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)

The effect of saline loading was compared in two types of experimental acute renal failure--due to i.m. administration of glycerol or to anoxia. In the glycerol model, chronic saline loading for about three weeks prior to the experiment achieved almost complete prevention of the uremia. The blood urea and serum creatinine levels 24 h after the experiment were 44 +/- 2 and 1.3 +/- 0.3 se) mg/dl, respectively. The values for the water-drinking rats were 292 +/- 23 and 3.7 +/- 0.4 mg/dl, respectively. In the anoxic model of acute renal failure, produced by uninephrectomy and contralateral renal artery clamping, chronic saline loading reduced the severity of the resultant uremia, although less impressively than in the glycerol model. The blood urea and serum creatinine 24 h after the experiment were 148 +/- 15 and 1.8 +/- 0.2 mg/dl, respectively. The values for the water-drinking rats were 237 +/- 15 and 2.3 +/- 0.2 mg/dl, respectively. Plasma renin activity was similar in the saline-loaded rats in both the toxic and anoxic models. It seems, therefore, that all known models of acute renal failure have at least a common pathogenic mechanism, which can be influenced by chronic saline loading prior to onset of the disease, and which is most probably not renin dependent. In the anoxic model additional factors, which cannot be counteracted by chronic saline loading, are active in the development of uremia.
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PMID:Chronic saline loading in anoxic renal failure in rats. 101 45

1. Indomethacin inhibits prostaglandin synthesis and interferes with renin release; these effects were studied in rabbit renovascular hypertension. 2. Ten intravenous injections (3 mg day-1 kg-1 after two initial doses of 9 mg/kg) of indomethacin were given daily to ten normal rabbits, ten rabbits with two-kidney Goldblatt hypertension (2KH), tension (1KH). Twelve appropriate control rabbits received diluent phosphate buffer without indomethacin. Plasma renin activity and plasma prostaglandin E2 were measured by radioimmunoassay. 3. In the normal group, indomethacin significantly decreased plasma prostaglandin E2 (1-15 to 0-2 ng/ml, SEM 0-2; P less than 0-01) and plasma renin activity (20 to 3 ng h-1 ml-1, SEM 1, P less than 0-01). Plasma creatinine increased slightly but the mean blood pressure was not significantly changed by indomethacin. 4. Six of ten rabbits with 2KH showed results similar to those in the normal rabbits. In four of ten rabbits in which development of 2KH was accompanied by increments in plasma renin activity (18 to 31-5 ng h-1 ml-1, SEM 3 and 4 respectively; P less than 0-01) and plasma prostaglandin E2 (1-2 to 3-4 ng/ml, SEM 0-2 and 0-4 respectively; P less than 0-05), treatment with indomethacin produced renal failure (plasma creatinine increasing to 7-6 mg/100 ml), oliguria, malignant hypertension (mean blood pressure, 168 mmHg, SEM 7-7) and death within 5 days. 5. In 1KH, indomethacin decreased plasma renin activity and plasma prostaglandin E2, but caused increased mean blood pressure (102 to 121 mmHg, SEM 4 and 6 respectively; P less than 0-01) and decreased renal function (plasma creatinine 0-9 +/- 0-04 to 3-5 +/- 1 mg/100 ml, SEM 0-04 and 1 respectively; P less than 0-01). 6. Aggravation of hypertension was conditioned by pre-existing levels of renal function and, to a lesser extent, by plasma renin activities. 7. These results suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.
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PMID:Effects of indomethacin in rabbit renovascular hypertension. 107 20

1. A group of patients with essential hypertension was divided into three categories on the basis of the plasma renin activity. 2. There was no correlation between the plasma renin activity categorized as high, normal or low and the duration of hypertension, the incidence of left ventricular enlargement, the blood urea nitrogen, serum creatinine, cholesterol or uric acid respectively. 3. Analysis of data showed that the incidence of cardiovascular events in the hypertensive population correlated with the plasma renin activity only in combination with known risk factors.
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PMID:Plasma renin activity and cardiovascular disease. 107 64

