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)

1. Much more water was consumed than either 0.9% or 2.7% saline in response to various dipsogenic stimuli in untreated normal replete rats when they had free access to water, 0.9% and 2.7% saline. On the other hand, the rats drank more 0.9% saline than water and 2.7% saline when each solution is the sole drinking fluid offered. 2. A marked increase in preference for 0.9% saline was observed during the chronic i.c.v. injection of angiotensin II at a dose of 25 ng/hr for 7 consecutive days in the three bottle choice test. After the cessation of angiotensin II infusion, most rats (45 out of 50 rats) returned to drink much more water than 0.9% and 2.7% saline, similar to the drinking pattern of the 0.9% saline-treated control rats. However, some rats (5 out of 50 rats) still preferred 0.9% saline and this persisted for up to 3 months although these rats did not show a hypertensive state and an increase of plasma renin activity.
Gen Pharmacol 1994 Oct
PMID:Salt preference elicited by chronic intracerebroventricular angiotensin II. 787 46

Renin-like activity (RLA) and angiotensin I-converting enzyme-like activity (ACELA), two key enzymes of the renin-angiotensin cascade (RAS), were sought in the dogfish rectal gland. RLA was 1.1 +/- 0.2 ng Ang I/mg protein/hr after incubation with porcine angiotensinogen and 0.8 +/- 0.1 ng Ang I/mg protein/hr after incubation with homologous plasma. ACELA was 7.22 +/- 1.08 and 8.87 +/- 1.9 nmol hippurate generated/min/mg protein respectively, at 0 and 37 degrees. The presence of these enzymes may indicate the presence of an endogenous RAS-like system in the rectal gland. Angiotensin II (Ang II) and atrial natriuretic peptide (ANP) binding sites were demonstrated autoradiographically in the subcapsular region of the gland, suggesting a possible interaction of the two hormones in the blind outer ends of the rectal gland tubules. Immunoreactivities toward Ang II, ANP, bombesin, vasoactive intestinal polypeptide (VIP), glucagon, and somatostatin were differentially localized in the rectal gland within three concentric zones with potentially different functional activities. In the capsule, there was a strong positive ir-glucagon reaction and a slightly weaker reaction for ir-somatostatin and VIP. In the blind outer ends of the tubules (in the subcapsular zone), strong immunoreactivity was present toward all the tested peptides except glucagon and somatostatin. In the inner zone and in the central canal, only a weak immunoreactivity toward Ang II and glucagon was observed.
Gen Comp Endocrinol 1994 Feb
PMID:Renin-like activity, angiotensin I-converting enzyme-like activity, and osmoregulatory peptides in the dogfish rectal gland. 790 83

1. The effects of barnidipine, a new dihydropyridine Ca2+ antagonist, on cardiovascular and renin-angiotensin-aldosterone systems were investigated in conscious squirrel monkeys. 2. Barnidipine (0.3-3 mg/kg p.o.) produced a dose-related decrease in systolic blood pressure. The hypotensive action after 3 mg/kg p.o. lasted more than 8 hr. 3. Barnidipine increased heart rate, but did not affect the PQ-interval of the electrocardiograph. 4. Barnidipine (1 and 3 mg/kg p.o.) increased plasma renin activity dose-dependently. However, it had no significant effect on plasma aldosterone concentration. 5. These results indicate that barnidipine produces a sustained hypotension without affecting atrioventricular conduction time and plasma aldosterone concentration in conscious squirrel monkeys.
Gen Pharmacol 1994 May
PMID:Hemodynamic effects of barnidipine hydrochloride in conscious squirrel monkeys. 792 6

Urinary output, urinary sodium and potassium excretion, plasma electrolyte concentrations and osmolality, plasma renin activity (PRA), and plasma aldosterone and arginine-vasopressin (AVP) concentrations were determined in eight camels in Tadla (Morocco). After administration of furosemide (2 mg.kg-1 body wt) urinary water, sodium and potassium excretions increased, inducing hypovolemia (as reflected by 14.6% increase in hematocrit), hyponatremia (142 +/- 1.0 vs 150 +/- 2.1 mmol.liter-1 in controls; P < 0.05), plasma hypo-osmolality (287.5 +/- 11.5 vs 307 +/- 1.4 mOsm.kg-1 H2O in controls; P < 0.05), and hypokalemia (3.7 +/- 0.2 vs 4.6 +/- 0.1 mmol.liter-1 in controls; P < 0.05). Such body fluid volume and composition changes were associated with parallel increases in PRA and plasma aldosterone concentrations (5.9 +/- 0.6 vs 0.9 +/- 0.2 ng AI.ml-1.hr-1 and 132.4 +/- 35.5 vs 25.1 +/- 6.5 pg.ml-1 in controls, respectively; P < 0.05). They were also associated with a fourfold increase in plasma arginine-vasopressin concentrations (0.8 +/- 0.2 vs 0.2 +/- 0.1 pg.ml-1; P < 0.05). In furosemide-treated animals, plasma aldosterone concentrations correlated positively with PRA (r = 0.85; n = 64; P < 0.01) and negatively with plasma sodium concentrations (r = -0.80; n = 64; P < 0.01), suggesting that in sodium-depleted camels the nexus between the renin-angiotensin system and aldosterone was restored.
Gen Comp Endocrinol 1994 Aug
PMID:Renin-aldosterone axis and arginine-vasopressin responses to sodium depletion in camels. 795 53

