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 characteristics and localization of beta adrenoceptor subtypes in rat kidney sections have been examined using [125I]cyanopindolol and in vitro labeling combined with autoradiography. Binding was stereoselective since the (-)-isomers of propranolol and pindolol were some two orders of magnitude more effective as competitors than the (+)-isomers. Competition curves obtained using the subtype selective antagonists ICI 118,551 (beta-2) and betaxolol (beta-1) had low pseudo Hill coefficients and were resolved into two distinct components representing beta-1 (63%) and beta-2 adrenoceptors (37%). Combined autoradiographic and histochemical studies using nuclear emulsion-coated coverslips and alkaline phosphatase staining showed that the majority of receptors were in the renal cortex and in the outer band of the medulla with fewer receptors associated with the inner medulla, papilla and renal blood vessels. Delineation of beta-1 and beta-2 adrenoceptor subtypes with the selective antagonists betaxolol and ICI 118,551 indicated that the highly localized receptors were predominately of the beta-1 subtype, associated with glomeruli and with tubules that from their staining characteristics and topography represent distal and cortical collecting tubules with few if any receptors associated with proximal tubules. Beta-2 adrenoceptors were more diffusely distributed in the cortex and there were minor areas of localization in the inner medulla. Although some glomerular beta adrenoceptors probably play a role in control of renin release, their distribution throughout this structure indicates that they also control other functions. The distribution of beta adrenoceptors in tubules corresponds well with the known distribution of beta adrenoceptor-stimulated adenylate cyclase in rat kidney and indicates that these receptors subserve a physiological function.
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PMID:Localization of beta adrenoceptor subtypes in rat kidney by light microscopic autoradiography. 298 17

An enzyme immunoassay for serum 18-hydroxycorticosterone was established using alkaline phosphatase as a label. The antiserum for 18-hydroxycorticosterone was produced by immunization of rabbits with 18-hydroxycorticosterone 3-(o-carboxymethyl) oxime conjugated to bovine serum albumin. Sephadex LH-20 column chromatography was used to separate 18-hydroxycorticosterone from other steroids in serum samples. The minimal detectable amount of 18-hydroxycorticosterone was 50 pg/tube, and the measurable range was from 5 to 1000 ng/dl when a 1.0 ml serum sample was used. Intra- and inter-assay coefficients of variance were 5.0% (n = 6), and 5.8% (n = 6), respectively. In normal controls the serum 18-hydroxycorticosterone level was 4.8 approximately 34.0 ng/dl (mean +/- S.D. = 17.1 +/- 9.0 ng/dl) on an unrestricted diet. Seven out of 8 patients with aldosterone-producing adenoma had above-normal serum 18-hydroxycorticosterone levels. Serum 18-hydroxycorticosterone increased and decreased significantly following ACTH and dexamethasone administration, respectively. In essential hypertensive patients, serum 18-hydroxycorticosterone was high during a low-sodium diet and was suppressed remarkably by captopril. These observations support the previous reports that adrenal 18-hydroxycorticosterone synthesis is dependent on both ACTH and the renin-angiotensin system. The present method is sufficiently sensitive and producible, avoids the use of radioisotopes and is quite satisfactory for clinical use.
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PMID:[Enzyme immunoassay for serum 18-hydroxycorticosterone and its clinical application]. 300 75

Human fetal lung homogenates contain an inactive form of renin which may be revealed by trypsin treatment. When activated, this form of renin has some biochemical similarities with fetal kidney renin: the pH optimum of fetal lung renin is approximately 6.5; it is bound by Affigel Blue affinity chromatography resin; and is inhibited by a monoclonal antibody (R-3-36-16) raised to human kidney renin. Inactive renin, partially-purified from both fetal kidney and lung, differs from this in that the renal form is of low-molecular weight (LMW, 45,000 daltons), whereas that from fetal lung is of high molecular weight (HMW, 58,000 daltons). Using a sensitive alkaline phosphatase-anti-alkaline phosphatase (APAAP) procedure with a polyclonal anti-renin antibody (R-15), immunoreactive renin in fetal lung was found in vessels in mesenchyme between airways. The pattern of staining was distributed similarly to Factor VIII-related antigen, suggesting localization in endothelial cells.
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PMID:Renin in human fetal lung--a biochemical and immunohistochemical study. 305 97

