Cardiopulmonary Physiology Millersville University Dr. Larry Reinking Chapter 8 Regulation of Arterial Blood Pressure
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Cardiopulmonary Physiology
Millersville University Dr. Larry Reinking Chapter 8 - Regulation of Arterial Blood Pressure In terms of the body tissues, the most important aspect of the cardiovascular system is a continued and predictable flow of blood. Like an irrigation system, the best way to provide a predictable flow is to have a constant volume and closely regulated pressure head. In other words, pressure and rate of flow go hand-in-hand in the circulatory system. This chapter examines the mechanisms that maintain a constant pressure head in the cardiovascular system. Arterial Pressure Values In humans the typical arterial pressure, at rest, is 120/80 mm Hg (systolic/diastolic). These values seem to be ‘magic’ numbers in that many other mammals regulate arterial pressure at this level. This value for blood pressure is probably a compromise between sufficient pressure for tissue perfusion and the damaging effect of excessive pressure. Pulse pressure is the difference between systolic and diastolic pressures and equals 40 mm Hg under normal conditions. Mean arterial pressure cannot be determined by simply averaging systolic and diastolic pressures since an unequal amount of time is spent in each of these phases. It is determined by integrating the area on a pressure vs. time curve which gives a value of about 96 mm Hg. A reasonable approximation of the mean arterial pressure can be made by adding the diastolic pressure to one third of the pulse pressure. We will use the value of 100 mm Hg for mean arterial pressure because it is easy to remember. The above values are characteristic for healthy, young individuals. Blood pressure tends to rise with age due, in part, to arteriosclerosis. An equation that was previously introduced (chapter 3) will be useful for examining arterial blood pressure controls: 
where Pa is the arterial pressure, CO the cardiac output, RT the peripheral resistance and Pv is the venous pressure. Since cardiac output is the stroke volume (SV) times the heart rate (HR) we can expand the above equation to the following: 
Regulation of arterial pressure can be broken down into fast acting, short term controls and those that have a slow onset but act for a long duration. Short Term Controls Short term controls are immediate responses to disturbances in blood pressure that occur over periods of seconds, minutes or hours. Many of these responses are mediated by the nervous system. Since nervous mechanisms tend to adapt over time, many of these controls are not effective on a long term basis. Unlike long term controls, short term controls only make approximate corrections for disturbances in arterial blood pressure. The following are factors for consideration in short term control: Vasomotor Tone. The arteries, arterioles and veins are innervated only by sympathetic nerves . These sympathetic nerves are predominately vasoconstrictor fibers, however there are some sympathetic vasodilator fibers. Sympathetic vasodilator fibers appear to be relatively unimportant in humans, with a possible exception of the initiation of vasodilation in skeletal muscle at the onset of exercise. Vasoconstriction is brought about by the release of norepinephrine which binds to -receptors on the vascular smooth muscle. At rest, the vasomotor center of the brain sends continuous signals to the vascular smooth muscle via the vasoconstrictor fibers. Thus, under normal conditions, the blood vessels are partially constricted, a situation referred to as vasomotor tone. Note all organs are effected to the same degree by sympathetic stimulation. Sympathetic input (and response) is greatest in the kidney, gut, spleen and skin while sympathetic effects are less powerful in the skeletal muscle, cardiac muscle and brain. Vasodilation is brought about in two ways. The first, and most important, is inhibition of the vasomotor center, which will cause a decrease in sympathetic output to the vessels. In this case, vasodilation is really a case of less vasoconstriction. Secondly, vasodilation is directly mediated by nerves and includes a very minor -sympathetic vasodilation in the skeletal muscle, some sympathetic cholinergic mediated skeletal muscle vasodilation and, in the genital erectile tissue, parasympathetic vasodilation. It has been discovered in the last few years that these neuronal induced types of vasodilation are mediated by the local generation of nitric oxide (NO). Prior to the elucidation of its chemical structure, NO was known as the edothelium-derived relaxing factor (EDRF).
Vasoconstriction of arterioles increases peripheral resistance (RT in the previous equation). Upstream from the constriction, arterial pressure will rise. Downstream from this constriction pressures will drop and flow will be restricted in the capillary beds. As a result, capillary pressures drop and plasma volume increases (reference: microcirculation lab). Constriction of veins (venoconstriction) causes a decrease in venous volume, more blood return to the heart and, therefore, an increased cardiac output. Venoconstriction also causes a back-pressure on the capillary beds causing a fluid shift into the interstitial spaces.
