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)

In our previous studies, we showed an in vivo stimulating effect of the extract of the rat submandibular gland on plasma inactive renin release. In this study, we evaluated the effects of the rat submandibular gland extract and of some plasma active renin stimulants on inactive renin release from rat renal cortical slices. Adult male Wistar rats (250-350g) were kept on a regular diet (Na 260mg/100g) and nephrectomized under pentobarbital anesthesia (50mg/kg, i.p.). Five thin renal cortical slices were obtained from each kidney by using a razor blade. These renal cortical slices were incubated in Earle's buffer (pH7.4, Difco) at 37 degrees C for 30 min (preincubation), then transferred into 10ml fresh Earle's buffer with or without some agents and incubated at 37 degrees C for 1 hour (experimental incubation). For each experiment, 6 groups of 5 renal cortical slices were employed. The agents used in this study were as follows: isoproterenol (10(-5)M), furosemide (50 micrograms/ml), prostaglandin E1 (10(-5)M), prostaglandin I2 (10(-5)M) and the rat submandibular gland extract (100 microliters) which was obtained after homogenation with 10 x (w/v) 0.01M pyrophosphate buffer (pH6.5) including 0.1M NaCl. One ml of samples of this Earle's buffer were withdrawn every 20 min. Active renin in the samples was assayed by the commercial RIA-kit (Dainabot), and total renin was assayed after trypsin (Worthington) treatment (30 micrograms/300 microliters sample) at 4 degrees C for 10 min. Inactive renin was determined as the difference between total renin and active renin. Active and inactive renins increased linearly in the buffer without any agents (control) during the observation period (60 min). Isoproterenol (10(-5)M) stimulated the release of active renin significantly (p less than 0.01 vs. control) but did not affect the release of inactive renin. Furosemide (50 micrograms/ml) stimulated the release of active and inactive renins significantly at 20 and 40 min (p less than 0.05 vs. control) but did not affect the release of either renin at 60 min. Both prostaglandins E1 and I2 (10(-5)M) stimulated the release of active renin significantly (p less than 0.01 vs. control) but inhibited, on the other hand, the release of inactive renin significantly (p less than 0.01 vs. control). The rat submandibular gland extract (100 microliters) did not affect the release of active renin but stimulated the release of inactive renin significantly (p less than 0.05 vs. control).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Release mechanisms of inactive renin from rat renal cortical slices: role of the submandibular gland]. 211 63

Cultured bovine aortic endothelial cells (BAECs) express the complete renin-angiotensin system and secrete angiotensins. In this study, we examined the adrenergic influence on the secretion of angiotensins from BAECs. Angiotensins were determined by high-performance liquid chromatography and radioimmunoassay. At basal state, BAECs contain angiotensin I, angiotensin II, and angiotensin III at concentrations of 2.5 +/- 1.3, 4.8 +/- 2.3, and 3.4 +/- 1.5 pg/10(6) cells, respectively. Angiotensin I, angiotensin II, and angiotensin III concentrations in the culture medium were 8.3 +/- 4.4, 9.4 +/- 3.5, and 9.9 +/- 3.3 pg/10(6) cells, respectively. Isoproterenol (0.1-10 microM) increases secretion of angiotensins I, II, and III in a dose-dependent manner. Increase in angiotensin secretion induced by isoproterenol (10 microM) can be inhibited by beta 2-adrenoceptor antagonist ICI 118,551 (1 microM), but not by beta 1-adrenoceptor antagonist atenolol (1 microM). Forskolin (1-1,000 microM) mimics the isoproterenol-induced response. In contrast, alpha-adrenergic agonist phenylephrine (1-100 microM) inhibits the secretion. Pretreatment of BAECs with captopril (1 microM) inhibits the accumulation of angiotensin II and angiotensin III in the culture medium, but not angiotensin I. These findings suggest that BAEC production and/or secretion of angiotensins is regulated by adrenergic mechanisms.
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PMID:Endothelial renin-angiotensin pathway. Adrenergic regulation of angiotensin secretion. 215 59

