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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent research shows that the renin-angiotensin-aldosterone axis either maintains or causes some or all of the high blood pressure of most patients and demonstrates anew that renin-sodium profiling defines this involvement. Performed with a serum potassium measurement, this now reliable test is useful for primary screening and then, in conjunction with renal vein renin studies or an aldosterone profile, for diagnosis or exclusion of surgically curable renovascular or adrenocortical hypertensions. For the remaining majority with essential hypertension, renin profiling exposes the relative participation of either vasoconstriction or volume factors, thereby guiding simpler, more specific, and predictably effective antirenin or antivolume treatments. Renin profiling identifies those in whom treatment should begin with a beta-blocker as opposed to a diuretic while not infrequently also providing baseline information about severity and prognosis in individual patients.
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PMID:Renin profiling for diagnosis and treatment of hypertension. 3 92

Renal hypertension of the two-kidney type is divided into three stages. In the first, hypertension results from the vasoconstrictor effect of angiotensin II. This persists to some extent in the second phase but there is in addition a slow-developing pressor effect, also resulting from angiotensin II and probably attributable to sodium. In the first two phases removal of the abnormal kidney corrects the hypertension. This fails in the third phase because changes in the opposite kidney maintain hypertension. Renin and angiotensin are probably not involved at this stage.
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PMID:Mechanism of renal hypertension. 5 63

Hormonal contraceptive treatment results in considerable stimulation of the renin-angiotensin-aldosterone system. Hepatic synthesis of renin substrate increases by a factor of 2.5-4. As a result, more angiotensin I an angiotensin II are released. Angiotensin II stimulates adrenal aldosterone production, producing a higher plasma aldosterone concentration. Urinary aldosterone secretion rises less, probably because binding of aldosterone to plasma proteins is increased at the same time. Renin release is suppressed to 50% by negative feedback mechanisms. Other factors in the etiology of hypertension may include effects on sodium balance and on the sensitivity of the blood vessels to pressure-regulating substances.
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PMID:[Changes of the renin-angiotensin-aldosterone system under contraceptive steroids. Contribution to the etiology of hypertension under hormonal contraceptives]. 18 75

The renin-angiotensin system has an important role in maintaining elevated blood pressure levels in certain forms of experimental and human hypertension. Renin, an enzyme produced by the juxtaglomerular cells of the kidney, acts on a protein substrate found in the alpha 2-globulin fraction of the plasma to produce a decapeptide, angiotensin I. This decapeptide is not directly pressor, but on passage through the pulmonary circulation is converted to an octapeptide, angiotensin II, a very potent pressor substance which acts by causing constriction of arteriolar smooth muscle. In addition to its direct action which increases blood pressure, angiotensin II acts on the adrenal cortex to cause the release of the sodium-retaining hormone aldosterone. Recent evidence suggests that this action may be mediated by the heptapeptide, angiotensin III. Both renin and its protein substrate exist in multiple forms and renin may also exist as a high molecular-weight "pro-hormone," although the physiologic significance of these forms is not clear. The elucidation of the biochemistry of the renin-angiotensin system has provided us with inhibitors which allow the system to be blocked effectively in vivo. Thus, angiotensin antagonists such as Sar 1, IIe 8-angiotensin II and converting enzyme inhibitors such as BPP 9a (SQ 20881) have proved useful in the study of experimental and human hypertension.
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PMID:The biochemistry of the renin-angiotensin system and its role in hypertension. 19 Aug 80

1. Renin-associated, chronic psychosocial hypertension of 150-160 mmHg develops in groups of mice interacting socially in complex population cages. 2. The blood pressures of 16 males in a cage were measured and an intraperitoneal injection of the angiotensin coverting enzyme inhibitor captopril (SQ 14,225) was given. Three hours later blood pressures were measured again. 3. During the first 3 weeks of psychosocial hypertension SQ 14,225 was without effect. But at 1 month and subsequently up to 7 months, SQ 14,225 reduced blood pressure to the normal range of 120-130 mmHg. 4. Plasma renin activities were not related to the extent of blood pressure reduction by SQ 14,225. Hence other factors in addition to the renin-angiotensin mechanism play a part in maintaining chronic psychosocial hypertension.
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PMID:Effects of an angiotensin converting enzyme inhibitor on psychosocial hypertension in mice. 23 19

1. Aorta homogenate contains renin-like activity which on incubation generates angiotensin I over a wide pH range. 2. Rat aortic renin measured at an incubation pH of 6.5 rose and fell in parallel to plasma renin with salt depletion and salt-loading respectively. Renin little relationship with plasma renin. 3. Aortic renin (pH 6.5) was elevated in Goldblatt-two kidney hypertension and slowly fell for 24h after bilateral nephrectomy whereas the fall in plasma renin was complete by the first hour. Aortic renin (pH 5.3) was also high, but did not fall after bilateral nephrectomy. 4. Aortic renin (pH 6.5) is probably derived from plasma renin whereas renin measured at pH 5.3 is probably a tissue renin. 5. The prolonged half-life of aortic renin (pH 6.5) explains the observation that the renin-angiotensin system appears to be active in maintaining blood pressure for several hours after bilateral nephrectomy whereas the decline in plasma renin is rapid and does not continue significantly beyond 1 h.
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PMID:Role of persistent vascular renin after bilateral nephrectomy in Goldblatt-two kidney hypertension. 28 58

