As a result of the constriction and, consequently, the increased total peripheral resistance and arterial pressure, left ventricular afterload increases pari passu, providing the major haemodynamic determinant for the structural ventricular adaptation of left ventricular hypertrophy and the associated events of hypertensive heart disease.
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These precapillary changes are associated with generalized constriction of the postcapillary venules, which reduces total body venous capacity. The simultaneous events of arteriolar and venular constriction relate to several pathophysiological 1.
As a result, the circulating intravascular volume is redistributed from the periphery to the central circulation to increase venous return to the heart i. This intravascular volume redistribution phenomenon 1 has been demonstrated clinically in patients with essential hypertension as well as in naturally occurring or other experimental forms of hypertension.
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Thus, early in the development of hypertension, systemic venoconstriction may not be associated with intravascular volume contraction 1. However, as arteriolar and venular constriction 1 progresses, capillary hydrostatic pressure increases and circulating intravascular volume diminishes. This is probably the consequence of two factors: movement of plasma from the circulation into the extravascular compartment and renal excretion of some of the circulating volume as arterial pressure increases i. The intravascular i. Thus, as diastolic and mean arterial pressures or total peripheral resistance increase in hypertensive patients with essential hypertension or with 1.
In contrast, patients with parenchymal disease of the kidney demonstrate an increased plasma volume as diastolic 1. The four pressure determinants of transcapillary fluid migration elucidated by Starling. The role of pre- and postcapillary tone in regulating plasma volume. Contraction of plasma volume in men with essential hypertension as diastolic A or mean arterial B pressures increase or as total peripheral resistance increases in male hypertensive patients with essential hyprtension or renal arterial disease C.
Unlike polycythaemia rubra vera, there is neither a leucocytosis or thrombocytosis, nor is there associated splenomegaly. This relative increase in red cell mass with a reduced plasma volume has been measured in a large number of patients with essential hypertension. In contrast, some patients have a volume-dependent essential hypertension in whom the magnitude of plasma volume is directly related to the height of arterial pressure Table 1.
This, then, provides an explanation why those patients with essential hypertension have plasma volume contraction may lose effective control of arterial pressure when they are treated only with an adrenergic inhibitor or a direct acting, smooth muscle relaxing vasodilators e. Thus, plasma volume expands as pressure is reduced with treatment and, under these conditions, blood pressure control can then be restored with diuretic administration. Indeed, this explains 1. It provides an explanation for the transudation of protein through the retinal capillary bed in patients with accelerated hypertension as well as those with papilloedema associated with malignant hypertension see Chapter 2.
A third example relates to development of oedema in patients receiving calcium antagonists. This oedema is the consequence not of renal-mediated fluid retention but, rather, of the potent drug-induced precapillary arteriolar dilatation associated with reflex postcapillary constriction.
This is particularly experienced with prolonged standing or when seated for a long time with the legs dependent. High cardiac output hypertension A fourth example of the phenomenon of pre- and postcapillary constriction provides, in part, a pathophysiological explanation for the increased cardiac output and hyperdynamic circulation observed during development of essential hypertension. Thus, early in the elaboration of hypertension i.
This increased output is related to the translocation of the circulating intravascular volume from the periphery to the central circulation as a result of the postcapillary i. With progression of the hypertensive vascular disease and, as the pre- and postcapillary vasoconstriction increase further, the intravascular i. This contraction in circulating intravascular volume proportionally diminishes the cardiopulmonary volume, decreases right atrial venous return and, thus, the cardiac output is reduced to a more normal level than the output observed earlier in the disease.
Nephrosclerosis A fifth example, which has more recently become appreciated clinically, relates to the increased intraglomerular hydrostatic pressure in patients with hypertensive nephrosclerosis i. Thus, both afferent and efferent glomerular arteriolar constriction occurs in patients with prolonged systemic arterial hypertension, with renal parenchymal involvement favouring elevated glomerular hydrostatic capillary pressure, glomerular ultrafiltration of protein, and consequent hyalinosis and glomerulosclerosis.