Insulin-induced hypoglycemia causes an increase in plasma vasopressin (AVP) in healthy subjects but the response in diabetics is not established. We investigated the effect of insulin-induced hypoglycemia on ten insulin-dependent diabetics with asymptomatic hypoglycemia, and compared the results with those for seven healthy subjects. The lack of adrenergic symptoms of hypoglycemia in insulin dependent diabetics being attributed to a diminished beta-adrenergic sensitivity, the effect of isoprenaline infusion was investigated as control. Insulin-induced hypoglycemia resulted in both populations in significant increase (P less than 0.01) in AVP in addition to significant increases in heart rate, plasma epinephrine (E), norepenephrine (NE) and cortisol (COR). Effective osmolality and mean arterial blood pressure did not vary. Diabetics showed smaller increase in AVP (P less than 0.01) and heart rate (P less than 0.05) than controls. Maximal E, NE and COR values did not differ between the two populations. Isoprenaline infusion resulted in increase in heart rate and plasma renin activity, but AVP and COR did not vary in the two populations. In conclusion, insulin-induced hypoglycemia released AVP in diabetics with asymptomatic hypoglycemia, but the response was weaker than in healthy subjects. A causal hypothalamic alteration of beta-adrenergic or glycopenia sensitivity is discussed.
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PMID:Arginine vasopressin response to insulin-induced hypoglycemia in insulin-dependent diabetics with asymptomatic hypoglycemia. 219 Sep 3

Renal renin content and release decrease from outer to inner cortex; this may be due to a cortical-to-medullary gradient in glomerular density and/or renin content per afferent arteriole. Although low sodium diets have been reported to decrease the tissue renin gradient, little information is available on renin release by different areas of the renal cortex or the effect of a low sodium diet. In the present study, we examined basal- and isoproterenol-stimulated renin release and content in microdissected superficial, midcortical, and juxtamedullary afferent arterioles from rabbits on normal and low sodium diets. Renin content was 25.8 +/- 3.6, 1.4 +/- 0.32, and 0.27 +/- 0.09 ng angiotensin I (Ang I)/hour/arteriole in the superficial, midcortical and juxtamedullary arterioles, respectively. Dietary sodium restriction significantly increased it to 60.1 +/- 7.3, 13.8 +/- 3.1, and 1.48 +/- 0.6, respectively. Renin release was 0.64 +/- 0.13, 0.15 +/- 0.04, and 0.025 +/- 0.013 ng Ang I/hour/arteriole/hour incubation of arteriole in the superficial, midcortical and juxtamedullary arterioles, respectively. With sodium restriction it increased significantly for the superficial, (1.77 +/- 0.27) and midcortical (0.62 +/- 0.11) but not the juxtamedullary arterioles (0.038 +/- 0.02). With either diet, renin release and content among the three types of arterioles were significantly different. Isoproterenol (1.6 x 10(-4) M) significantly stimulated renin release from all three types of arterioles whether rabbits were fed a normal or low sodium diet; however, only in the superficial arterioles was the increase (delta) greater with dietary sodium restriction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renin release from microdissected superficial, midcortical, and juxtamedullary afferent arterioles in rabbits. 223 84

In vitro release of renin, angiotensinogen and aldosterone was studied in control (CT) and nephrotic rats. Nephrotic syndrome (NS) was induced by a single injection of puromycin aminonucleoside (PA). The in vitro systems used were: renal cortical slices (RCS), liver slices (LS) and adrenal glands, all incubated in Krebs-Ringer buffer. Renal renin content (RRC) and isoproterenol-induced renin secretion (RS) also were studied. RS, RRC and angiotensinogen release were measured indirectly by radioimmunoassay (RIA) of angiotensin I (ANG I); aldosterone was estimated by direct RIA. Basal RS was not modified in NS: 385 +/- 196 (CT) vs 344 +/- 149 ng ANG I/mg protein/h (NS), p greater than 0.05. Isoproterenol increased RS significantly in both CT and NS groups: 535 +/- (CT) and 685 +/- 231 ng ANG I/mg protein/h (NS) (p less than 0.05 vs. basal RS). RRC was similar in both groups: 2.17 +/- 0.62 (CT) vs 2.05 +/- 0.49 micrograms ANG I/mg protein/h (NS), p greater than 0.05. Angiotensinogen release from LS increased in nephrotic rats from 10 +/- 3.2 (CT) to 12 +/- 1.9 pmoles angiotensinogen I/mg tissue/2h (NS), p less than 0.05. Aldosterone release increased markedly from adrenal glands of rats with NS (1649 +/- 1111 pg aldosterone/mg tissue/h) with respect to control rats (257 +/- 85), p less than 0.05 In vitro studies were performed six days after PA-injection, when nephrotic rats had ascitis, edema, proteinuria, hypoproteinemia, hypercholesterolemia, hypertriglyceridemia, low sodium and aldosterone excretion, low levels of plasma angiotensinogen and high levels of plasma renin and aldosterone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiology of experimental nephrotic syndrome induced by puromycin aminonucleoside in rats. II. In vitro release of renin, angiotensinogen and aldosterone. 226 44

