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

Renal arteriography gives a reliable anatomic delineation of the renal vasculature. However, the presence of renal arterial disease does not determine the physiologic significance of the lesion. The intravenous infusion of saralasin, a specific angiotensin II antagonist, has been investigated as a method for identifying patients with hypertension dependent upon excessive angiotensin II activity. Correlations between the blood pressure response to saralasin infusion, peripheral and differential renal vein plasma renin levels and renal angiography have been obtained in 35 hypertensive patients. The results suggest that a hypotensive response to saralasin infusion provides an adjunct to renin determinations for recognizing angiotensinogenic renovascular hypertension. However, false negative responses to saralasin occur. The reasons for these negative responses need to be determined before saralasin infusion can be employed as the sole screening test for renovascular hypertension.
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PMID:Clinical experience with saralasin infusion in hypertensive patients. 59 Dec 50

We assessed the role of the renin-angiotensin system in the response of the renal circulation to restriction of sodium intake in 38 normal patients. Both saralasin (10 to 30 ng/kg/min), an angiotensin antagonist, and SQ 20881 (30 to 300microgram/kg), a converting enzyme inhibitor, induced a dose-related increase in renal blood flow (xenon 133 washout) only when the resin-angiotension system was activated by restriction of sodium intake to 10 MEq/day. Increasing doses of saralasin (100 to 1,000 ng/kg/min) reduced renal blood flow, presumably due to the angiotensin-like action of this partial agonist. The renal vascular response to SQ 20881 paralleled the endocrine response: An identical threshold dose (30 microgram/kg) increased renal blood flow and reduced plasma angiotensin II concentration, which fell despite a progressive rise of plasma renin activity. Plasma bradykinin concentration did not change in response to SQ 20881, which also blocks kininase II. Both agents also induced a small but consistent and statistically significant reduction in arterial blood pressure, which will be important in assessing the pathogenetic significance of a blood pressure reduction in patients with hypertension. This study indicates that angiotensin mediates the renal vascular response to restriction of salt intake in normal man and provides an approach to assessing the role played by angiotensin in the pathogenesis of functional renal disease.
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PMID:Renal vascular response to interruption of the renin-angiotensin system in normal man. 59 39

Prevention of conversion of angiotensin I to angiotensin II by means of a converting enzyme inhibitor, the nonapeptide SQ 20.881, in chronic hypertensive mice was followed by a drop in blood pressure in all mice independent of the ethiology of hypertension; in conscious normotensive mice was observed a significant decrease in blood pressure, which, however, was less than that observed in the hypertensive mice.
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PMID:Effects of the nonapeptide SQ 20.881 on the blood pressure of conscious normotensive and chronic hypertensive mice. 60 80

Angiotensin II was infused at rates varying from 0.1 to 10 ng/kg per minute into 49 subjects with hypertension and 26 normotensive subjects and changes in blood pressure, plasma angiotensin II, and plasma renin activity (PRA) were determined after 20 and 30 minutes at each dose. Similar dose-related increases in angiotensin II and blood pressure occurred with a threshold of 1 ng/kg per minute in the normotensive and hypertensive subjects. Whereas angiotensin II induced a significant, dose-related decrement in renin activity in the normotensive subjects, with a threshold of 1.0 ng/kg per minute, no significant change in renin activity occurred in either the normal-renin or high-renin hypertensive subjects. In a separate study, nine normotensive and six hypertensive sodium-restricted subjects were given a converting enzyme inhibitor, SQ 20881, 30 microgram/kg. Despite a significantly greater fall in blood pressure (P less than 0.006) and angiotensin II concentration (P less than 0.045) in the hypertensive subjects, they did not have a greater rise in plasma renin activity. We conclude that angiotensin II reduces renin release in normal man at infusion rates that yield plasma angiotensin II levels within the physiological range but has a strikingly reduced influence on renin release in hypertension. In high-renin hypertension due to renal artery stenosis or nephrosclerosis, renin release is presumed to be relatively autonomous because of a dominant, intrarenal mechanism. The mechanism in normal-renin essential hypertension is not clear, but the abnormality could well be related to the pathogenesis of the hypertension.
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PMID:Failure of renin suppression by angiotensin II in hypertension. 61 2

Hypertension in patients on chronic hemodialysis is thought to be largely of two types--volume dependent or renin dependent. If renin-dependent hypertension is mediated by angiotensin II, then angiotensin II antagonism should lower blood pressure. To test this hypothesis, the angiotensin II antagonist saralasin was given to 15 hypertensive patients on chronic hemodialysis. Patients were separated into two groups by their blood pressure response. In responders blood pressure was 191/112 mm Hg and fell to 147/85 during saralasin administration (P less than 0.01). In contrast, nonresponders had blood pressures of 190/111 mm Hg before and 188/110 during saralasin administration. Five responders subsequently ahd nephrectomies with normalization of their blood pressures. Plasma renin activity averaged 70 ng/ml . 3 h of angiotensin I in responders and increased to 110 after saralasin (P less than 0.05), while nonresponders had values of 21 before and after saralasin. These results offer strong support for the hypothesis that renin-dependent hypertension is an important mechanism in certain patients on chronic hemodialysis and that such patients will respond to angiotensin II antagonism.
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PMID:Effect of saralasin in hypertensive patients on chronic hemodialysis. 61 54

