Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the effect of prostaglandin inhibition on the renal blood flow of the ischemic kidney, we administered indomethacin to 10 anesthetized dogs with renal artery stenosis and contralateral nephrectomy. Following the operation to produce renal ischemia, there was an increase of blood pressure associated with an increase of renin and the prostaglandins F1 (PGF1), and E (PGE). The administration of indomethacin to the intact, normotensive animals caused the anticipated decrease of prostaglandin E, renin, and renal blood flow. However, in the hypertensive dogs, indomethacin caused a paradoxical 45 per cent increase in the renal blood flow, despite a 44 per cent decrease of prostaglandin E. PGF1, PGE, renin, and erythropoietin exhibited the anticipated decreased levels. The study suggests that prostaglandins may not be the sole important factor in the regulation of renal blood flow in the presence of ischemia. Other important factors likely include the renin-sensitive angiotensin, the adrenergic, and the kallikrein-kinin systems.
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PMID:Paradoxical increase of renal blood flow in anesthetized hypertensive dog treated with indomethacin. 48

We have described a case which documents two possible surgical correctable causes for hypertension in a 55-year-old white man. Preoperative renal arteriograms and renal vein renin determinations suggested the possibility of renal artery stenosis due to fibromuscular hyperplasia. At operation, a pheochromocytoma was found in the left suprarenal area. The presence of two unusual causes for hypertension in a single patient suggests that more than one remediable cause of hypertension should at least be considered in a given hypertensive patient.
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PMID:Pheochromocytoma and fibromuscular hyperplasia. 50 91

The rare opportunity arose to assess in detail the renin-angiotensin system before and after the development of a renal artery stenosis with severe hypertension. Peripheral plasma concentrations of renin, angiotensin II, and aldosterone were known to be normal before the development of renal artery stenosis, and there were no lateralising features on renal vein sampling. Acute hypertension associated with very high peripheral plasma concentrations of renin and angiotensin II, and with pronounced lateralisation on renal vein sampling followed the development of acute unilateral renal artery stenosis. These measurements all returned to normal after nephrectomy, conforming with the pattern of changes previously established only in experimental animals.
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PMID:Renal artery stenosis with severe hypertension. A rare case with detailed assessment of renin-angiotensin system before and after development of lesion. 50 79

A positive saralasin test in patients with angiographic evidence of renovascular disease and other positive functional tests gives further assurance that these patients will achieve normal or substantially reduced blood pressure postoperatively. In our experience with proved renovascular hypertension there was a 19% incidence of falsely negative saralasin tests. Therefore, saralasin should not be used as the sole screening test in hypertensive patients suspected of having surgically correctable lesions. There is a direct correlation between elevated renin activity and a positive saralasin test. In some patients saralasin may be more sensitive than any other currently used test to detect overactivity of the renin-angiotensin system. This would determine those patients with technical errors in renin sampling and assays. Of the 16 patients (all normotensive) who had 6-month followup tests 5 had elevated peripheral renin activity, probably owing to furosemide stimulation. Of these 5 patients 2 had a positive postoperative saralasin test, raising the question of potential falsely positive responses in cases of essential hypertension and coincidental non-functional renal artery stenosis. Patients with high renin essential hypertension may respond to saralasin, even in the absence of renal artery lesions. A saralasin test should be done in a hospital where all specific conditions can be met and potential complications handled promptly.
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PMID:Saralasin test as a diagnostic and prognostic aid in renovascular hypertensive patients subjected to renal operation. 54 21

The findings at preoperative nephroangiography of 42 hypertensive patients with unilateral renal artery stenosis or occlusion were correlated with the blood pressure response following surgery and also with the preoperative renal vein renin activity ratio. A stenosis reducing luminal area by at least 90 per cent (or occlusion) and the presence of collateral circulation are considered to be highly suggestive of renovascular hypertension.
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PMID:Unilateral renal artery stenosis and hypertension. II. Angiographic findings correlated with blood pressure response after surgery. 54 71