With therapeutic reduction of afferent and efferent arteriolar resistance with angiotensin-converting enzyme inhibitors or angiotensin II receptor blockade , glomerular hydrostatic pressure will also diminish in association with reduced filtered protein and reversal or inhibition of further progression of glomerular sclerosis see Chapter 6. These findings provide credibility to the concept that angiotensin II participates in the progression of nephrosclerosis in essential hypertension as well as in diabetic renal disease; they also strongly suggest that inhibition of angiotensin II confers significant benefit to these patients.
Fluid volume partitions As originally postulated by Starling, local haemodynamic and other pressure alterations are responsible for the movement of water across the major body fluid 1.
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These factors include the local compartments 1 capillary hydrostatic and local tissue pressures as well as the protein oncotic pressures, intravascularly and extravascularly. In general, total body water is normal in essential hypertension and seems to be normally distributed between the extracellular and intracellular fluid compartments. However, although there is much epidemiological evidence suggesting deranged sodium handling in patients with hypertension, there is little evidence supporting the concept that total body sodium is increased in hypertensive disease or that it is associated with expanded total body water or, even, increased blood pressure sensitivity.
In contrast, emerging data suggest other effects of sodium excess on heart, aorta, kidney, and vessels. In addition, there is good clinical investigative evidence that the extracellular fluid volume may be maldistributed in hypertension. Thus, as intravascular i. This movement of fluid from the intravascular to the extravascular including interstitial fluid compartments has specific pathophysiological 1. Sodium metabolism As suggested above, many epidemiological studies have demonstrated a direct correlation between the magnitude of dietary sodium intake and the prevalence of hypertension in many populations.
Other studies have shown that in those societies with daily sodium dietary intakes of i. The major problem lies in the elusive ability to define just which patients with essential hypertension are sodium sensitive and those which are not. The best proof in the individual patient is to restrict sodium intake to see if blood pressure becomes reduced. The subject currently remains one of great controversy. As we describe later, salt excess is associated with structural and functional derangements of the target organs of the disease.
Hormonal alterations Because of the controversial role of sodium in essential hypertension, many studies have focused upon the role of adrenal corticosteroids and their regulatory genes in the pathogenesis of hypertension in at least some patients. There have been very few patients with essential hypertension who have demonstrated an abnormality of steroidal mechanisms underlying the hypertension disease process.
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In general, aldosterone seems to be synthesized, released, and excreted in proportion to the levels of stimulation of the renin—angiotensin system in patients with essential hypertension; there does not seem to be any clearcut derangement in adrenal steroid biosynthesis in such patients. Recent studies in many of these secondary hypertensions have demonstrated specific genetic enzymatic abnormalities that account for the steroidal defect.
Hormonal alterations have been demonstrated in other patients with hypertension Table 1. Neural mechanisms The autonomic nervous system normally participates in the control of arterial pressure; this role may be altered in patients with essential hypertension. One would normally expect that, as arterial pressure increases, heart rate should slow.
However, most patients with essential hypertension demonstrate a faster resting heart rate than normal. In addition, increased release, sensitivity, and excretion of norepinephrine noradrenaline has been repeatedly demonstrated in patients with essential hypertension and, more frequently, in patients with borderline or earlier stages of the disease.
The elevation of serum catecholamine concentration in these patients, however, is not nearly as high as in patients with phaeochromocytoma. It is of interest that in patients with less severe essential hypertension, particularly those with a hyperdynamic betaadrenergic circulatory state with or without idiopathic mitral valve prolapse syndrome , serum norepinephrine noradrenaline concentration is frequently elevated.
This finding provides one explanation for the altered haemodynamic findings as well as the augmented myocardial contractility, the idiopathic mitral valve prolapse, and the associated cardiac dysrhythmias. In general, there have been no alterations reported in catecholamine biosynthesis or in release or reuptake of these substances, although increased responsiveness of beta-adrenergic receptor sites has been reported see Chapter 5.