Chronic daily administration of cilazapril (1 X 10 mg/kg/day p.o., from age 4 to 14 weeks) to young spontaneously hypertensive rats (SHR) prevented the development of hypertension. The antihypertensive effect of a single dose of cilazapril persisted greater than 24 h. Discontinuation of long-term treatment resulted in an increase of systolic arterial blood pressure (SAP) to control hypertensive levels within 4 days. Following 10 weeks of drug administration, comparative hemodynamic studies were carried out on age-matched (14 weeks) control SHR and cilazapril-treated SHR. Cilazapril-treated SHR had a significantly lower mean arterial blood pressure (MAP) and total peripheral vascular resistance than did control SHR. The antihypertensive effect of cilazapril was not associated with changes in heart rate (HR). The myocardial performance parameters, cardiac output, and stroke volume, were similar in treated and control SHR, suggesting that the antihypertensive effect of cilazapril following chronic administration to SHR is mainly due to a reduction in peripheral vascular resistance. Vasopressor responses to angiotensin I were significantly lower in cilazapril-treated SHR than in control SHR. By contrast, pressor responses to angiotensin II and a high dose of norepinephrine (1.0 microgram/kg i.v.) were significantly enhanced. Isoproterenol elicited a fall in blood pressure in both groups, the extent of which was dependent upon the magnitude of basal blood pressure levels. Chronic cilazapril treatment resulted in a reduction of heart weight, suggesting that the drug may prevent development of cardiac hypertrophy in SHR. Kidney and adrenal weights were unaffected by the chronic treatment. Specific renin activities (SRA) in tissues of SHR were increased by factors of 20 (plasma) or 2 (kidney and adrenal) following cilazapril administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cilazapril prevents hypertension in spontaneously hypertensive rats. 242 85

The effect of a beta-adrenoceptor agonist on the release of the components of the vascular renin-angiotensin system was examined in vitro. Isolated rat mesenteric arteries were perfused in an open system with Krebs-Ringer solution and released immunoreactive angiotensin II (ANG IIir) into the perfusate was directly determined using a Sep-Pak C-18 cartridge connected to the perfusion system. Renin activity in the concentrated perfusate was also determined. Isoproterenol (1 nM-1 microM) increased the release of ANG IIir in a dose-dependent manner. The increase in ANG IIir release during isoproterenol (1 microM) infusion was inhibited by propranolol (1 microM) or captopril (2 microM). Isoproterenol-induced increment of ANG IIir release was blocked by the selective beta 2-adrenoceptor antagonist, ICI 118,551 (1 microM), but not by the selective beta 1-adrenoceptor antagonist, atenolol (1 microM). Renin activity in the perfusate was measurable, but did not increase in response to isoproterenol (1 microM) infusion. There was no significant difference in the response of ANG IIir release to isoproterenol between spontaneously hypertensive rats and Wistar-Kyoto rats. The present results indicate that locally generated ANG II is released by beta 2-adrenoceptor activation. The beta-adrenoceptor agonist and the vascular renin-angiotensin system may play an important role for the regulation of peripheral vascular tone.
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PMID:Role of vascular angiotensin II released by beta-adrenergic stimulation in rats. 243 81