This reflex involves nerve endings in the blood vessels of the neck and thorax. When stretched by increased arterial pressure, these nerves are excited and send signals to the brain. The appropriate brain centers respond by slowing the heart rate and by promoting vasodilation. There are two concentrations of baroreceptors (pressure sensors, also called pressoreceptors) in humans. The first is on the carotid sinus at the bifurcation of the internal and common carotid artery. These signals are carried to the brain by afferent fibers of the glossopharyngeal nerve. This point is an ideal position for monitoring pressure supply to the brain. The second concentration of baroreceptors lies on the aortic arch and these signals are carried by afferent fibers of the vagus nerve to the medulla of the brain. This location is a good point for monitoring the body pressure supply, in general.
In the above diagram, note that the overall responses to increased arterial pressure are vasodilation, mediated by the vasomotor center and decreased cardiac performance as influenced by the vagal center. Primary Function of the Baroreceptor Reflex - This reflex primarily buffers short term challenges to arterial blood pressure. Such a challenge would be encountered when going from a lying to a standing position. If the afferent nerves are blocked, in a dog, blood pressure has wide fluctuations but the average value remains at 100 mm Hg. In other experiments, the mean blood pressure was artificially raised to 200 mm Hg, afferent signals to the brain increased for one to two days and then returned to baseline. In this case the baroreceptor reflex 'adapted' so that it buffers changes at the new, average blood pressure. The above experiments indicate that the baroreceptor reflex has little importance in the long term regulation of average arterial pressure. Carotid Sinus Syndrome - In some cases, control by the baroreceptor reflex can be too effective. In older people especially, the carotid artery can harden and narrow. If pressure is placed on the neck, such as with a tight collar, strong afferent signals are sent to the brain causing extreme bradycardia and vasodilation. Dizziness, fainting (syncope) or cardiac arrest can result from stimulation of this type of over-excitable carotid sinus. Sometimes the carotid arteries are surgically 'stripped' of nerves to treat this syndrome. 2. Other Stretch Receptors Stretch receptors in the pulmonary artery and atria also help to buffer changes in blood pressure. These receptors act in a fashion similar to the systemic arterial baroreceptors in that they inhibit the vasomotor center via vagal input. Their action is much less pronounced than the previously discussed baroreceptor reflex. Atrial stretch also causes a reflex increase in the heart rate (Chapter 6, p. 3). A portion of this response is caused by an increased firing rate of the SA node. The remainder of the effect is mediated by a vagal reflex through the medulla (the Bainbridge reflex) and results in increased sympathetic stimulation of the heart. This reflex has a different purpose than the previous reflexes. Rather than altering blood pressure, this reflex adjusts the heart performance to match venous return. Thirdly, atrial stretch results in the release, into the circulation, of a peptide (Atrial Natriuretic Peptide, ANP) that causes a sodium diuresis by inhibiting the renin-angiotensin-aldosterone system and ADH release. This peptide has wide implications for volume and pressure control and will be dealt with in more detail at a later point. 3. Chemoreceptors The carotid bodies (at the bifurcation of the carotids) and the aortic bodies (on the aortic arch) receive a rich flow of blood and have the primary function of sensing arterial oxygen, carbon dioxide and pH levels. This information is used primarily to control pulmonary ventilation. As a secondary function, the carotid and aortic bodies also influence blood pressure. If the blood pressure drops, these bodies receive less perfusion and become hypoxic, hypercapnic and acidic. This situation causes an afferent signal, via the vagi, to excite the vasomotor center and blood pressure increases due to increased sympathetic discharge. This is a weak reflex and is not initiated until blood pressure drops below 80 mm Hg. 4. CNS Ischemic Response The central nervous system ischemic response is the most powerful response to diminished blood pressure. When brain perfusion becomes inadequate (ischemia), CO2 levels rise in the cerebrospinal fluid. Elevated CO2, in turn, has a potent stimulatory effect on the vasomotor center and results in intense sympathetic output. Arterial pressure will rise to levels as high as 270 mm Hg, the limit of cardiac abilities. The intense vasoconstriction will completely shut down some areas of the circulation such as the kidneys. Unlike other reflexes that are mediated by peripheral sensors, this response is directly initiated by an organ that is in trouble. The CNS ischemic response is a 'last ditch' effort used only in emergency situations. If brain ischemia is prolonged (>10 minutes) vasomotor activity is lost and the blood pressure drops to 40-50 mm Hg.
