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)

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

Besides 55 patients with renal artery stenosis in our department 5 occlusions of renal artery and some other rare but clinically very important causes of renovascular hypertension are reported. All these casuses of an angiotensin-renin mechanism given in general the indication for operative procedure. The very low risk of renovascular revascularisation justifies this operative indication.
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PMID:[Particular causes of renovascular hypertension]. 64 90

Plasma renin activity (PRA) and concentration, measured after acid treatment of the plasma (PRC3.3), were determined on the same plasma samples in different conditions. Log PRA and log PRC3.3 were significantly (P less than 0.001) and similarly related to sodium intake, age, and plasma aldosterone concentration in normal subjects. The correlation coefficient between log PRA and log PRC3.3 was 0.49 in 80 sodium-replete and sodium-deplete normal subjects, and it was 0.84 in 84 hypertensive patients untreated or under treatment with thiazides. On the contrary, during beta adrenergic blockade, PRA decreased significantly (P less than 0.001) by 62% while the changes in PRC3.3 were not significant. At maximal exercise, PRA increased significantly by 168% while the PRC3.3 increase of 24% was not significant. In hypertensive patients with unilateral renal artery stenosis the ipsilateral renal vein/artery ratio was higher for PRA (2.46) than for PRC3.3 (1.56), whereas both ratios on the controlateral side were similar and close to one (1.14 and 1.06). The conditions in which PRA and PRC3.3 determinations are concordant or discordant are discussed.
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PMID:Relative significance of plasma renin activity and concentration in physiologic and pathophysiologic conditions. 65 65

Percutaneous transluminal dilatation of a left sided renal artery stenosis was performed in a 61 year old patient with hypertension. Biochemical and hemodynamic activity of the renal artery stenosis was demonstrated by measurement of renal venous renin-activity and determination of renal plasma flow and of pre- and poststenotic blood pressure values. Shortly after the dilatation procedure hypertension disappeared and renal plasma flow increased. The described procedure might be an alternative method to renal vascular surgery.
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PMID:Percutaneous transluminal dilatation: a new treatment of renovascular hypertension? 67 42

A patient had unilateral renal artery stenosis and, at the same time, bilateral polycystic kidney disease. The renal venous renin ratio of 151:40, together with a high peripheral plasma renin activity, indicated that the hypertension was partially caused by renopressor mechanism. Correction of the obstructive lesion permitted a better control of hypertension with antihypertensive drugs, and the peripheral and renal venous renin activity returned to normal. The success in detecting one pathogenic mechanism responsible for arterial hypertension should not deter further diagnostic efforts.
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PMID:Renal artery stenosis and polycystic kidney disease. 67 87

Pressor responses to norepinephrine (NE) infusions were examined in normal rabbits, in rabbits with renal artery stenosis of over 30 days' duration (chronic renal hypertensive rabbits), and in rabbits with renal artery stenosis of 3 days' duration (3-day clipped rabbits). The 3-day clipped rabbits did not have hypertension, but they showed the same increased pressor responses to NE as did the chronic renal hypertensive rabbits, which was about 2.5 times that of the normal rabbits. Plasma renin activity (PRA) was the same in the 3-day clipped rabbits as in the normal group, but in the chronic renal hypertensive rabbits the PRA was significantly below normal. Infusions of angiotensin II (A II) in either subpressor or pressor amounts potentiated the pressor responses to NE in normal rabbits, whereas, in 3-day clipped rabbits and chronic renal hypertensive rabbits, A II in subpressor or pressor doses did not alter the pressor responses to NE. Infusion of the A II antagonist, [1-sarcosine, 8-isoleucine]angiotensin II, did not alter the pressor responses of normal rabbits to NE, but this A II analogue completely abolished the pressor hyperresponsiveness to NE in the 3-day clipped rabbits and greatly reduced the NE hyperresponsiveness in the chronic renal hypertensive rabbits; this A II antagonist did not alter the control arterial pressure in any of the three groups of rabbits. These studies show that the increased pressor response to NE in rabbits with renal artery stenosis occurs before the onset of hypertension and thus is not merely a result of the hypertension. Also, these results provide evidence that A II plays an important role in the increased pressor responses to NE in hypertensive and prehypertensive rabbits.
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PMID:Pressor responses to norepinephrine in rabbits with 3-day and 30-day renal artery stenosis. The role of angiotensin II. 67 26