The cardioselectivities of five beta-adrenoceptor antagonists were compared. Six normal subjects received, in a double-blind random order, 200 mg acebutolol, 50 mg atenolol, 10 mg betaxolol, 100 mg metoprolol, 80 mg propranolol, and placebo. All beta-adrenoceptor antagonists produced a similar reduction in exercise tachycardia. Isoprenaline infusions in incremental doses were given. Dose-response curves were constructed and the doses of isoprenaline required to increase heart rate by 25 beats/min (I25), forearm blood flow by 3 ml/100 ml/min (IF3), and finger tremor by 200% (IT200), and decrease diastolic blood pressure by 25 mm Hg (ID25), after each treatment were compared. After propranolol, I25, ID25, IF3, and IT200 were greater (p less than 0.02) than after atenolol, betaxolol, and metoprolol; I25, ID25, and IT200 were greater than after acebutolol. After acebutolol I25, ID25, and IF3 were greater than after atenolol and betaxolol; IT200 was greater than after betaxolol. Atenolol and betaxolol caused less reduction in the isoprenaline-induced changes in blood glucose, plasma potassium, lactate, renin activity, and serum insulin than propranolol. Acebutolol caused less attenuation of blood glucose and plasma lactate, and metoprolol less attenuation of plasma renin activity, than propranolol. It is concluded that acebutolol, atenolol, betaxolol, and metoprolol cause less blockade of beta 2-adrenoceptors than propranolol, and atenolol and betaxolol are more cardioselective than acebutolol.
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PMID:A comparison of the cardioselectivity of five beta-adrenoceptor blocking drugs. 244 Nov 75

After a 2-week placebo period, 30 men, aged 60 years (mean), with mild or moderate hypertension were randomly assigned to one of three treatment groups: pindolol, 10 mg b.i.d.; epanolol, 200 mg b.i.d.; and epanolol, 400 mg q.d. At the end of the placebo period and of 4 weeks of active treatment, heart rate, blood pressure, plasma renin activity (PRA), and nonepinephrine (NE) concentration of subgroups of subjects, were measured during isoproterenol infusion (30 ng/kg.min-1 for 15 min) and submaximal ergometric exercise (89 W, mean). Sitting heart rates were reduced with 200 mg b.i.d. epanolol (p less than 0.01) but unchanged with pindolol and 400 mg q.d. epanolol. Reductions of systolic and diastolic blood pressures occurred in all treatment groups but were most pronounced with pindolol. Isoproterenol-induced cardioacceleration and rise in PRA and plasma NE concentration were abolished by pindolol but only attenuated by epanolol. Pindolol also abolished the isoproterenol-induced reduction in diastolic blood pressure; epanolol had no effect on it. The hemodynamic and hormonal responses to exercise were attenuated by pindolol and epanolol in proportion to their beta-blocking activities. In the doses used, epanolol had moderate beta 1-selective blocking action. The intrinsic sympathomimetic activity of epanolol is dose dependent.
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PMID:Antihypertensive and hormonal responses to beta-blockade with intrinsic sympathomimetic activity: pindolol versus epanolol. 244 3

The ontogeny of renin secretion from renal cortical slices was studied in two groups of fetal (107-109 days of gestation and 131-136 days of gestation; term is 145 days), newborn (3-9 days old), and adult nonpregnant sheep. Isoproterenol (ISO; 10(-8)-10(-5) M) significantly increased active renin secretion in all age groups (P less than 0.05), with newborns having the highest values at all concentrations. However, the percent changes in active renin secretion were similar among all ages. Inactive renin secretion also increased with ISO stimulation, with newborns having the highest rate of inactive renin secretion. The percent of total renin in the active form differed among ages, ranging at base line from 60 +/- 10% in fetuses at greater than 130 days of gestation to 88 +/- 6% in fetuses at less than 110 days of gestation (P less than 0.05). Propranolol (1 microM) inhibited ISO (10(-6) M)-stimulated active renin secretion at all ages. On the other hand, the prostaglandin (PG) synthase inhibitor aspirin (1.6 x 10(-5) M) did not inhibit ISO (10(-6) M)-mediated increases in active renin secretion in fetal (greater than 130 days of gestation) kidney slices and produced values intermediate between base line and ISO alone in newborns and adults.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ontogeny of isoproterenol-stimulated renin secretion from sheep renal cortical slices. 250 35


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