Twenty-seven patients with mild to moderate essential hypertension were randomized to receive therapy with either hydrochlorothiazide or diltiazem. After a placebo run-in period of 2 weeks, patients received increasing doses of either drug for 14 weeks. Those in whom hypertension was effectively controlled continued for 26 weeks of total treatment. Those not controlled, i.e. blood pressure greater than 140/90 mm Hg or less than 10 mm Hg reduction of pressure, were unblinded and crossed over to therapy with both drugs. Eleven of 14 patients (79%) were effectively treated with diltiazem alone, and 8 of 13 patients (62%) were effectively treated with hydrochlorothiazide alone. Supine blood pressures fell from 152 +/- 5/97 +/- 1 to 142 +/- 4/87 +/- 3 mm Hg in the 11 patients treated with diltiazem, from 152 +/- 2/99 +/- 1 to 134 +/- 3/88 +/- 2 mm Hg in the 8 patients treated with hydrochlorothiazide, and from 151 +/- 4/104 +/- 3 to 140 +/- 5/92 +/- 1 mm Hg in the 8 patients who received both drugs (p less than 0.01 for each group). Diltiazem patients had significant increases in alkaline phosphatase and urinary magnesium. Hydrochlorothiazide patients had increases in serum uric acid, serum globulin, CO2 content, and plasma renin activity. Serum potassium, serum chloride, urinary osmolality, and urinary calcium decreased after treatment with hydrochlorothiazide. Patients receiving both drugs had increases in serum glucose, serum BUN, serum uric acid, serum globulin, and CO2 content. These patients had decreased serum chloride and urinary calcium. Diltiazem monotherapy was comparable to hydrochlorothiazide in efficacy of lowering blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal-metabolic consequences of antihypertensive therapy with diltiazem versus hydrochlorothiazide. 332 Jul 20

1. The distribution of enzymatic activities was determined in subcellular fractions of rat kidney cortex homogenates after various homogenization procedures. The specific activities of kininogenase (KGA), BAEE esterase (pH 8.5), alkaline phosphatase and glucose-6-phosphatase were, on average, 3.4 times higher in the microsomal fraction than in the whole homogenate. The total amount of these activities in the microsomal fraction after gentle, ordinary and forced homogenization were about 15, 40 and 65% of total recovered activities, respectively. These results confirmed the localization of KGA in the microsomal fraction.2. Renin activity was primarily recovered in the heavy mitochondrial fraction. When the force of the homogenization was increased some renin activity was shifted to the soluble fraction.3. When a mixture of renin and purified urinary KGA was given intravenously to an anaesthetized rat, a hypotensive response due to the KGA was followed by a hypertensive renin response. Over a certain range of concentrations KGA and renin could be measured simultaneously. In fractions of kidney homogenates, however, KGA activity was too low to be measured by this method.
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PMID:Subcellular localization of renin and kininogenase in the rat kidney. 432 58

Collagenasic dispersion of rabbit kidney cortex followed by centrifugation on discontinuous sucrose gradient, allowed the simultaneous isolation of a microvascular fraction and of glomerular and tubular fractions. The microvessels were characterized by an overall diameter of 22 micron and the presence of granular and smooth muscle cells. Measurement of cellular renin activity and the muscle specific enzyme creatine kinase showed that these vessels were arteriolar in nature and that they contained the preglomerular arterioles. The glomerular or tubular contamination rates were assessed by means of enzymatic markers. Thus, in the arterioles, potassium fluoride-resistant acid phosphatase was some 10 times lower than in the glomeruli. The specific tubular enzymes gamma-glutamyl-transpeptidase and alkaline phosphatase were about 20 times lower in the arterioles than in the tubular fraction. The possibility of obtaining these fractions may facilitate many types of study on renal hemodynamic and glomerulo-tubular feedback control.
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PMID:Isolation and characterization of a microvascular fraction from rabbit kidney cortex. 614 66

Effect of vitamin E-deficiency on renin release was examined with rat kidney cortical slices. Male Wistar rats were fed either a control or a vitamin E-deficient diet for 4 weeks. When kidney cortical slices were incubated in a Krebs-Ringers' bicarbonate solution (pH 7.4) at 37 degrees C, the rate of renin release into the incubation medium in vitamin E-deficient group was significantly higher than that in the control group. However, dietary supplementation of alpha-tocopheryl acetate (TOCA) or N,N'-diphenyl-p-phenylenediamine (DPPD) to the vitamin E-deficient rats for 5 d suppressed the stimulation of renin release from kidney cortical slices by vitamin E-deficiency. On the other hand, the release of protein, acid phosphatase and alkaline phosphatase during incubation of kidney cortical slices was not affected by vitamin E-deficiency or supplementations of TOCA and DPPD. These findings indicate that vitamin E-deficiency specifically stimulates renin release from kidney cortical slices and this effect is attenuated by the dietary supplementation of TOCA or DPPD.
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PMID:Stimulation of renin release from rat kidney cortical slices by vitamin E-deficiency. 636 85