Eight dromedary camels were studied for 24 days under control conditions (3 days), and during water deprivation (14 days) and rehydration (7 days) in Tadla (Morocco), during the summer. During dehydration, food intake gradually fell and was zero on the last day and animals lost about 30% of their body weight. However, most of this reduction in weight was attributed to water loss, since body weight of the animals returned to control values following rehydration. Dehydration was associated with a decrease in plasma volume (-42 +/- 3%) and a concomitant rise in plasma Na concentration (from 154 +/- 2 to 191 +/- 3 mM). These changes were accompanied by increased plasma arginine-vasopressin (from 0.2 +/- 0.1 to 5.7 +/- 2.2 pg ml-1) and plasma renin activity (from 1.2 +/- 0.2 to 20.0 +/- 5.2 ng Al ml-1 hr-1), without significantly changed plasma concentrations of aldosterone and atrial natriuretic peptide. Dehydration was associated with increased urine osmolality (from 952 +/- 515 to 1963 +/- 498 mosm kg-1 H2O), reduced urine production (from 4565 +/- 2230 to 817 +/- 178 ml day-1), and increased Na excretion. Most of these parameters returned to control values during initial rehydration, except for plasma renin activity, which remained elevated for 7 days, and diuresis, which rose to 12773 +/- 6707 ml day-1 on Day 7 of rehydration.
Gen Comp Endocrinol 1993 Mar
PMID:Hormonal control of water and sodium in plasma and urine of camels during dehydration and rehydration. 833 27

Systemic hypovolemia and hypotension increase plasma renin activity (PRA) in fowl, but it is not clear whether this response is mediated directly by reduced renal arterial perfusion pressure (RAPP) or indirectly via renal nerves activated when systemic baroreceptors detect hypotension. To evaluate the influence of RAPP on renin release, arterial and renal venous blood samples were collected as RAPP was reduced step-wise from 108 mm Hg (control) to 71 and 47 mm Hg. PRA in systemic arterial (aPRA) and renal venous (vPRA) plasma was measured as the rate of fowl angiotensin I (ANG I) generation. Basal vPRA (2.47 +/- 0.6 ng x ml-1 x min-1) tended to be higher than aPRA (1.24 +/- 0.3 ng x ml-1 x min-1). When RAPP was reduced to 47 mm Hg both vPRA (4.35 +/- 0.6 ng x ml-1 x min-1) and aPRA (1.91 +/- 0.3 ng x ml-1 x min-1) increased significantly. Significant negative slopes (P = 0.01) were obtained when changes in aPRA or vPRA were regressed on RAPP. Mean systemic arterial pressure did not change during reductions in RAPP, nor did angiotensinogen concentrations differ when systemic arterial (472 +/- 30 ng/ml) and renal venous (460 +/- 27 ng/ml) plasma values were compared. Renal plasma flow was fully autoregulated as RAPP was reduced from 108 to 47 mm Hg; consequently, RAPP-induced increases in vPRA cannot be attributed to hemoconcentration of secreted renin. These results demonstrate that reductions in RAPP directly stimulate renin release from domestic fowl kidneys.
Gen Comp Endocrinol 1993 Mar
PMID:Reduced renal arterial perfusion pressure stimulates renin release from domestic fowl kidneys. 833 29

The role of the renin-angiotensin system (RAS) in the control of blood pressure and drinking was investigated in fresh water (FW)- and seawater (SW)-adapted eels, Anguilla anguilla, by comparing the effects of pharmacological manipulation through the use of papaverine (stimulator) and captopril (inhibitor) on the endogenous system. In SW eels basal blood pressure levels were lower (23.3 +/- 0.8 mm Hg) with correspondingly higher basal drinking rates (0.51 +/- 0.07 ml/kg/hr) and plasma AII concentrations (32.89 +/- 4.19 fmol/ml) compared to FW eels (33.8 +/- 1.3 mm Hg, 0.06 +/- 0.02 ml/kg/hr, 9.72 +/- 0.60 fmol/ml, respectively). In FW eels papaverine caused immediate hypotension with full recovery, decrease in plasma osmolality, and increase in drinking rate and plasma AII concentration, but in SW eels, hypotension with full recovery and an increase in plasma osmolality, drinking rate, and plasma AII concentration occurred. In FW eels captopril had no effect on the parameters measured, but in SW eels it caused a sustained decrease in blood pressure and a decline in the basal drinking rate and plasma AII concentration. Papaverine was also administered 15 min after captopril. In FW eels this manipulation caused hypotension only after the papaverine injection, followed by a partial recovery. Osmolality was unaffected, the previously observed papaverine-induced dipsogenic response was blocked, and the rise in plasma AII concentrations was smaller than with papaverine only. In SW eels there was an immediate hypotension after captopril administration with full recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
Gen Comp Endocrinol 1995 Oct
PMID:The role of the renin-angiotensin system in the control of blood pressure and drinking in the European eel, Anguilla anguilla. 857 57

