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)

We hypothesize that hemodilution in the early stages of water immersion plays an important role in vasopressin (AVP) suppression and subsequent diuresis. Ten men (19-24 years) were immersed to the neck in a semireclining position for 8 h in 34.6 degree C tap water. After 8 h of immersion there were decreases (p less than 0.05) in plasma volume (PV) of 15.6%, extracellular volume (ECV) of 18.8%, interstitial volume (ISV) of 19.6%, and red cell volume of 10.7%. Hemodilution (hyposmotem years) were immersed to the neck in a semireclining position for 8 h in 34.6 degree C tap water. After 8 h of immersion there were decreases (p less than 0.05) in plasma volume (PV) of 15.6%, extracellular volume (ECV) of 18.8%, interstitial volume (ISV) of 19.6%, and red cell volume of 10.7%. Hemodilution (hyposmotem years) were immersed to the neck in a semireclining position for 8 h in 34.6 degree C tap water. After 8 h of immersion there were decreases (p less than 0.05) in plasma volume (PV) of 15.6%, extracellular volume (ECV) of 18.8%, interstitial volume (ISV) of 19.6%, and red cell volume of 10.7%. Hemodilution (hyposmotem of 4 mosmol/kg H2O) and near maximal suppression of AVP (to 0.5 pg/ml) and plasma renin activity (to 0.4 ng Ang 1 .ml-1.h-1) were evident by hour 2 of immersion. The early hemodilution (2-2 h) was due to a slight increase in PV with no change in plasma Na+ or osmotic content, even though urine volume and UosmV increased significantly. The hyposmotemia and PRA suppression continued throughout immersion in spite of the progressively increasing diuresis and decreasing PV. These findings suggest the transfer of hypotonic fluid into the vascular system; this fluid does not appear to come from the intracellular volume. We conclude that hyposmotemia is an important part of the mechanism contributing to AVP suppression during water immersion.
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PMID:Hemodilution, vasopressin suppression, and diuresis during water immersion in man. 725 90

Previous studies suggest that beta-adrenergic receptor agonists and other hypotensive agents stimulate water intake via the renin-angiotensin system (RAS). However, a recent study reported that acute peripheral administration of Losartan, an angiotensin II (AII) type I receptor antagonist, failed to inhibit isoproterenol-induced water intake. In the current study we assessed the role of chronic Losartan treatment on isoproterenol-induced water intake. Male Sprague-Dawley rats were divided into two groups (n = 10/group). The experimental group was chronically treated with Losartan in the drinking water (120 mg/kg/day). Rats in the control group were maintained on normal tap water. At the end of each week, water intake in response to isoproterenol was determined. On the days of the dipsogenic study, water intake was determined 1 h prior to and 2 h following SC injection of isoproterenol (25 micrograms/kg). Isoproterenol-induced water intake in the experimental group was significantly lower than the control rats by 71% and 88% at the end of weeks one and two respectively (p < 0.01). Following ten days of Losartan treatment, dipsogenic response to AII likewise demonstrated a complete blockage of AII receptors (75% decrease compared to the controls). These data strongly suggest that water intake in response to isoproterenol is mediated in part by the RAS.
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PMID:Chronic Losartan treatment blocks isoproterenol-induced dipsogenesis. 756 31