Over an 18-month period nine infants in a neonatal intensive care unit developed hypertension (blood pressure, 115/88 to 280/140 mm Hg) at 2 to 45 days of age. Eight of the nine infants had indwelling umbilical artery catheters prior to onset of hypertension; six of the nine infants had evidence of a patent ductus arteriosus. Peripheral plasma renin activity was greater than 300 ng/ml/3 hr in six of eight infants. Angiograms were abnormal in six of seven infants and computerized renal scans were abnormal in all nine infants. One infant had congenital renal artery stenosis. Eight of nine infants had evidence of unilateral or bilateral renal artery thrombi which were felt to have emanated from an umbilical artery catheter or a ductus arteriosus. Hypertension in all infants was successfully controlled medically (follow-up of 3 to 27 months; mean, 14.4 months). Blood pressures remained normal when medication was discontinued. In our experience, neonatal renovascular hypertension is no longer uncommon, responds to aggressive medical management, and rarely requires early nephrectomy. Neonatal renovascular hypertension was usually associated with umbilical artery catheters positioned above the level of the renal arteries.
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PMID:Nonsurgical management of renovascular hypertension in the neonate. 68 86

A new method was developed for separate kidney function studies by catheterizing the ureters and exteriorizing the catheters through the urethra into the vagina. Renal artery plication was performed to reduce blood flow to one kidney by 66 +/- 5%. Arterial pressure increased from 107 +/- 2 to 131 +/- 3 mmHg and remained elevated for 28 days. Plasma renin activity was increased for the first 7-10 days only. Sodium and water excretion were markedly reduced in the kidney with the stenosed renal artery and after the first 2 days Na and water excretion were incresed in the contralateral kidney. These changes in Na and water excretion were frequently associated with similar directional changes in glomerular filtration rate (GFR) and renal plasma flow. An exception was noted in that renal sodium and water excretion remained low throughout the 28 days in the kidney with the constricted renal artery, whereas GRF returned to near the control level by the end of 2 wk. Altered filtration fraction did not appear to be a determining factor in control of the rate of Na excretion. It is suggested that GFR, the renin-angiotensin-aldosterone system, and other as yet undefined factors are involved in salt and water homeostasis during unilateral renal artery stenosis with hypertension.
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PMID:Separate renal function studies in conscious dogs with renovascular hypertension. 69 70

From our consecutive series of renal vein renin studies in 170 patients with kidney disorders and hypertension, we present those cured by surgical correction of a unilateral renal artery stenosis during the period 1973--75. The renin secretion patterns of these patients range between no demonstrable abnormality, even with a stimulating procedure using dihydralazine 7.5 i.v., and massive renin secretion already during basal conditions. Thus, the renin secretion may not be increased even after stimulation in some patients with durable unilateral renovascular hypertension. This fact may be explained by the rise of the systemic blood pressure, eventually maintained by sodium and water retention and accompanied by adaptive changes in the contralateral kidney. The perfusion pressure is thereby kept normal in the affected kidney, eliminating a stimulus for renin secretion. It is likely that many cases of renovascular hypertension pass through an early stage where no involvement of the renin-angiotensin system may be discovered. Of course, these patients will also benefit from surgery. The conclusion is that renin studies for diagnostic purposes should be performed when patients are on treatment and kept normotensive for some time, and that an additional challenge of the perfusion pressure, i.e., by use of dihydralazine, intravenously should be performed.
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PMID:Observations on the use and limitations of renal vein renins in hypertensive patients. 69 82

The effect of saralasin, a competitive inhibitor of angiotensin II, was assessed in hypertensive patients with unilateral renal artery stenosis after furosemide application. A significant fall of systemic arterial blood pressure, an increase of renal venous renin activity, significantly on the stenosed side in patients without arteriosclerosis of the contralateral kidney, and an almost equal decrement of renal blood flow in both kidneys were observed. Conceivably saralasin exerts different sodium-dependent effects on peripheral angiotensin II and specific intrarenal vascular receptors.
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PMID:Effects of saralasin on blood pressure, renin and renal blood flow in unilateral renovascular hypertension. 69 87


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