Abstract
To determine the contribution of renal nerves to natriuresis produced by selective alpha-2 adrenergic receptor activation in volume-loaded. Inactin-anesthetized rats, responses to B-HT 933 (20 micrograms/kg/min, i.v.) were compared in the chronically denervated kidney with responses in the contralateral innervated kidney. Plasma vasopressin concentration was maintained at high physiological levels by constant infusion of arginine vasopressin (170 pg/kg/min, i.v.). Control rats received arginine vasopressin and saline only. Arterial pressure and heart rate were decreased significantly by B-HT 933 (12 mm Hg and 80 beats/min. respectively). Glomerular filtration rate was not altered in innervated or denervated kidneys, whereas renal blood flow was decreased slightly, but significantly, in denervated but not innervated kidneys. B-HT 933 increased urine flow and total and fractional sodium excretion significantly in innervated kidneys but not in denervated kidneys when compared with control animals. Urine osmolality was also decreased significantly in innervated kidneys, but remained hyperosmotic to plasma. The data indicate that, in the presence of fixed levels of arginine vasopressin, chronic renal denervation prevented the natriuretic and diuretic effect of B-HT 933 in anesthetized rats. These results suggest that central and/or peripheral effects of alpha-2 adrenergic receptor activation were involved in producing natriuresis in the innervated kidney by decreasing renal sympathetic nerve influence on tubular sodium reabsorption.
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