Blockade of the renin-angiotensin system was studied in male Sprague-Dawley rats during long-term inhibition of nitric oxide synthase. Nitro-L-arginine-methyl ester (L-NAME) was placed in the drinking water for 4 weeks (approximately 100 mg/kg per day). Separate groups of rats were coadministered the angiotensin II antagonist A-81988 in the drinking water ranging from approximately 0.001 to 1 mg/kg per day. Control groups received only tap water or A-81988 alone. Each week, rats were placed in metabolic cages, and tail-cuff blood pressures and blood samples were taken. L-NAME produced a sustained elevation in tail-cuff pressure that was completely prevented by A-81988. No changes in creatinine clearance, sodium excretion, plasma creatinine concentration, or blood urea nitrogen were observed. Food and water intakes were identical in all groups. Water excretion was significantly increased in L-NAME-treated animals regardless of additional inhibitor treatment, suggesting a possible role for nitric oxide synthase in the control of water excretion; this effect was independent of blood pressure. Although less potent than A-81988, the angiotensin II antagonist losartan and the angiotensin converting enzyme inhibitor enalapril also blocked L-NAME-induced hypertension. In a separate series of experiments, rats were not given A-81988 until 2 weeks after hypertension had fully developed in L-NAME-treated rats. Within 1 week of treatment with the angiotensin II antagonist, tail-cuff pressure returned to normal. We conclude from these studies that long-term inhibition of endogenous nitric oxide production produces an angiotensin II-dependent form of hypertension.
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PMID:Angiotensin blockade reverses hypertension during long-term nitric oxide synthase inhibition. 768 26

Adult male golden hamsters were maintained on powdered Purina chow and tap water, and were permitted continuous access to either a 15% or a 30% ethanol solution (v/v); after an initial 4-5 weeks of ethanol availability, hamsters had stabilized their intakes and were deriving an average of 1.25 and 1.96 g/day of absolute ethanol from the 15% and 30% solutions, respectively. When salt was added to the diet in increasing concentrations ranging from 4% to 10% over a period of 40 days, hamsters reduced chow-derived calories by up to 35%, increased tap water consumption by up to 50%, and increased consumption of ethanol solutions by up to 100%; when unadulterated Purina chow was reinstated, intakes of chow-derived calories, tap water, and ethanol solutions returned to baseline levels. Hamsters that were continuously maintained on unadulterated Purina chow, but with chow-derived calories matched to that of animals on the salt-adulterated diet, significantly increased their ethanol intake, but not their tap water intake; the increase in their ethanol intake was only about half as large as that of hamsters that had salt added to the diet, but the increase persisted even after ad lib feeding was reinstated. The results indicate that the addition of salt to the diet of hamsters produces large increases in ethanol consumption; furthermore, the increased ethanol intake is not simply the result either of a nonselective increase in fluid consumption or of the reduction in food intake that accompanies the addition of salt to the diet. Results are related to the possible role of the renin-angiotensin system in the control of ethanol consumption in the golden hamster.
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PMID:Dietary salt and voluntary ethanol consumption in golden hamsters. 786 52

To determine whether chronic treatment with enalapril initiated early in life prevents glomerular injury secondary to normal aging, CF1 mice received enalapril (20 mg/L, n = 10) or nifedipine (40 mg/L, n = 10) in their drinking water from the time of weaning to 12 months of life. Control mice (n = 10) received tap water ad libitum. Immunocytochemical detection of renin confirmed that angiotensin-converting enzyme inhibition resulted in recruitment of renin-containing cells along the preglomerular vessels. Morphometric analysis of glomeruli included assessment of glomerular diameter and the percentage of mesangial area per glomerulus. Glomerular diameter and mesangial area were higher in control mice (99.7 +/- 0.5 microns, 12.7 +/- 0.3%) than in enalapril-treated mice (88 +/- 0.8 microns, 8.6 +/- 0.6%) (P < .05). Glomerular diameter and mesangial area in the nifedipine-treated group (99.1 +/- 0.9 microns, 12.4 +/- 0.9%) were not different from control mice. These results demonstrate that angiotensin-converting enzyme inhibition prevents the glomerular enlargement and mesangial expansion observed during natural aging. In addition, control glomeruli expressed alpha-smooth muscle actin in a mesangial distribution. This effect was prevented by enalapril treatment but not by nifedipine. We conclude that long-term treatment with enalapril from early life prevents the early changes associated with glomerular injury and expression of alpha-smooth muscle actin in the glomerulus. alpha-Smooth muscle actin may participate in and serve as an early marker of the glomerular injury during the normal aging process.
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PMID:Intraglomerular expression of alpha-smooth muscle actin in aging mice. 820 23

