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)

A large part of renin was revealed to be stored in the remin granules as a soluble but hard to release form. Over 70% of the total renin in the granules could be released when the granules were ruptured by hypo-osmotic shock. Renin release from the isolated granules was limited within 20% of the total renin during incubation at 37C in an isotonic medium. 2. Without mechanical or osmotic shock renin granules were quite stable in a cold isotonic solution. Renin release from the isolated granules was not so much influenced by addition of cations which significantly stimulate renin release in vivo. Some cellular components may be required for the release process of renin from the granules as a mediator. 3. The molecular weight of the stored renin in the granules was shown to be 43,000 which was the regular size. Acidification of the extract of the renin granules altered neither molecular size of renin nor renin activity.
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PMID:Storage form of renin in the dog kidney. 70 78

The role of the renin angiotensin system was evaluated in 18 normotensive patients with chronic congestive heart failure and in 5 controls. No correlation was observed between plasma renin activity and cardiac index. There was a significant inverse correlation between renin and pulmonary capillary wedge pressure (r = -0.61, P less than 0.01). Renin values of the patients appeared to be increased when compared with controls with similar left ventricular filling pressure. Specific angiotensin II inhibition by saralasin decreased arterial pressure in 8 out of 14 patients: their renin was significantly higher than that of the remaining 6 patients (P less than 0.01). The 2 patients with the lowest renin levels responded to saralasin with a blood pressure increase. Left ventricular filling pressure decreased in all but these latter 2 patients with either little change or an increase in stroke volume. Thus, renin levels appear to be increased in normotensive patients with congestive heart failure when related to left ventricular filling pressure. Renin via angiotensin II plays a role in the blood pressure control of many patients with congestive heart failure. In some patients angiotensin II blockade appears to improve cardiac function by unloading the left ventricle.
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PMID:Congestive heart failure in normotensive man. Haemodynamics, renin, and angiotensin II blockade. 70 15

In 34 patients saralasin was infused after variable degrees of sodium depletion in order to differentiate between essential and renin-induced hypertension. After sodium-depletion of short duration mean arterial pressure dropped more than 10 mm Hg in 9 of 25 patients with essential and in 7 of 9 patients with renin-induced hypertension. After long-lasting sodium depletion the fall of mean arterial pressure exceeded 10 mm Hg in 11 of 16 patients with essential and in 8 of 9 patients with renin-induced hypertension. Thus saralasin did not discriminate essential and renin-induced hypertension. Also, plasma renin concentration before and after saralasin did not allow to differentiate between the two forms of hypertension. The changes of renin during infusion of saralasin was negatively correlated to the change of blood pressure. Renal vein renin ratio in patients with renovascular hypertension was not modified by saralasin. Renin and aldosterone changed inversely during saralasin infusion.
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PMID:[Saralasin-induced changes of blood pressure, renin and aldosterone in essential and renal hypertension (author's transl)]. 71 15

The presence and absence of renin activity and juxtaglomerular cells (JGC) in the kidney have been extensively studied among the vertebrates. Renin and JGC have been found in the kidneys of tetrapods and teleostean fishes. Therefore the renin-angiotensin system probably appeared first during early evolution of teleosts. However, the findings of various investigators need to be analyzed precisely to summarize and the subjects remained for further research need to be pointed out. There still remains a possiblity that a similar hormone is present in the cyclostomes and elasmobranchs. There are some discrepancies between the renal renin activity determined biochemically and the histological visualization of the granules in some primitive bony fishes. There are contradictory reports regarding the presence of macula densa in nonmammalian kidney. The fact that JGC are present extrarenally in sea-horses may suggest some function of this system. Renin-like activity has been reported extra-renally in various mammalian tissues and in the corpuscles of Stannius (CS) in teleosts. Physiological roles of these extrarenal renin have not been clarified. It has been demonstrated that CG contain 'hypocalcin' which lowers plasma Ca level. It is of interest in determining the possible relationship between the renin-angiotensin substances in CS and hypocalcin.
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PMID:Occurrence of the renin-angiotensin system in the vertebrates. 73 40

Comparative biochemistry of renins and angiotensins was discussed. Renin extracted from hog kidney was different from that from mouse submaxillary glands in immunoreactivity and carbohydrate content. Rat kidney renin was also different from hog kidney renin in the amino acid composition. The presence of big and big-big renins was pointed out immunochemically. These big renins were considered to be precursors of kidney renin. Angiotensins in mammalian and nonmammalian species produced by renal or extrarenal renin have been differentiated by some biochemical and pharmacological criteria. Some of these angiotensins were analyzed sequentially. The replacements of amino acid residues at positions 1, 5, and/or 9 of angiotensin I have been demonstrated in nonmammalian species. Specific pressor activities have been determined using synthetic angiotensins by a 4 point assay in rat. Specific pressor activities of various angiotensins were obtained from the dose-blood pressure-response curves using a single angiotensin sample per assay rat.
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PMID:Comparative biochemistry of renins and angiotensins in the vertebrates. 73 41

