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)

To determine how endothelins affect regional kidney blood flow and responses to increased renal artery pressure (RAP), an extracorporeal circuit was established to control RAP independent of the mean systemic arterial pressure (MAP). RAP was first set at approximately 65 mm Hg, and endothelin-1 (1 ng/kg/min for 30 min then 0.4 ng/kg/min) or vehicle was infused into the renal artery, or the ET(A)/ET(B) antagonist TAK-044 (3 mg/kg plus 3 mg/kg/h) or vehicle was administered intravenously. RAP was then progressively increased in steps from approximately 65 to approximately 160 mm Hg. When RAP was approximately 65 mm Hg, endothelin-1 increased renal vascular resistance (RVR, 72%), and reduced cortical (CBF, 26%) but not medullary blood flow (MBF). TAK-044 reduced MAP (12%) and RVR (15%) and increased CBF (21%) but not MBF. When RAP was increased, renal blood flow (RBF), glomerular filtration rate, and urine and sodium excretion increased, while MAP fell. These responses were unaffected by endothelin-1. TAK-044 potentiated the increases in RBF and reductions in MAP in response to increased RAP, but did not affect urine and sodium excretion. Plasma renin activity was reduced by endothelin-1 and increased by TAK-044. Thus, both exogenous and endogenous endothelins reduce CBF but not MBF, and reduce plasma renin activity, but neither affect pressure natriuresis.
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PMID:Effects of renal arterial endothelin-1 and endogenous endothelins on regional kidney blood flow and renal antihypertensive mechanisms in anesthetized rabbits. 1107 Apr 16

1. Inhibition of the renin-angiotensin system (RAS) during kidney development produces chronic alterations in renal morphology and function that have been characterized in detail in adult animals. The aim of the present study was to determine the consequences of neonatal angiotensin-converting enzyme (ACE) inhibition on renal haemodynamics and function in rats at a much earlier age, namely 3-4 weeks. 2. Male Wistar pups received daily intraperitoneal injections of enalapril (10 mg/kg) or isotonic saline from birth until 24-28 days of age, when renal haemodynamics and function were assessed using clearance techniques under pentobarbital anaesthesia. 3. Enalapril-treated rats showed significant reductions in glomerular filtration rate (GFR; -44 +/- 6%; P < 0.05), effective renal plasma flow (ERPF; -33 +/- 6%; P < 0.05) and filtration fraction (-16 +/- 3%; P < 0.05) compared with saline-treated controls. Although mean arterial pressure tended to be lower in enalapril-treated rats, this group demonstrated a significant increase in renal vascular resistance compared with control rats (RVR; 46 +/- 6 vs 32 +/- 3 mmHg/mL per.min per g.kidney weight, respectively; P < 0.05). In enalapril-treated rats, urine osmolality was reduced (-59 +/- 5%; P < 0.05) and urine flow rate and fractional urinary excretion rates of sodium and potassium were markedly elevated compared with controls (P < 0.05). Enalapril-treated rats showed severe renal histological abnormalities, including wall thickening of cortical arterioles, papillary atrophy and tubulointerstitial alterations, mimicking those described previously in similarly treated rats examined in adulthood. 4. In conclusion, neonatal ACE inhibition in rats induces pronounced alterations in renal haemodynamics and function, characterized by reductions in ERPF and GFR, increased RVR and impaired tubular sodium and water reabsorption, which are evident at weaning.
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PMID:Renal haemodynamics and function in weanling rats treated with enalapril from birth. 1617 49


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