The effect of inhibiting the renin-angiotensin system was evaluated in male Sprague-Dawley rats with reduced renal mass produced by right nephrectomy and infarction of two-thirds of the left kidney. Separate groups of rats were then administered the angiotensin receptor antagonists, A-81988 or losartan (DuP 753), the angiotensin converting enzyme inhibitor, enalapril, or vehicle (tap water) in their drinking water for 4 weeks. Tail cuff blood pressures and blood samples were obtained weekly. Excretory function during week 4 was evaluated using metabolic cages. Rats with reduced renal mass were characterized by a significant elevation in systolic blood pressure and urinary protein excretion along with a reduced urine osmolality. At 1 mg/kg/day, A-81988 prevented the hypertension and the development of proteinuria. A-81988 administration also improved urinary concentrating ability because urine osmolality was significantly higher in this group compared to untreated controls. The same dose of losartan or enalapril was ineffective at controlling the development of the hypertension, indicating that A-81988 is more potent in vivo. Despite the maintenance of systemic hypertension, losartan significantly blunted the proteinuria compared to vehicle-treated controls. At a dose of 10 mg/kg/day, losartan and enalapril also prevented the increase in systolic blood pressure and proteinuria and produced an increase in urine osmolality. These data support the hypothesis that angiotensin receptor antagonists have beneficial effects in forms of renal failure associated with proteinuria and diminished concentrating ability.
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PMID:Angiotensin II receptor blockade improves renal function in rats with reduced renal mass. 824 38

We profiled the concentrations of angiotensin I (Ang I), angiotensin II (Ang II), and angiotensin(1-7) [Ang(1-7)] by the combination of radioimmunoassay and high performance liquid chromatography in the blood of 14-week-old male Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) drinking either tap water or a solution containing ceranapril (30 mg/kg) or lisinopril (20 mg/kg) for 14 days. Differences in the chemical and pharmacokinetic properties of the two converting enzyme inhibitors ruled out class-related effects. Plasma renin activity, angiotensin converting enzyme (ACE) activity, and plasma levels of Ang I and Ang II were the same in vehicle-treated WKY and SHR. In contrast, plasma levels of both Ang(1-7) and vasopressin in SHR were 3.7-fold and 2.6-fold higher, respectively (p < 0.05). Angiotensin converting enzyme inhibition reduced the blood pressure of WKY and SHR, and augmented their intake of water and output of urine. These changes were associated with increases in renin activity and plasma levels of Ang I and Ang(1-7). In both WKY and SHR, lisinopril had a greater effect in inhibiting plasma and cerebrospinal fluid ACE, reducing levels of plasma angiotensinogen, and increasing the concentrations of authentic Ang II. The principal finding of this study is that plasma Ang(1-7) is the sole component of the circulating angiotensin system that is elevated in the established phase of genetic hypertension. The finding that chronic inhibition of ACE augments circulating levels of Ang(1-7) evidenced the existence of functional pathways for the alternate processing of Ang I.
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PMID:Angiotensin(1-7) in the spontaneously hypertensive rat. 828 65

1. To examine whether an angiotensin-converting enzyme (ACE) inhibitor prevents left ventricular (LV) hypertrophy even in low-renin hypertension, we studied the effect of the administration of perindopril on cardiac hypertrophy induced by partial renal ablation in hypertensive rats. 2. Rats that had undergone partial nephrectomy were randomly divided into four groups that received the following as drinking water: Group A, tap water; Group B, 1% sodium chloride (NaCl); Group C, NaCl + perindopril 3 mg/kg per day; and Group D, NaCl + perindopril 1 mg/kg per day. Plasma renin activity (PRA), angiotensin-II (AII) concentration and cardiac tissue AII were measured. 3. Supplementation of NaCl following nephrectomy increased the blood pressure and cardiac weight compared with rats that had undergone nephrectomy alone (P < 0.05). Treatment with perindopril (3 mg/kg per day) did not affect the blood pressure and plasma AII but inhibited the increase of cardiac weight (P < 0.05). Left ventricular AII was decreased in cases of reduced renal mass hypertension, but was not changed by treatment with perindopril. 4. These results demonstrate that perindopril may be able to prevent LV hypertrophy even in low-renin hypertension, which was not mediated by a reduction of blood pressure or suppression of the circulating and cardiac renin-angiotensin systems. Other mechanisms of ACE inhibitors may contribute to the cardioprotective effects.
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PMID:The angiotensin-converting enzyme inhibitor, perindopril, prevents cardiac hypertrophy in low-renin hypertensive rats. 846 69