The effects of chlorthalidone, spironolactone and propranolol in reducing blood pressure were compared in the same 11 normoreninemic hypertensive patients. All three drugs decreased the blood pressure significantly and no agent had a superior blood pressure-lowering effect. The blood pressure did not normalize. The data suggest that no one variable--volume factors, relative hyperactivity of the renin-aldosterone system or beta-adrenergic hyperactivity--is the prime mover in normoreninemic hypertension. Long-term treatment with chlorthalidone resulted in slight hyperreninism (26.3 +/- 4.9 ng-ml-1-3 hours-1) (mean +/- standard error) with concomitant changes in plasma aldosterone (23.0 +/- 3.2 ng-100 ml-1). The body weight decreased significantly (--1.8 kg, P less than 0.005). Plasma potassium concentrations were low (3.2 +/- 0.1 mEq-liter -1). Creatinine clearance was unimpaired (117 +/- 6 ml-min-1). Treatment with spironolactone resulted in more marked hyperreninism (47.0 +/- 14.3 ng-ml-1-3 hours-1) and hyperaldosteronism (61.9 +/-11.8 ng-100 ml-1). The body weight decreased significantly (--1.9 kg, P less than 0.004). Significant hyperkalemia occurred (4.4 +/- 0.1 mEq-liter-1). The glomerular filtration rate decreased significantly to 93 +/- 3 ml-min-1 (P less than 0.004). Treatment with propranolol resulted in marked suppression of the plasma renin activity (1.8 +/- 0.2 ng-ml-1-3 hours-1) and plasma aldosterone levels (8.9 +/- 1.3 ng-100 ml-1). A significant increase in body weight occurred (+2.3 kg, P less than 0.013). The plasma potassium concentration increased to a level not significantly different from the value found after treatment with spironolactone (4.2 +/- 0.1 mEq-liter-1). The creatinine clearance decreased significantly to 99 +/- 5 ml-min-1 (P less than 0.008). Hyperreninemia (by spironolactone and chlorthalidone), effective hyperaldosteronism (by chlorthalidone) and volume retention (by propranolol) are considered to represent expressions of mechanisms counteracting the depressor effects of these different pharmacologic maneuvers, leading to the maintenance of supranormal blood pressure.
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PMID:Intrapatient comparison of treatment with chlorthalidone, spironolactone and propranolol in normoreninemic essential hypertension. 110 6

Prostaglandins PGE-1 or PGA-1 (0.5 to 1 mug per min) were infused into the stenosed renal artery of anesthetized hypertensive dogs. Increased urine volume, sodium and potassium excretion, and p-aminohippurate clearance were found during the prostaglandin infusion period in the infused kidney as compared to the control periods before infusion. Creatinine clearance was increased during infusion of PGE-1. The noninfused, nonischemic kidney showed no effect at the time of infusion with PGE-1 but in the case of PGA-1, the p-aminohippurate and creatinine clearances and urine diuresis were decreased. As a result, the mean aortic blood pressure decreased. Both prostaglandins increased the renal vein renin in the infused kidney. PGA-1 did affect renin release of the noninfused kidney, but PGE-1, which is rapidly inactivated by the lung, did not have this effect. Renin release seems to be influenced by electrolyte diuresis operating through the macula densa mechanism. However, the lowering of blood pressure seen in this study cannot exclude the involvement of the stretch receptors (the juxtaglomerular cells) for renin release. The increased renin release after prostaglandin administration seems to be a protective renal mechanism against the drug-induced hypotension. It seems to be induced by the direct sodium and water diuretic effects of prostaglandins.
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PMID:Direct effect of prostaglandins in renal function and renin release in the presence of renal ischemia in the dog. 111 61

Three patients with right renal tumors extending into the inferior vena cava underwent ligation of the left renal vein coincident with right nephrectomy and en bloc resection of the vena cava. Two patients exhibited no postoperative renal dysfunction while the third demonstrated renal dysfunction which cleared by 9 days postoperatively. Features of the temporary renal dysfunction included proteinuria, elevated serum creatinine levels, oliguria, hypertension, elevated peripheral venous renin level, as well as radiographic evidence of swelling the kidney. The collateral venous drainage of the left kidney makes it possible to ligate the main vein of a solitary kidney with survival of the patient. However, postoperative temporary renal dysfunction may occur and a plan to deal with this problem should be fromulated.
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PMID:Ligation of the renal vein in the solitary kidney: effects on renal function. 111 94

Seven groups of rabbits were studied before or at various intervals after the subcutaneous administration of 50 percent glycerol in isotonic saline (14 ml/kg). A sharp increase in plasma crystalloid osmolarity, due to glycerol reabsorption from the subcutaneous tissue, was detected at 1.5 and 6 hours and was maximal between 12 and 20 hours. Plasma renin activity did not change at 1.5 hours, but it was significantly elevated at 6 hours and maximally increased between 12 and 20 hours. The increase of plasma crystalloid osmolarity might contribute to renin release in this experimental model. Changes in renal renin levels after the administration of glycerol were not significant, although lower renal renin values were consistently found in rabbits with more severe impairment of renal function. Plasma renin substrate increased later than plasma renin activity (20 hours) and remained high after plasma renin activity had returned to normal (48 hours). The increase of plasma renin substrate was interpreted as mainly due to the impairment of renal function, since a positive correlation was found between plasma creatinine and plasma renin substrate.
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PMID:Changes in plasma renin substrate, plasma and renal renin, and plasma osmolarity during glycerol-induced acute renal failure in rabbits. 111 58