1. Angiotensin II blockade before and after marked sodium depletion in patients with hypertension [unilateral renovascular (eight), bilateral renovascular (four) and essential (four)] was performed by intravenous administration of the angiotensin II antagonist Sar1-Ala8-angiotensin II (saralasin). 2. On normal sodium intake, saralasin decreased mean blood pressure by 8 mmHg in the unilateral renovascular group, by 6 mmHg in the bilateral renovascular group and increased it by 3 mmHg in the essential hypertensive group. After sodium depletion saralasin decreased mean blood pressure by 33 mmHg, 35 mmHg and 18 mmHg respectively. The saralasin-induced decrease in blood pressure significantly correlated with the log of the initial plasma renin activity. 3. Saralasin infusion decreased effective renal plasma flow (ERPF) in all three hypertension subgroups, both on normal sodium intake and after sodium depletion. Glomerular filtration rate decreased in direct relation to the hypotensive effect of saralasin but ERPF showed this relationship only after sodium depletion. On normal sodium intake saralasin increased filtration fraction by 17%, but decreased it by 7% after sodium depletion. 4. It is concluded that the hypotensive action of saralasin closely correlates with the value of circulating plasma renin activity, apparently independent of the aetiology of the hypertension. The decrease in ERPF during saralasin infusion in the patients on normal sodium intake seems mainly related to the agonistic activity of saralasin, but that after sodium depletion to the hypotensive effect of saralasin.
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PMID:Angiotensin II blockade before and after marked sodium depletion in patients with hypertension. 62 Apr 96

Previous work has shown that parathyroidectomy protected Sprague-Dawley rats against mineralocorticoid hypertension. 2 In order to explain this protection, we studied vascular reactivity to noradrenaline and angiotensin II in several groups of rats with and without their parathyroid and thyroid glands. Work was performed in vagotomized, anaesthetized rats after ganglionic blockade with pentolinium, and atropine sulphate. 3 The reactivity to noradrenaline was significantly lower in parathyroidectomized rats, especially at the beginning of mineralocorticoid treatment. 4 Autotransplantation of parathyroid glands in thyroparathyroidectomized rats re-established normal cardiovascular reactivity and development of hypertension. 5 Cardiovascular reactivity to angiotensin II was not affected in parathyroidectomized rats and was lowered in thyroparathyroidectomized thyroxine-treated rats.
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PMID:Effect of parathyroidectomy on cardiovascular reactivity in rats with mineralocorticoid-induced hypertension. 62 36

We have studied the effects of intravenous infusion of saralasin, a competitive antagonist of angiotensin II, in 27 hypertensive patients: 13 had essential hypertension, 14 had renal lesions which involved the renal artery in 9 cases. In essential hypertensives saralasin administration did not significantly lower blood pressure, even after mild salt depletion. It induced a decrease in blood pressure in 7 patients with renal abnormalities (5 with renal artery stenosis, 2 with unilateral parenchymal disease). It may be suggested that in these cases hypertension was dependent, at least partly, on the renin-angiotensin system. In agreement with other investigators, we have found a relationship between the level of plasma renin activity and the blood pressure decrease obtained by saralasin. In patients with unilateral renal artery stenosis, blood pressure decrease was related to renal vein ratio of plasma renin activity.
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PMID:[Clinical usefulness of saralasin in human hypertension (author's transl)]. 64 79

The angiotensin II (AII) antagonist [Sar1-Ala8]AII (Saralasin) was injected into the brain ventricles (IVT) and intravenously (IV) in five different types of hypertensive unanesthetized rats. Renal hypertension was studied 16-22 days after kidney clipping. Intravenous infusions of cumulative doses (0.1-100 microgram/kg per min) and IVT injections (5-40 microgram) of Saralasin did not change mean arterial pressure (MAP) in controls and in one-clip, one-kidney Goldblatt hypertension, whereas MAP decreased in one-clip, two-kidney Goldblatt hypertension following IV and IVT Saralasin. In two-clip, two kidney hypertensive rats, IVT Saralasin decreased MAP but was ineffective when infused IV. Both IV and IVT Saralasin increased MAP in DOC hypertension. In spontaneously hypertensive (SH) rats, IV Saralasin increased MAP; IVT injection decreased MAP. The effect of IVT Saralasin in SH rats persisted 15-20 h after nephrectomy. We conclude that plasma AII may contribute to peripheral and central mechanisms of blood pressure regulation. The dissociation of the effects of IV and IVT Saralasin and the persistance of blood pressure decrease in nephrectomized SH rats following IVT Saralasin further support a role for locally formed brain angiotensin.
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PMID:Effects of central and peripheral angiotensin blockade in hypertensive rats. 64 31

Transient hypertension occurred in 3 patients shortly after blunt injury to the abdomen. Renal trauma was suspected in all 3 patients and radiological evidence for renal injury was present in 2. Plasma renin activity definitely was elevated in 1 patient and probably was elevated in another. There was a decrease in blood pressure in all 3 patients during infusion of the angiotensin II analogue--saralasin--showing that the hypertension in these patients was angiotensin-mediated. Renal function as reflected by the blood urea nitrogen, creatinine and electrolytes was not impaired significantly. Thus, acute hypertension after blunt abdominal trauma may be angiotensinogenic and is not necessarily sustained.
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PMID:Renin angiotensin involvement in transient hypertension after renal injury. 65 Jul 71


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