During the last few years, several studies including six randomised, controlled trials reevaluating therapeutic paracentesis in the management of cirrhotic patients with tense ascites have been reported. The main findings of these investigations are: (i) Repeated large-volume paracentesis (evacuation of 4-6 l/day until complete mobilization of ascites) or total paracentesis (complete mobilization of ascites in only one tap) associated with i.v. albumin infusion (6-8 g/l of ascitic fluid removed) are more effective in eliminating the intra-abdominal fluid than conventional diuretic therapy, are associated with a lower incidence of complications and considerably reduce the duration of hospital stay and the cost of treatment; (ii) The mobilization of ascites by paracentesis without albumin infusion is associated with an impairment in effective circulating blood volume, as indicated by a decrease in cardiac output, central venous pressure, pulmonary capillary wedge pressure and plasma concentration of atrial natriuretic peptide and a marked elevation of plasma renin activity and aldosterone concentration. In 20% of patients this circulatory disturbance is accompanied by the development of renal impairment and/or dilutional hyponatraemia. These changes can be detected within the first 24 h following complete mobilization of ascites and do not occur when plasma volume is expanded with albumin; (iii) Hemaccel and dextran 70 appear to be as effective as albumin in preventing renal and electrolyte complications after paracentesis; (iv) Therapeutic paracentesis is an alternative treatment to peritoneovenous shunting in cirrhotic patients with refractory ascites.
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PMID:Paracentesis in the management of cirrhotic ascites. 849 65

The effects of nifedipine and enalapril on age-associated renal interstitial fibrosis were investigated in 60 CF1 female mice. Mice received 20 mg enalapril (ENAL) per L (N = 20), or 40 mg nifedipine (NIF) per L (N = 20) in their drinking water. Control (CONT) mice received tap water ad libitum. The percentages of both interstitial peritubular sclerosis (IPS) in cortex and interstitial medullary sclerosis (IMS) were determined. Kidney tissue was studied using immunological techniques and optical (OM) and electron microscopy (EM) to analyze the expression of renin. alpha-SM-actin and vimentine expression were also evaluated. The results showed that blood pressure levels in ENAL or NIF animals were not different from those of CONT. Renin expression was observed in arcuate vessels (AV) in ENAL animals, whereas no renin staining in AV was found in either NIF or CONT animals. Renin immunoreactivity in the juxtaglomerular apparatus was more intense in ENAL mice, as compared with NIF or CONT animals. Laboratory testing showed the following values: proteinuria (mg/mL): CONT 6.1 +/- 0.6, NIF 11.2 +/- 2.3, and ENAL 1.0 +/- 0.6 (P < 0.05); creatinine: CONT 1.37 +/- 0.24, NIF 0.87 +/- 0.16, and ENAL 0.63 +/- 0.1 (P < 0.01). The percentages of interstitial sclerosis were: %IPS: CONT 18.12 +/- 1.1, NIF 17.40 +/- 0.9, and ENAL 3.42 +/- 1.3 (P < 0.01); %IMS: CONT 23.41 +/- 1.5, NIF 21.80 +/- 1.9, and ENAL 6.12 +/- 1.2 (P < 0.01). Percentages of alpha-SM-actin expression were: CONT 13.10 +/- 1.9, NIF 13.80 +/- 0.2, and ENAL 1.00 +/- 0.1 (P < 0.01). Vimentine staining showed no differences among the groups. It was concluded that enalapril reduces the peritubular and medullar interstitial fibrosis, whereas nifedipine has no effect.
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PMID:Renal interstitial sclerosis in aging: effects of enalapril and nifedipine. 873 1


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