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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long considered a single clinical entity, essential hypertension is now recognized as a heterogeneous spectrum of pathophysiologic disturbances, based on extensive clinical, pharmacologic and biochemical evidence. Two distinctly different mechanisms for long-term vasoconstriction can be identified and quantified in the spectrum of patients with essential hypertension, although the causes of this group of disorders are still obscure. The first vasoconstrictor mechanism is renin-angiotensin mediated and involves an increase in vascular smooth muscle cytosolic free calcium mobilized from intracellular sites. The degree of activity of this mechanism can be assessed by plasma renin level and/or by the hypotensive response to circulating anti-renin-system drugs (such as CEI inhibitors and beta blockers). The second vasoconstrictor mechanism, on the other hand, is renin-independent. It appears to require antecedent renal sodium retention and to be related to abnormal membrane influx of calcium. A low plasma renin level identifies this kind of vasoconstriction, which is also characterized by a low serum ionized calcium. Low-renin vasoconstriction is correctable by sodium depletion or by calcium channel or alpha adrenergic blockade. Depending on the state of sodium balance, these two vasoconstrictor mechanisms contribute reciprocally to maintenance of arteriolar tone in models of experimental hypertension, normotensive and hypertensive people, and in the vasoconstriction of edematous states, such as congestive heart failure. One of the two mechanisms also sustains diastolic hypertension in the experimental and clinical forms of renovascular hypertension and primary aldosteronism. Thus, both experimentally and clinically, at the polar extremes of the range of plasma renin values, one of the two mechanisms predominates: it is possible that, in the medium range of renin values, both mechanisms contribute to vasoconstriction. In our proposed unifying, analytic model, arteriolar vasoconstriction is associated with increased intracellular calcium and decreased magnesium levels in vascular smooth muscle. In the vasoconstriction consequent to sodium-volume expansion, cytosolic calcium is increased by an increased membrane influx. In renin-mediated vasoconstriction, receptor-operated channels mobilize cytosolic calcium instead from intracellular stores. These interrelationships provide a basis for stratifying hypertensive patients pathophysiologically and for applying simpler, more specific, and more rational therapies. Thus, the array of modern pharmacologic agents can often be rationally directed at one or the other, or both, of these two vasoconstrictor mechanisms.
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PMID:Recognizing and treating two types of long-term vasoconstriction in hypertension. 305 33

Two different mechanisms for long-term vasoconstriction that sustain diastolic hypertension in the experimental and clinical forms of primary aldosteronism and renovascular hypertension can also be identified and quantified among patients with essential hypertension. The first is renin-independent, requires antecedent sodium retention, and appears related to abnormal membrane transport of calcium. This vasoconstriction is identified by low plasma renin and ionized calcium values and is correctable by sodium depletion or calcium channel or alpha-blockade. The second is renin-mediated but also involves an increase in cytosolic calcium. This mechanism is quantifiable by the plasma renin level and by the hypotensive response to an anti-renin-system drug (CEI inhibitor, saralasin, beta-blocker). At the very extremes of the range of plasma renin values encountered in hypertensive patients, one of the two mechanisms predominates, whereas in the medium range of renin values either or both mechanisms can be operative.
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PMID:Pathophysiology of diastolic hypertension. 307 77

Ten years of experience with three different converting enzyme inhibitors (CEI; teprotide, captopril and enalapril) in over 300 hypertensive patients reveals that CEI act largely to block renin-angiotensin mediated vasoconstriction. Thus, their effectiveness or lack of it is predicted by the baseline plasma renin measurement. Accordingly, responses to these pharmacological agents can be used to identify and quantify renin-mediated vasoconstriction in the spectrum of hypertensive diseases. The converse is also generally true. Patients failing to respond to CEI exhibit low renin values and their increased peripheral resistance appears related to other mechanisms, possibly involving a subtle increase in total body sodium. Thus, low renin states such as low-renin essential hypertension, primary aldosteronism, and anephric man exhibit little or no response to CEI. The relationship between the renin system activity and effectiveness of CEI reflects a specific interference with a particular pathogenic mechanism which is further supported by the fact that two other types of renin system inhibitors (beta-blockers and saralasin) are similarly effective or ineffective according to the operant renin profile also by studies in patients with congestive heart failure without hypertension in whom the same relationships can be demonstrated. Like hypertensives, heart failure patients exhibit a broad spectrum of renin activity values, and their pretreatment renin levels predict the responses to CEI. We have also found that plasma renin values in heart failure are dependent on sodium intake. When salt is administered, renin falls and patients then become unresponsive to CEI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Converting enzyme inhibition to identify and treat renin-mediated or sodium-volume related forms of increased peripheral resistance in hypertension and in congestive heart failure. 608 35