Angiotensin II exerts its action via at least two distinct receptor subtypes designated AT1 and AT2. AT1 receptors seem to be responsible for most of the known angiotensin II effects while the role of AT2 receptors is not yet clear. Adipocytes of adult rats express exclusively the AT1 subtype. Angiotensin II stimulates prostacyclin release in adult rat adipocytes and in mouse preadipocytes. In the latter prostacyclin release is completely blocked by an AT2 receptor antagonist. Adipocyte angiotensin II receptors seem to be regulated by age and fat mass. Blockade of these receptors by an AT1 antagonist seems to prevent adipose tissue hypertrophy. Moreover, adipose tissue contains all the main components of the renin-angiotensin system such as angiotensinogen, angiotensin converting enzyme, angiotensin II and angiotensin II receptors. Angiotensinogen expression in adipocytes is stimulated by a high fat diet concurrent with enlargement of fat mass, associated with insulin resistance. Angiotensin converting enzyme inhibitors improve insulin sensitivity. Taken together, there is evidence of interaction between insulin and angiotensin II in regulation of adipose tissue metabolism and cellularity. Clarification of these interactions could lead to significant progress in pharmacological treatment of obesity and its comorbidity.
Gen Physiol Biophys 1995 Oct
PMID:The role of angiotensin II and its receptors in regulation of adipose tissue metabolism and cellularity. 878 38

Renin-like activity (RLA), angiotensin I converting enzyme-like (ACELA), and kallikrein-like activity (KLA), activities of the key enzymes of renin-angiotensin and kallikrein-kinin systems, were sought in the kidney of the African lungfish Protopterus annectens during the aquatic phase. RLA, examined by RIA (using porcine angiotensinogen as substrate), was 0.38 +/- 0.05 ng angiotensin I/mg protein/hr. ACELA and KLA were investigated in assays spectrophotometrically. ACELA, measured at 37 and at 20 degrees , was, respectively, 1.55 +/- 0.55 and 0.61 +/- 0.23 nmol hippurate/min/mg protein. KLA was 7.34 +/- 0.93 mU/mg protein in the crude kidney extract and 31.05 +/- 7.50 mU/mg protein after electrophoretic purification. Renal kininogenase activity was inhibited by 100% by D-Phe-Phe-Arg-chloromethyl ketone (10 microM), 98% by phenylmethylsulfonyl fluoride (2 nM), and 91% by aprotinin (1000 kIU). The apparent molecular weight of the renal kininogenase on SDS-PAGE was 27,000 Da. Both the renal enzyme and the purified glandular kallikrein, used as a control, have the same mobility on polyacrylamide gel electrophoresis. Immunoreactivities toward angiotensin II and bradykinin were localized by double immunostaining in the same cells of the proximal tubules. Putative angiotensin II receptors were demonstrated immunohistochemically, in the supranuclear region of proximal tubular cells, using an antibody to the sequence between amino acids 225 and 237 of the mammalian AT1 receptor.
Gen Comp Endocrinol 1996 Jul
PMID:The kallikrein-kinin and renin-angiotensin systems in the kidney of an African lungfish, Protopterus annectens. 881 41

Plasma prorenin and renin, serum insulin-like growth factor I (IGF-I) and IGF-binding protein (IGFBP-2 and IGFBP-3) concentrations were measured in 22 randomly selected male and female patients with insulin-dependent diabetes mellitus (IDDM) or non-IDDM (NIDDM). Plasma prorenin concentration was significantly elevated in patients with proliferative retinopathy (1869.5 +/- 785.0 mUL-1, mean +/- SEM) compared to patients with nonproliferative retinopathy (325.5 +/- 73.2 mUL-1, P < 0.003) and those without retinopathy (318.6 +/- 47.3 mUL-1, P < 0.007). Similarly, serum insulin-like growth factor-I (IGF-I) concentration in patients with proliferative retinopathy (126.3 +/- 21.5 micrograms L-1) was significantly higher than in patients with nonproliferative retinopathy (126.3 +/- 14.85 micrograms L-1, P < 0.004) and without retinopathy (135.2 +/- 37.26, P < 0.05). There was moderately strong positive correlation between plasma prorenin and serum IGF-I concentrations (r = 0.56, P < 0.01). Plasma prorenin concentration was uninfluenced by change in renal function (creatinine clearance, serum creatinine or BUN), but IGF-I levels were inversely related to creatinine clearance (r = 0.67, P < 0.002). There was no demonstrable relationship between IGF-binding proteins and prorenin or renin concentrations. In view of some overlap between plasma prorenin and serum IGF-I concentrations in diabetic patients with proliferative and nonproliferative retinopathy, measurement of both markers may be more useful in predicting the development of proliferative retinopathy in patients with diabetes mellitus than either measurement alone.
Gen Pharmacol 1996 Mar
PMID:Relationship between prorenin, IGF-I, IGF-binding proteins and retinopathy in diabetic patients. 891 51


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