Recall that veins are capacitance vessels that contain a major portion of the circulating blood. The primary effect of sympathetic induced constriction of the veins is to reduce the volume of blood contained in this portion of the circulation. As a result, more blood is returned to the heart and, in accordance with the Frank-Starling principle, cardiac output increases. 6. Abdominal Compression Reflex An additional consequence of sympathetic out put from the vasomotor center is excitation of skeletal muscles and, especially, the abdominal muscles. This excitation increases muscle tone, compresses the abdomen and moves blood from the abdominal veins toward the heart. As a result cardiac output and blood pressure increase. This response is called the abdominal compression reflex. 7. ADH Another response to a drop in blood pressure is the release of a large amount of antidiuretic hormone (vasopressin) by the posterior pituitary. ADH is a potent vasoconstrictor and will also cause the retention of water by the kidneys (Chapter 7, p. 3). Water retention, in turn, expands blood volume, increases cardiac output and arterial blood pressure. 8. Adrenal Catecholamines Sympathetic stimulation also causes the adrenal medulla to release epinephrine and norepinephrine into the circulation. These compounds will have a positive chronotropic and inotropic effect on the heart. Epinephrine has mixed effects on vessels in various parts of the circulation. In cutaneous vascular beds, for example, it causes vasoconstriction but in skeletal muscle it promotes vasodilation. During strenuous exercise, peripheral resistance can actually drop due to the extensive skeletal muscle vasodilatory effect of circulating epinephrine. 9. RAAS The renin-angiotensin-aldosterone system plays a crucial role in the short regulation blood pressure since angiotensin II is a powerful and vasoconstrictor. The vasoconstrictor aspects of the RAAS take about 10-20 minutes to become fully effective. This effect is much slower than that of catecholamines and about half the speed of vasopressin. The duration of vasoconstriction, however, is much longer. The renin-angiotensin-aldosterone system also alters fluid volume and, thus, is critical part of long term regulation. 10. Delayed Compliance Recall (Chapter 3) that tone of the smooth muscle in blood vessel walls can 'adapt' to new situations by the process of stress-relaxation. An increase in blood volume will cause an initial increase in arterial pressure than will then drop due to the relaxation of blood vessels. This mechanism will allow a person to adapt to 30% increase or a 15% decrease in blood volume. 11. Fluid Shift A change in arterial pressure will result in a similar change in capillary pressure. If capillary pressure increases, more fluids will move from the capillary lumen into the interstitial spaces. As a result, blood volume decreases followed by a decrease in cardiac output and arterial blood pressure. A decrease in capillary pressure has an opposite effect. Long Term Controls Long term regulation of arterial blood pressure takes place over periods of days to years. Although the onset on these controls are slow, they are precise and powerful. Unlike a short term control which may be only an 80% fix, long term controls completely correct a disturbance in the average arterial blood pressure. In addition, these long term controls are durable; they will not adapt over time. Long term controls are mediated by the kidney. Renal Function Curve The most important aspect of long term control is the effect of blood pressure on renal function. An increase in blood pressure alters renal function and causes an increase in urine output and sodium excretion. These responses are called, respectively, a pressure diuresis and a pressure natriuresis. If arterial blood pressure drops, urine and sodium output decline. The renal function curve depicts this relationship: Figure 8.2 The Renal Function Curve 
Changes in urine and sodium output alter blood volume, cardiac output and, ultimately, blood pressure. Note that urine production stops at a blood pressure of about 50 mm Hg arterial pressure. This curve explains why a change in peripheral resistance can only have short term effects on blood pressure. Although there may be a substantial, short term increase in pressure, it can only be transient due to renal influence on extracellular fluid volume. Control Amplification - Renal Function and the Microcirculation Long term controls are very powerful because of an indirect effect on the microcirculation. An increased blood volume and cardiac output will enhance tissue nutrition, thus producing more constriction of the precapillary sphincters (refer to microcirculation lab). As a result, peripheral resistance increases and the blood pressure is further elevated. This sequence of events can be illustrated as follows: 