A sensitive solid phase enzyme-linked immunosorbent assay (ELISA) has been developed using two anti-human renin monoclonal antibodies, which were shown to bind both human as well as primate renin at two different epitopic sites. One monoclonal antibody (3-36-16) was used to coat each well of a 96 well microtitre plate in which renin, contained in 5 to 20 ul of plasma, was allowed to react. Plates were then incubated with the gamma globulin (gamma G) fraction of a rabbit anti-human renin serum followed by development with sheetp anti-rabbit gamma G conjugated to alkaline phosphatase. Quantification was carried out by the addition of the alkaline phosphatase substrate, p-nitrophenylphosphate, which produced a colorimetric reaction. The sensitivity of the assay is 25 pg ml-1. The method recognises both active and inactive renin from plasma, kidney, amniotic fluid and chorionic cells. Plasma renin can be measured within 6 hours when values are greater then 150 pg ml-1 or within 24 hours when plasma values are less than 150 pg ml-1. The ELISA has already been used to measure total immunoreactive renin in plasma obtained from patients with several forms of hypertension. The values ranged from 25 pg ml-1 in patients with primary aldosteronism to as large as 60 ng ml-1 in a patient with a renin-secreting tumour.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A multirange ELISA for the measurement of plasma renin in humans and primates. 640 Mar 74

To study the hormonal and metabolic effects of prostacyclin (PGI2), 6 healthy women were infused iv with PGI2 (1, 2, 4, and 8 ng/kg/min. each for 20 min) dissolved in glycine buffer, or with glycine buffer only. Serial blood samples collected before, during and after the infusion were assayed for FSH, LH, prolactin, growth hormone, thyrotrophin, oestradiol, progesterone, testosterone, cortisol, thyroxine, triiodothyronine, renin, aldosterone, glucose, insulin, glucagon, cholesterol, high density lipoprotein-cholesterol, triglycerides, alkaline phosphatase, alanine and aspartate aminotransferases, bilirubin, sodium, potassium, chloride, calcium, inorganic phosphorous, creatinine and uric acid. PGI2 infusions were accompanied by increased levels of prolactin, growth hormone and cortisol, probably due to the stressful side-effects during PGI2 infusion. In addition, plasma renin activity, glucagon and blood glucose increased, whereas the other variables measured did not change. These PGI2-effects should be kept in mind, when PGI2 is used in clinical practice.
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PMID:Hormonal and metabolic effects of intravenous infusion of prostacyclin in healthy women. 675 11

In order to help clarify the role of the renin-angiotensin system in the evolution of the post-hemorrhagic circulatory shock syndrome, captopril, a potent inhibitor of the conversion of angiotensin I to angiotensin II, was infused into a hemorrhagic shock model in the cat. The hemorrhage protocol had arterial blood withdrawn until a mean arterial blood pressure (MABP) of 40 mm Hg developed. Oligemia was maintained for a period of 2.5 hr, after which time, all remaining shed blood was reinfused and the cats observed for an additional 2 hr. Coincident with the large reduction in MABP, superior mesenteric artery flow (SMAF) was similarly reduced as recorded by a noncannulating electromagnetic flow probe fitted around the artery. Post-oligemic plasma activities of cathepsin D (CD) and alkaline phosphatase (AP) were elevated 11-fold and 3-fold respectively; intestinal morphological damage was graded at 2.8 +/- 0.6 on a 0-4 scale of increasing severity (control: 0.03 +/- 0.02). Captopril was administered at an initial priming dose of 0.5 mg/kg followed by a continuous infusion of 0.5 mg/kg/hr. Improved post-reinfusion maintenance of MABP and SMAF was noted. Plasma elevations in enzyme activity were more moderate: 8-fold for CD, 1.5-fold for AP. Intestinal morphologic damage was graded at 2.5 +/- 0.3. Blockade of angiotensin II formation by captopril thus demonstrated beneficial effects on post-oligemic hemodynamic status and on the degree of cellular enzyme release without significant improvement in intestinal morphology.
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PMID:Captopril and the intestinal response to hemorrhagic shock. 675 18


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