Abstract
To evaluate the hypothesized renal actions of corticotropin releasing hormone (CRH), adult male conscious normally hydrated or volume-expanded rats (6 ml saline) were injected iv with various doses of CRH (1–5 μg). Some groups of rats were injected with arginine vasopressin (AVP) antagonist (2 or 10 μg) iv prior to CRH (5 μg). Urine was collected for volume, Na, K, and cyclic guanosine monophosphate (cGMP) determination. AVP and atrial natriuretic pepride (ANP) were determined in blood by radioimmunoassay. Blood pressure (BP) was measured by telemetry. In both normally hydrated and volume expanded conscious rats, the biphasic effects of CRH injected iv were observed. Initially, within the first hour, CRH caused dose-dependent antidiuresis, decreased sodium, potassium and urinary cGMP excretion. Plasma AVP was already increased significantly (p < 0.01) within 5 min after injection from 3.9 ± 0.5 pg/ml to 15.5 ± 3.3 pg/ml (n = 15) at 15 min, then declined by 30 min to the concentration reached at 5 min and was maintained for 180 min. Changes in plasma ANP followed a mirror image of AVP. Plasma ANP correlated with the decrease of ANP synthesis in the left ventricle. Four hours after the injection, a marked diuresis, natriuresis, kaliuresis and an increase in urinary cGMP occurred. This was accompanied by increased ANP mRNA in the right atrium at 180 min. All urinary changes were reversed by a V2 receptor antagonist (2 or 10 μg) given iv. Control injection of saline evoked an immediate (3–5 min) increase in BP, and this elevation was markedly inhibited by CRH (5 μg). Heart rate was further increased. We hypothesize that the renal effects are mediated by vasodilation induced by CRH that decreases the baroreceptor input to the brain, leading to the rapid release of AVP which acts on the heart and inhibits ANP release and synthesis. These effects could be of physiological significance during the stress.
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