Clinical data, arteriographic findings, peripheral and renal vein plasma renin activity (PRA) studies and responses to prostaglandin A1 infusion are presented from observations in seven hypertensive patients with renal artery stenosis. PGA1 infusion caused an increase in PRA and urine sodium excretion but no significant change in blood pressure. Exaggerated increases in PRA were observed in five patients. With cessation of PGA1 infusion PRA returned toward pre-infusion levels. In two patients bilateral renal and peripheral vein PRA's were determined before and during PGA1 infusion. PGA1 caused a greater increase in renal vein PRA than in peripheral vein PRA indicating a direct enhancement of renin secretion. These studies indicate possible relationships between the vasoactive prostaglandins and the renin-angiotensin system in the pathogenesis of hypertension due to renal artery stenosis.
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PMID:Effect of prostaglandin A1 infusion in hypertensive patients with renal artery stenosis. 56 75

The prognostic value of renal vein and peripheral renin levels was analyzed in 66 patients with unilateral renal artery stenosis who underwent corrective surgery. Patient selection for operation was independent of renin results. Fifty-three percent of those with confirmed renovascular hypertension had renal vein renin ratios less than 2.0, ie, within the 95% confidence limit for the control group of 82 patients with essential hypertension. Thirty-four patients with clearly lateralizing renin data (ipsilateral:contralateral greater than or equal to 1.5 and contralateral:peripheral less than or equal to 1.3) were benefited by operation, but 23 additional patients with nonlateralizing data also benefited. No proposed scheme for renin data analysis detected more than 75% of those with renovascular hypertension. Although lateralizing renin data are highly predictive of operative benefit, nonlateralizing data do not necessarily herald operative failure and should not be dogmatically used to exclude surgical intervention.
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PMID:Predictive value of renin determinations in renal artery stenosis. 57 97

Male Sprague-Dawley rats with unilateral renal artery stenosis and a contralateral untouched kidney develop a malignant hypertension (MH) which is characterized by high blood pressures, sodium and water depletion, and subsequent activation of the renin-angiotensin system. In the present studies we found plasma arginine vasopressin (AVP) concentrations-3-fold higher than those in rats with benign renal hypertension, and 4- to 5-fold higher than those in normotensive control rats. Analysis of individual values showed considerable scatter; about 50% of the values fell in the range of benign hypertensive or control rats. When a specific AVP antiserum was injected, iv, into eight conscious unrestrained MH rats, BP transiently fell toward control values in four; in one, BP fell by only 10 mm Hg, and three other MH rats showed no response. In the same rats, injection of a specific angiotensin II antiserum always induced a transient fall in BP. On the basis of these and previously reported observations, we conclude that, subsequent to sodium and water loss and activation of the renin-angiotensin system, vasopressin release is stimulated in a significant number of MH rats and that, in these rats, vasopressin may cause significant systemic vasoconstriction. Thereby vasopressin may contribute to the development of malignant renal hypertension in rats.
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PMID:Plasma vasopressin concentrations and effects of vasopressin antiserum on blood pressure in rats with malignant two-kidney Goldblatt hypertension. 61 98

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

The effect of total adrenalectomy on the mechanisms of arterial pressure control was studied in uninephrectomized rats with and without renal artery stenosis (Goldblatt one-kidney model). Four groups of rats were prepared and maintained on high-salt intake (1% NaCl): uninephrectomized-KI; KI + adrenalectomy-KIAx; uninephrectomized with renal artery stenosis-GI; and GI with adrenalectomy-GIAx. Over 3 wk blood pressure rose significantly in both GI and GIAx but the degree of increase in GI was greater. Hyponatremia, hyperkalemia, and increased plasma urea nitrogen were observed in both KIAx and GIAx. Plasma renin concentration (PRC) and plasma renine activity (PRA) were markedly increased and plasma renin substrate (PRS) was decreased in both adrenalectomized groups. Infusion of saralasin resulted in significant and similar reductions in mean arterial pressure (MAP) in KIAx and GIAx, but had no effect on MAP in KI and GI. These results allow approximations of the contribution to total MAP of identifiable components, which are: the total adrenal component, the renin-angiotensin system component, which partially compensates for loss of the adrenal secretions, and the independent effect of the renal artery clip. Thus, a multifactorial analysis of GI hypertension is provided.
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PMID:Adrenal gland in experimental renal hypertension. 62 42


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