In experimental situations, a 2% increase in blood volume produces a 5% increase in filling pressure, a 5% increase in cardiac and, surprisingly, a 50% increase in arterial pressure. Influence of Salt on Extracellular Fluid Volume and Blood Pressure An increase in salt intake usually has a much greater influence on blood pressure than increased water intake. Salt has a strong influence on extracellular fluid volume for two reasons. First, an increased salt level in the blood alters blood osmolality and stimulates antidiuretic hormone release. As a result there will increased water reabsorption in the kidneys. Secondly, increased blood osmotic concentration stimulates the brain’s thirst center, more fluids are consumed and extracellular fluid volume increases. In comparison, increased water intake lowers blood osmolality and therefore ADH release and thirst are inhibited. Renin-Angiotensin-Aldosterone System As we saw in the previous section, The RAAS influences peripheral resistance via the production of angiotensin II. However, as explained with the renal function curve, this can only be a transient effect. The long term actions of the RAAS stem from its ability to alter renal function. The release of angiotensin II stimulates aldosterone release and, as a result, distal tubule sodium and water reabsorption increase. In effect, the RAAS causes a shift in the renal function curve. An increase in circulating angiotensin II causes a shift of the curve to the right. Thus, at a ‘normal’ renal function (normal urine production) there is an increased arterial blood pressure. In dogs, experiments have shown that a 2.5x elevation of angiotensin II caused a sustained 15 mm Hg increase in mean arterial pressure. In these same experiments, arterial pressure dropped to 75 mm Hg when angiotensin II production was completely blocked. RAAS and Salt Intake The most important aspect of the renin-angiotensin-aldosterone system may be in moderating the effects of salt intake on fluid volumes. In the presence of the RAAS a large intake of salt, in a normal subject has a small effect on blood pressure. During blockade of the RAAS, the same salt intake can cause the arterial pressure to rise by 60 mm Hg. The following diagram depicts the interaction of salt intake and the RAAS: 
Atrial Natriuretic Peptide (ANP) As noted in earlier chapters, stretching of the atria causes the release of a peptide hormone that promotes salt excretion (i.e., a natriuresis). Such an event would be the consequence of hypervolemia. This released peptide, which plays a major role in volume and pressure regulation, is called atrial natriuretic peptide. (A few years ago, the chemical nature of this hormone was unknown and it was called atrial natriuretic factor; this name persists in the current literature.) Atrial natriuretic peptide inhibits vasopressin release, interferes with the RAAS and increases urine flow. All of these actions reduce extracellular fluid volume, thus reversing the original stimulus. The following diagram (figure 8.3) summarizes the known actions of ANP: Figure 8.3 Actions of Atrial Natriuretic Peptide (ANP) 
Recently, two other ANP like peptides have been discoveved, brain natriuretic peptide and type C natriuretic peptide. The role and significance of these molecules is uncertain. Endothelin Endothelin is a recently discovered peptide hormone that is secreted by cardiac and vascular endothelial cells. It is the most potent known vasoconstrictor and has activity at concentrations of 10-10 M. Actually, endothelin is a family of peptides based on a similar 21 amino acid sequence. At this date, at least four forms of endothelin have been identified (ET-1, ET-2. ET-3 and VIC, vasoactive intestinal constrictor). In addition to causing constriction of vascular smooth muscle, endothelin causes bronchoconstriction, contraction of intestinal smooth muscle and has a positive inotropic effect on cardiac muscle. All of these actions are a result of endothelin-mediated increases in intracellular calcium levels. Another interesting feature of endothelin is that it also acts as a growth factor, causing proliferation of vascular and cardiac muscle. This effect may be significant in understanding the pathophysiolgies of, respectively, pulmonary hypertension and cardiac hypertrophy during heart disease. Endothelin levels increase during heart disease. This observation and the various actions of endothelin suggest that it is involved in a wide range of disease states including hypertension, coronary artery disease, renal failure, congestive heart failure, myocardial infarction, and pulmonary disorders. Obviously, the endothelin area is an active focus of cardiovascular research. The development of endothelin 'blockers' , for example, could have tremendous potential for the treatment of heart disease. Hypertension Hypertension is defined as a persistent arterial blood pressure that exceeds 140/90 mm Hg. This term does not refer to an excitable, anxious personality. In the United States, at least 30 million individuals have hypertension (1993 estimate) and about 12% of the deaths in this country can be linked be to this disease. Clinical observations over the past decade have determined that the presence of hypertension is the most reliable factor for predicting mortality in individuals with cardiovascular diseases. Hypertension is a problem for two reason; increased cardiac after-load and vascular damage. Increased Cardiac After-load - As previously discussed (p.1, chapter 6), striated muscle performs poorly with after-load type work. When presented with high arterial pressures, left ventricular muscle hypertrophies and can actually triple in size. Unfortunately, the coronary blood supply does not increase in proportion with the muscle increase. Thus, poor blood flow to the myocardium develops. This situation becomes progressively worse throughout the course of severe hypertension. Vascular Damage - Persistent high blood pressure will damage the