The renin-angiotensin-aldosterone hormonal axis is the major long-term servocontrol for regulation of both arterial blood pressure and sodium balance. It supports normotension or hypertension via angiotensin vasoconstriction and angiotensin plus aldosterone-induced renal sodium retention. Normally, in the presence of hypertension or sodium-volume excess, plasma renin activity promptly falls to zero. Accordingly, any renal secretion of renin in the face of high blood pressure is abnormal. In established essential hypertension varying degrees of abnormal plasma renin activity operate to cause or sustain the hypertension; only very low plasma renin values reflect a normal renal response. Human hypertensive disorders comprise a spectrum of abnormal plasma renin-sodium volume products. High renin, intensely vasoconstricted, hypovolemic forms (e.g., malignant, renovascular) are one extreme of the spectrum; "wet"-volume-excess low-renin forms are the other extreme (e.g., primary aldosteronism, low-renin essential hypertension). These varying, but abnormal renin-sodium products are caused by a renal lesion in which a subpopulation of ischemic nephrons hypersecretes renin and retains sodium despite systemic hypertension and sodium excess. Thus, hypertensive patients cannot suppress their renin secretion normally. The hypertension from this renal lesion is correctable by agents that reduce renin secretion or block its effect (beta blockade, CEI, renin inhibition, or angiotensin II antagonism). None of these agents lower blood pressure after binephrectomy, verifying the renal origin of renin in the cardiovascular control system. In essential hypertension, the plasma renin level appears as a continuous variable associated with greater risk of ischemic injury.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The renin system and new understanding of the complications of hypertension and their treatment. 849 72

Although vascular compliance, deltaV/deltaP, is abnormal in essential hypertension and can be improved by antihypertensive drug therapy, it is not clear whether drug-induced changes in compliance are attributable solely to lower achieved blood pressure (BP), and thus equally likely with different drugs possessing similar antihypertensive efficacy. Therefore, we used computerized arterial pulse waveform analysis (CAPWA) to measure capacitive (C1) and oscillatory (C2) components of arterial compliance in essential hypertensive subjects (n = 39) before, and 1 and 3 months after achieving normotensive BP values with administration of either dihydropyridine calcium channel antagonists (CaBl, n = 11), converting enzyme inhibitors (CEI, n = 9), angiotensin receptor blockers (ARB, n = 9), or beta-blockers (BBl, n = 10). Despite equivalent effects on BP (CABL: -19 +/- 4/-15 +/- 2 mm Hg; CEI: -12 +/- 3/-13 +/- 2 mm Hg; ARB: -10 +/- 3/-12 +/- 2 mm Hg; and BBl: -14 +/- 3/-12 +/- 2 mm Hg; P <.005 for each drug v pretreatment), CaBl, CEI, and ARB significantly increased arterial compliance (CaBl: %deltaC1 = 30.0 +/- 5.8, %Delta C2 = 43.7 +/- 23.3; CEI: %deltaC1 = 32.7 +/- 5.4, %deltaC2 = 26.7 +/- 7.1; ARB: %deltaC1 = 36.3 +/- 11.8, %deltaC2 = 43.6 +/- 23.1; P <.01 for CaBl, CEI, and ARB v pretreatment), but BBl did not (%deltaC1 = -3.9 +/- 7.6, %deltaC2 = -7.0 +/- 11.5, P = not significant v pretreatment, sig = 0.01 v other drugs). We conclude that for an equivalent effect on BP, arterial compliance improves after therapy with some, but not all antihypertensive drugs. We hypothesize that a greater clinical benefit may result from the preferential use of drugs that concomitantly improve arterial compliance.
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PMID:Differential effects of antihypertensive drug therapy on arterial compliance. 1246 Jul 7