Seventy-three rabbits (2 to 3 kg in weight) were studied during a control period and after receiving 50% glycerol (G) or mercuric chloride (M) with or without indomethacin (I) (controls received the diluent used for I). Plasma creatinine, plasma renin activity, blood pressure, sodium and potassium concentrations, hematocrit value, urinary output, body wt and histologic appearance of the kidney were determined. I enhanced the incidence and severity of the acute renal failure produced by G but failed to aggravate that produced by M. Because the dose of I used in this study blocked the synthesis of renal prostaglandins in the rabbit, we suggest that renal prostaglandins protect against the development of G-induced acute renal failure (a circulatory type of renal failure) in this animal model. Furthermore, the failure of I to aggravate M-induced acute renal failure indicates that it is unlikely that I aggravates G-induced acute renal failure by a direct nephrotoxic effect. No evidence was found for other possible side actions of I being responsible for the observed aggravation.
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PMID:Indomethacin enhancement of glycerol-induced acute renal failure in rabbits. 112 91

In 5 patients with polycystic kidney disease and creatinine clearances ranging from 4 to 40 ml/min, relationships between changes in blood pressure, sodium balance, body fluid compartments, plasma renin activity (PRA), urinary aldosterone excretion, and plasma aldosterone concentrations were studied during periods of low, medium, and high sodium intake. Total body water (TBW), total exchangeable body sodium (TEBS), and extracellular volume (ECV) were measured by isotope dilution techniques, plasma volume with Evan's blue dye, and PRA and aldosterone by radioimmunoassay. Low sodium intake reduced kidney function, blood pressure, and serum sodium, while PRA reached its highest levels. Subsequent increases in sodium intake improved kidney function and increased blood pressure. Plasma volume increased slightly and ECV markedly, while PRA dropped to 15 percent of the value noted after the low sodium intake. TBW and TEBS showed inconsistent changes. Aldosterone changes correlated closely with PRA. Blood pressure showed a negative correlation with PRA, but a positive one with body weight and cumulative sodium balance, and with plasma and extracellular volumes.it is suggested that whereas renin and aldosterone are involved in the maintenance of circulatory homeostasis during sodium loss, sodium retention causes an increase in blood pressure by concomitant changes in body fluids.
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PMID:Relationships of the renin-angiotensin-aldosterone system and sodium balance to blood pressure regulation in chronic renal failure of polycystic kidney disease. 112 29

The relative effects of des-a-Asp-angiotensin 3I and angiotensin II on renal function, including renin secretion, were investigated in normal and sodium-depleted dogs. Intrarenal arterial infusion of the heptapeptide fragment into normal dogs at a rate which was calculated to increase blood levels by only 7 ng/100 ml decreased renal blood flow from 254 +/- 9 ml/min to 220 +/- 12 and 219 +/- 12 ml/min (P less than 0.01 for both values) after 10 and 30 minutes of infusion, respectively; renin secretion decreased from 502 +/- 214 ng/min to 253 +/- 109 and 180 +/- 53 ng/min (P less than 0.05 for both values). Infusion of angiotensin II at the same rate decreased renal blood flow from 251 +/- 26 ml/min to 224 +/- 22 and 220 +/- 16 ml/min (P less than 0.01 and 0.025, respectively) and decreased renin secretion from 374 +/- 25 ng/min to 166 +/- 76 and 131 +/- 37 ng/min (P less than 0.025 for both values). Neither peptide significantly changed mean arterial blood pressure, creatinine clearance, or excreted sodium in these dogs. Infusion of des-1-Asp-angiotensin II into sodium-depleted dogs decreased renin secretion from 1094 +/- 211 ng/min to 768 +/- 132 and 499 +/- 31 ng/min (P less than 0.025 for both values) after 10 and 30 minutes of infusion. Angiotensin II infusion decreased renin secretion from 1102 +/- 134 to 495 +/- 235 and 502 +/- 129 ng/min in these dogs (P less than 0.05 and 0.025, respectively). Neither peptide significantly altered renal blood flow, arterial blood pressure, creatinine clearance, or excreted sodium in the sodium-depleted dogs. The data demonstrated that these two peptides have similar effects on the renin secretory mechanism and the vascular receptor at the level of the renal arterioles.
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PMID:Des-1-Asp-angiotensin II. Possible intrarenal role in homeostasis in the dog. 114 85


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