endothelium of blood vessels. This damage causes narrowing of vessels (arteriosclerosis) and potentiates the possibility of blood clot formation on the vessel walls. Small vessels may actually burst with prolonged, severe hypertension. The most serious types of vessel damage include 1) coronary blood vessel arteriosclerosis, 2) cerebral hemorrhage (i.e., a stroke), 3) damage to the vessels of the retina and 4) damage to vessels of the renal glomerulus. The last type of damage will lead to renal insufficiency, worsened hypertension due to a shift in the renal vascular curve and, ultimately, renal failure. Classification of Hypertension In only about ten percent of the cases can a clear cause for the elevated blood pressure be determined. When a clear cause can be identified, the term secondary hypertension is used. Most types of hypertension are primary hypertension ( also called essential hypertension or idiopathic hypertension), that is, there is no clear etiologic factor. Systolic hypertension is the result of hardening of the arteries and is most common in the elderly. In this type of hypertension a normal stroke volume produces only elevated systolic pressure. Systolic hypertension is also seen in cases of high cardiac output. The most common type of hypertension is diastolic hypertension and is usually associated with vasoconstriction. Causes of Secondary Hypertension The following types of hypertension have clear pathophysiological causes and, therefore, are potentially treatable: Endocrine Hypertension - This type of hypertension is the most common type of secondary hypertension and is the result of overproduction of a hormone, typically by a tumor: Chromaffin tissue tumor - This type of tumor, in the adrenal medulla, produces excess amounts of epinephrine and, especially, norepinephrine. The -receptor activation by norepinephrine causes vasoconstriction while the cardiac -receptor effects include increased heart rate and stroke volume. Conn’s Syndrome - Conn’s syndrome is the result of an adrenal cortex tumor that secretes excess aldosterone. Salt and water retention result in excess extracellular fluid volume and hypertension. As a result of increased potassium secretion, this syndrome is characterized by low serum potassium and muscle weakness. (Recall that potassium secretion is linked to sodium reabsorption in the distal tubule.) Cushing’s Syndrome - As a result of another type of adrenal cortex tumor, glucocorticoids such as cortisol are produced in excess. These hormones increase sensitivity to norepinehrine and like aldosterone, but to a lesser degree, have sodium retaining actions. Renovascular Hypertension Renovascular hypertension is the result of a narrowed renal artery. The resulting decreased sodium load and decreased blood flow to the juxtaglomerular apparatus causes activation of the renin-angiotensin-aldosterone system. In experimental situations a type of renovascular hypertension, called Goldblatt hypertension, can be induced by placing a restricting clip on the renal artery. Oral Contraceptives In a small number of cases, women taking oral contraceptives develop hypertension. Blood pressure usually returns to normal when the contraceptive therapy is stopped. Essential Hypertension (Idiopathic Hypertension) Essential hypertension is, in all probability, a collection of many diseases which may involve defects in any of the blood pressure controls that have been discussed in this chapter. This area of medicine has an enormous amount of literature, numerous opinions, many conflicting findings and can be quite confusing. The following are some features and ideas concerning essential hypertension: Vascular Reactivity - In most cases of essential hypertension there is increased vascular reactivity to situations, like exercise or stress, that increase sympathetic output. It is uncertain if the cause is increased background sympathetic output or hypertrophy of smooth muscle. In addition, individuals with essential hypertension have exaggerated vascular responses to external stimuli such as angiotensin injections, salt loading or norepinephrine infusions. Psychogenic Factors - On a short term basis, anxiety, fear and stress can cause elevated blood pressure via increased sympathetic output. In certain stressful occupations (e.g., air-traffic controllers, bus drivers) the incidence of long term hypertension is higher than the normal population. Certain personality types have also been linked with a higher occurrence of hypertension. Shift in the Renal Function Curve - In essential hypertension there is a shifting of the renal function curve to the right: Figure 8.4 Hypertension and the Renal Function Curve
