Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies in our laboratory indicated that a blunted (40-50%) renal excretory response to isotonic intravenous saline loads occurred in conscious, renal-denervated dogs after 70% of the atrial mass was removed. The blunted responses could not be explained by differences in the responses of arterial pressure, renal nerve activity, or by measured changes of plasma immunoreactive atrial natriuretic peptide (iANP), arginine vasopressin (AVP), plasma renin activity (PRA), or aldosterone (Aldo). The present study was designed to determine whether the central nervous system (CNS) was the source of an unidentified substance, which could account for the blunting of the urine excretory response seen in the atrial-resected dogs. Renal denervation was performed in all dogs to eliminate alterations in efferent renal sympathetic nerve activity derived from reflexes activated during volume expansion. Cardiac denervation (CDX) was used to eliminate sensory cardiac afferent nerve activity to the CNS. A group of five renal-denervated dogs was given an isotonic volume load (400 ml/30 min) before and after complete CDX. Plasma AVP was fixed at normal plasma levels of 3 pg/ml by continuous intravenous infusion. Na and H2O excretion were not different in renal-denervated dogs compared with combined renal and cardiac denervation during the 5 h after the saline load. Plasma AVP and Aldo were unchanged with the volume loads, although PRA rose gradually over the 5 h after the saline loads. Plasma iANP increased transiently in the combined renal and cardiac-denervated state rising from a control of 65-120 pg/ml at the end of the load period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Saline diuresis and natriuresis in unanesthetized dogs: a missing atrial factor? 141 4

The purpose of this study was to determine (1) if the acute in vivo administration of cocaine and the cocaine metabolite ecgonine methyl ester (EME) activates the renin-angiotensin system (RAS) and alters cardiovascular function during pregnancy and (2) whether heart function is decreased in rabbits chronically exposed to cocaine or EME in vivo. The acute in vivo effects on plasma renin activity (PRA) were examined when cocaine (2 mg/kg) or EME (2 mg/kg) was administered intravenously. Arterial blood samples were withdrawn for hormonal analysis. Arterial pressure was measured using a COBE CDX III transducer and a Micro-Med 100 blood pressure analyzer. Hematocrit was measured using a microcapillary technique and serum protein was analyzed using refractometry. In chronic cocaine and EME studies, cardiovascular function was monitored in rabbits that were chronically exposed to cocaine or EME via Alzet osmotic pumps (1.66 microg/h for 14 d) implanted subcutaneously. On d 14, the animal was euthanized, and the heart was removed and exposed to 15 min of global ischemia using the Langendorff method. Coronary flow and left ventricular pressure (LVP) were assessed. The acute administration of cocaine or EME increased PRA and mean arterial pressure (MAP) in pregnant rabbits within 5 min. Coronary flow and LVP were significantly lower in the cocaine and EME-treated rabbits than in vehicle female rabbits.
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PMID:Cocaine activates the renin-angiotensin system in pregnant rabbits and alters the response to ischemia. 1227 Nov 52