The complex hormonal action of angiotensin II in the long-term control of blood pressure or sodium metabolism, or in renal hypertension, is not completely understood. Structure-activity relations with analogues of angiotensin II gave information about the functions responsible for pressor and myotropic response in the molecule that led to the synthesis of competitive antagonists of this hormone. These antagonists, however, show variable agonist/antagonist ratios in different species or different tissues of the same species. This fact necessitates further work to induce tissue specificity. Although des-Asp1-angiotensin II ("angiotensin III") has been recognized as a hormone, its exact role in the biosynthesis of aldosterone is yet to be discovered. The antagonists such as des-Asp1-[Ile8]-angiotensin II or des-Asp1-[Thr8]-angiotensin II have provided important leads in this direction. Many of the biologic effects of angiotensin I have been attributed to its conversion to angiotensin II by the converting enzyme. Recent investigations indicate that angiotensin I itself may play a direct role; however, most of these studies were carried out by inhibiting the converting enzyme activity with peptides obtained from the venom of Bothrops jararaca. Since these peptides also potentiate bradykinin action, the observed biologic activities could be caused by either angiotensin I or bradykinin. Bsides, converting enzyme is no longer thought to be a single enzyme and its nature varies from species to species and from tissue to tissue in the same species. Renin inhibitors related to renin substrate or pepstatin are not freely soluble in plasma and are not effective under physiologic conditions. This points to the importance of renin inhibitors isolated from kidney or other natural sources. Thus, although the renin-angiotensin system appears to be an integral part of the problem of hypertension, characterization of various converting enzymes, roles of extrarenal renin, isorenin, tonin, and brain-renin, and the involvement of other humoral, neurogenic, and immunogenic factors should be pieced together to get a clear picture of the hypertension problem.
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PMID:Pathogenic factors involved in renovascular hypertension. State of the art. 32 61

Renin-aldosterone profiling was used to classify patients with hypertension: 243 patients with essential hypertension were classified by renin-urinary sodium indexing; 107 were reclassified by response to administration of furosemide and intravenous saline; 45 were further classified by response to a low-sodium diet. Arbitrary "normal ranges" were determined in 89, 32, and 38 volunteers, respectively. Patients with low-renin apparently do not have "high-volume" hypertension. Rather, they show a primary renal abnormality in renin secretion and become relatively deficient in angiotensin II and aldosterone when they are subjected to diuresis. They can maintain aldosterone secretion under normal conditions because their adrenal aldosterone receptor is supersensitive to angiotensin II. No evidence of abnormal sympathetic neural activity was found among the renin subgroups. Renin-aldosterone profiling in current clinical practice seems useful mainly in the detection of patients with curable forms of secondary hypertension. Aldosterone/renin ratios may be particularly helpful in diagnosis when obtained after a patient has undergone expansion or contraction of his extracellular fluid volume.
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PMID:Renin-aldosterone profiling in hypertension. 33 42

Post-transplant hypertension has been observed in 98 renal allograft recipients who had good renal function and whose follow-up was more than 15 months. The role of the original diseased kidneys as well as the role of the renal pressor system was studied with emphasis on late hypertension. Post-transplant hypertension was found to be a multifactorial phenomenon with frequency decreasing as a function of prolonged graft survival. Renal artery stenosis was an infrequent but significant cause of hypertension and was found in 10 of 29 arteriograms performed. Renin studies performed in 34 hypertensive patients and in a control group of 11 recipients showed that elevation of plasma renin activity and of plasma aldosterone level is frequent but difficult to interpret, particularly when a renal artery stenosis is observed. These investigations may be useful in recognizing the role of retained diseased kidneys in sustaining hypertension. Plasma aldosterone was found elevated in nearly all of the patients. The role of corticosteroids and the similarity of post-transplant hypertension, in some cases, with the one kidney model of experimental hypertension are discussed.
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PMID:Late hypertension following renal allotransplantation. 37 92

Furosemide and hydrochlorothiazide were compared for treatment of black patients with mild to moderate hypertension in a randomized, open-label, crossover study design. Hydrochlorothiazide produced a significantly greater fall in mean arterial (24.7 vs 16.0 mm Hg, P less than .01) and diastolic (17.3 vs 10.1 mm Hg, P less than .01) blood pressure (BP) in 16 patients. Addition of methyldopa in nine patients produced a significantly greater fall in mean arterial (38.8 vs 31.9 mm Hg, P less than .05) and diastolic (28.9 vs 23.4 mm Hg, P less than .05) BP with hydrochlorothiazide vs furosemide. Renin status was categorized before and after treatment. Patients with low and normal renin activity were equally responsive to both diuretics. Hydrochlorothiazide caused a greater reduction in plasma potassium (0.26 mEg/L). Serum parathyroid hormone was not chronically elevated with furosemide. In this study, hydrochlorothiazide was more effective than furosemide for treatment of mild to moderate hypertension in black patients; renin classification did not predict diuretic responsiveness.
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PMID:Antihypertensive comparison of furosemide with hydrochlorothiazide for black patients. 38 33


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