Furthermore, the reported altered responses to upright tilting, Valsalva manoeuvres, and tyramine stimulation of norepinephrine noradrenaline release from nerve endings may provide a useful indication of adrenergic neural participation in certain patients with essential hypertension. Several years ago, the clonidine suppression test was introduced to differentiate patients with phaeochromocytoma from those patients with essential hypertension who demonstrate smaller elevations of plasma catecholamines.
Clonidine a centrally acting adrenergic inhibitor administration will suppress elevated catecholamine levels to Table 1. Renopressor system The enzyme renin is released from the juxtaglomerular apparatus of the kidney through several mechanisms Table 1.
Renin acts on its circulating peptide substrate angiotensinogen, produced in the liver, resulting in the 1. The generation of the pressor octapeptide angiotensin II 1 octapeptide apparently generates other peptides whose actions are under active investigation. Angiotensin II has a number of sites of action, most notably in blood vessels and adrenal cortex, to produce vasoconstriction and aldosterone release, respectively.
In addition, angiotensin is also generated locally in heart, vessels, kidneys, and other organs with specific local actions Table 1. The precise roles for these local systems are not yet clearly known but intracellular generation of angiotensin II affects muscle protein synthesis, with inherent implications relating to the development or reversal of vascular and ventricular hypertrophy.
Local generation of angiotensin II may be of particular importance in: a the function of the cardiac or arteriolar myocyte which produces the peptide an intracrine function ; b the effect on neighbouring cells an autocrine function ; or c association with other hormones e. Measurement of plasma renin activity PRA has important clinical implications not only in the classification of patients with essential hypertension, but in other hypertensive diseases including renal arterial disease and steroidal forms of hypertension see Chapters 2, 6 and 7.
In this fashion, certain agents may exert their physiological actions most subtly by acting in concert with other substances. It is well known, for example, that angiotensin II can augment or amplify adrenergic function by its interaction with norepinephrine noradrenaline at certain brain centres, as well as at peripheral ganglionic or postganglionic sites.
Angiotensin may also interact with kinins and prostaglandins in kidney, with atrial peptides at nerve endings, on the cardiac myocyte at the vascular smooth muscle membrane, and with other peptides e. Another possible example of this modulatory cardiovascular action occurs with L-arginine, nitric oxide, and bradykinin at the endothelial level to alter local haemodynamic functions. Endothelial dysfunction i. These dysfunctions may be modified by agents that are used to manage these conditions and, hence, may reverse endothelial dysfunction.
Their effects upon cells and their possible roles in atherogenesis. In: Atherosclerosis. KT Lee ed. Annals N. The first report demonstrating that the ;4 initial functional derangement of the ventricle myocytic stretch initiates the process of hypertrophy through stimulating DNA-mediated protein synthesis. It provides a model for many subsequent studies.
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Hypertension 18 Suppl. Most interestingly, these mitogenic factors in atherosclerosis may be the same factors that participate in hypertension, thereby offering a conceptual explanation as to how one disease exacerbates the other. Page IH: Hypertension Mechanisms. Grune and Stratton, Orlando, FL; Page IH: Pathogenesis of arterial hypertension. Page lecture: The mosaic of hypertension: past, present, and 6 Suppl. These future.
Hypertension ;6 three references provide discussions on the mosaic concept of Page relating to the multifactorial nature of hypertension and left ventricular hypertrophy. These three references are clinical Cardiol. The third reference provides that first support to the former discussions on the clinical, structural, and functional progression of hypertensive heart disease. Relationship to arterial pressure levels in different hyper— These three references are Circulation ;4 studies that develop the concept of fluid volume alterations in clinical hypertensionand the functional correlates of PRA in patients with essential hypertension.
Sealeyj E, Laragh JH: The renin—angiotensin—aldosterone system for normal regulation of blood pressure and sodium and potassium homeostasis. In: Hypertension: Pathophysiology, Diagnosis, and Management.
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