Thus, a normal urine output is associated with an elevated mean arterial pressure. This shift to the right could be caused by a large number of factors that include, for example, a) constriction of the renal arteries via anatomical defects or hormonal influences b) increased sodium reabsorption by the distal tubule or c) renal disease. Renal function declines in older people and may contribute to age related hypertension by causes a shift in the renal performance curve.. Genetic Factors - Essential hypertension appears to be a genetically determined illness that is inherited in a polygenetic fashion. Like other polygenetic traits such as height, there will be distribution of individuals; those on the upper end of the curve will have hypertension. The expression of essential hypertension is further complicated by environmental risk factors such as diet. Identical twins have similar blood pressures as adults. Blacks have twice the incidence of hypertension and 17 times the incidence of kidney failure when compared to the white population in the U.S. Sodium and Hypertension - In 1981 the American Heart Association recommended that Americans alter their eating habits and strive to reduce sodium intake from a national average of 12 grams per day to four or five. It is widely agreed that there are sodium sensitive individuals who will develop hypertension. For the general, normotensive portion of the population, however, a relationship between dietary sodium and hypertension is inconclusive. The hypothesized sodium-hypertension link is based on the following types of indirect evidence: Cross Cultural Studies - 'Primitive societies' such as inland Amazonas tribes have very low salt intakes, low blood pressure, no strokes and no age related increase in blood pressure. Traditional cultures with high salt intake (e.g., Japanese fishing villages where salted fish is part of the daily diet) have elevated blood pressure and a high incidence of strokes. Renal Disease - Humans and laboratory animals with impared renal function are sensitive to dietary salt intake. An increased sodium load will result in an elevated arterial pressure. Animal Models - A number of laboratory animal strains exist that spontaneously develop hypertension. In many of these strains an increased dietary sodium causes increased blood pressure. It is interesting that if a kidney is transplanted from a 'genetic hypertensive' animal, the recipient of the organ soon develops hypertension. This evidence suggests a renal origin for this disease. Diuretics and Antihypertensives - Diuretics are known to increase the excretion of sodium and to lower blood pressure in certain individuals, especially those with renal disease. Most antihypertensive drugs work better with sodium restriction. Attempts to illustrate a firm link between sodium intake and blood pressure in the general population have not been very successful. The Intersalt Study, for example, involved more than 10,000 healthy subjects and showed that over a wide range of salt intakes, mean arterial blood pressure varied by less than one mm Hg. Sodium and Chloride - In sodium sensitive individuals and lab animals sodium must be accompanied by chloride to induce hypertension. An intake of a large amount of sodium bicarbonate, for example, does not produce an elevated blood pressure. The same is true for chloride in the absence of sodium. Potassium - It has been argued that the low blood pressure seen in cultures having a low sodium diet is really due to high potassium intake. Several (but not all) all epidemiological studies have shown a that blood pressure is inversely related to the dietary intake of potassium. Calcium - Diets high in sodium are usually low in calcium. Diets low in calcium have been linked to hypertension during pregnancy. At least two studies have shown that individuals that consume <300 mg calcium/day have two to three times the likelyhood of developing hypertension as compared to those consuming >1200 mg calcium/day. Similar types of results have been found with animal models. Sodium Pump, Calcium and ANP - It is suspected that some forms of essential hypertension involve an ANP mediated ihhibition of the sodium-potassium pump in vascular smooth muscle. The following diagram depicts a possible scenario: Figure 8.5 Possible Role of ANP and Sodium Pumps in Vasoconstriction
An inhibited sodium pump would decrease the transmembrane sodium gradient and diminish the amount of sodium entering through the Na/Ca exchanger. Intracellular levels of calcium would rise and, as a result, more muscle contraction occur. Vasoconstriction is the final result of this scheme. Magnesium - Magnesium is also suspected as playing a role in hypertension. In Finland, heart disease and hypertension is much higher in areas that have low magnesium levels in the soil. In the mid 1980's the Finnish government conducted a field trial in which potassium and magnesium chloride were added to table salt in certain regions of the country. The results were striking. After four years of data collection it was found that the areas that received magnesium and potassium spiked table salt had lower average blood pressures and a 25% reduction in heart attack deaths. Nitric Oxide - Recall that nitric oxide mediates vasodilation (Chapter 8, p.2). In one strain of spontaneously hypertensive rats, the elevated blood pressure has been linked to a deficient production of nitric oxide. No human case of nitric oxide deficiency has been demonstrated yet. Essential Hypertension Summary Comment The previous section deals with various aspects of essential hypertension and, as you have noticed, is a 'laundry list' without much of a unifying theme. In this regard, the above section mirrors the current understanding and treatment of essential hypertension. This is a complex and frustrating area in clinical medicine that will require much more study before integrative concepts become evident. Sources and Further Reading Grossman, J.D. and J.P. Morgan. 1997. Cardiovascular effects of endothelin. News Physiol. Sci. 12: 113-117. Chapter 8 Yüklə 46,49 Kb. Dostları ilə paylaş:
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