The effect of the microtubule inhibitors colchicine and vinblastine on renin release in vivo and in vitro was studied. Injection of 0.5 mg/100 g i.v. of colchicine or vinblastine to furosemide treated rats on a low salt diet resulted in a decrease of plasma renin as well as plasma angiotensinogen concentration during a 5 h observation period. Renin release from rat kidney slices was diminished by vinblastine (5 x 10(-5) M), when basal or stimulated (by isobutylmethylxanthine and isoproterenol) renin release was measured. Colchicine at 5 x 10(-5) M had no effect under these conditions. Renin release from the isolated perfused rat kidney was increased 2--3 fold by vinblastine (10(-5) M) or colchicine (10(-4) M). The maximal response of renin release to isoproterenol (10(-7) M) was not changed when vinblastine (10(-5) M) or colchicine (10(-4) M) were present in the perfusion medium. The contrasting results cast considerable doubts on the suitability of microtubule inhibitors in studies on renin secretion.
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PMID:The influence of vinblastine and colchicine on renin secretion in vivo and in vitro. 73 53

Renin substrate concentrations and the release of renin in response to the rapid removal of 15 ml/kg weight blood or subcutaneous administration of 500 microgram/kg body weight isoproterenol were measured in control rats and animals recovering from prior myohemoglobinuric acute renal failure (recovery rats). Blood for these assayas was drawn from chronically implanted aortic catheters, obviating the need for animal handling and anesthesia. Baseline plasma renin titers of recovery rats were modestly elevated but renin substrate concentrations were the same as in controls. Hemorrhage produced equivalent changes in blood pressure and plasma renin titer in the two groups. Isoproternol injection in recovery rats caused a somewhat greater blood pressure fall and almost twice the rise in plasma renin concentration observed in control rats. The marked resistance of recovery animals to a second bout of acute renal failure thus cannot be attributed to impaired renin release or inadequate plasma renin substrate.
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PMID:Renin release and the refractoriness to acute renal failure of rats recovering from prior renal failure. 74 30

The effect of papaverine on renal function and renin release was investigated in dogs in vivo and in vitro. Intrarenal arterial infusion of 0.1 mg/kg/min of papaverine for 10 minutes caused a significant rise in renal blood flow, a significant decrease in renal vascular resistance, clearance and extraction ratio of creatinine and PAH and in the amount of filtered sodium, without altering arterial blood pressure. There was a significant increase in sodium excretion and in the excreted percentage of filtered sodium (TRFNa). Renin activity (PRA) of arterial blood and renal venous blood, veno-arterious PRA-difference and renin secretion increased significantly after papaverine infusion. In order to eliminate the effect of hemodynamic changes on renin secretion, the effect of papaverine (10(-5), 10(-4)M) was investigated in vitro in surviving canine kidney cortex slices. Papaverine caused a significant increase in renin release and in tissue cAMP concentration. This supports the assumption that the increase in renin secretion might be due to a direct effect on the juxtaglomerular apparatus, by blocking phosphodiesterase activity and by increasing the renal cAMP level.
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PMID:Effect of papaverine on renin release in dogs in vivo and in vitro. 75 46

We studied the relative rates of release of active and inactive renin by the kidney in anesthetized pigs. Renin concentration was determined in arterial and renal venous plasma as follows: (1) before and after stimulation of renin release with isoproterenol or furosemide, (2) after suppression of renin release by extracellular fluid volume expansion, and (3) after administration of propranolol or indomethacin. Inactive renin was activated by dialysis of plasma at pH 3.3 for 24 hours. Renin concentration was estimated by radioimmunoassay determination of angiotensin I after a 3-hour incubation with excess homologous renin substrate. Following isoproterenol, the release of active renin increased from 8 +/- 4 (SEM) to 58 +/- 34 ng/min, and inactive renin increased from 53 +/- 33 to 321 +/- 136 ng/min. Similarly, furosemide stimulated the release of both active and inactive renin. Both forms of renin were suppressed by propranolol or indomethacin. Although changes in renin release following volume expansion were not statistically significant, the direction of change for both forms of renin was similar. Following logarithmic conversion of the rate of release, the plot of active vs. inactive renin formed a straight line. Values for active renin as a percentage of the total renin in simultaneously drawn arterial and renal venous plasma samples were not different. Thus, under the conditions of these experiments, release of active and inactive renin appears to be controlled by similar mechanisms. Both stimulation and suppression of renin release result in parallel changes in release of the two forms. Data on relative amounts of active renin in arterial and renal venous plasma suggest that there is no systemic conversion of the two forms.
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PMID:Release of active and inactive renin by the porcine kidney. 75 31

Effects of several sulfhydryl reagents on the reaction of renin and angiotensinogen were investigated by measuring the production of angiotensin I. Renin and angiotensinogen were prepared from the kidneys of dogs and from plasma of nephrectomized dogs, respectively. The amount of angiotensin I generated was increased with application of dithiothreitol, dithioerythritol and 2,3-mercapto-1-propanol. The greatest enhancement of the generation of angiotensin I was observed with dithiothreitol. Dithiothreitol had no influence on renin activity, on radioimmunoassay for angiotensin I and the recovery of synthetic angiotensin I from the incubation medium. When heterologous angiotensinogen was used, a great enhancement of generation of angiotensin I was observed. Dithiothreitol did not accelerate the reaction following replacement of the natural substrate, angiotensinogen, with the synthetic tetradecapeptide as substrate. It is postulated that dithiothreitol augments angiotensin I generation by acting on the angiotensinogen and not on the renin.
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PMID:Effect of dithiothreitol of the reaction of renin and angiotensinogen. 75 47


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