Abstract
To investigate the role of the sympathetic nervous system in the sodium retention after systemic vasodilation, 15 hypophysectomized dogs undergoing saline diuresis (5 ml/min) had the left kidney denervated (5% phenol in 70% ethanol). After stable urine flows were obtained, control clearances for inulin, PAH, free-water, distal chloride delivery and fractional distal chloride reabsorption were obtained. In 8 dogs, diazoxide (D) as a bolus (5 mgm/kg) was infused; in 7, sodium nitroprusside (N) was infused. During both infusions, mean arterial pressure dropped from 133±6 (x±SEM) to 83±7 torr (p <.01). With D, UNaV from the right kidney fell from 23±7 to 7±2 uEq/min (p<.01). CIN and CPAH decreased slightly but significantly (p<.05). CH2O + CCI decreased from 6.1±.3 to 2.1±.8 (p<.01) and 6.7±.1 to 3.1±1.1 (p<.01) ml/min/100 GFR, respectively. CH2O + CCI/CH2O was not affected. No significant changes on the left were noted. With N, no changes occurred in CIN or CPAH. UNaV decreased on the right from 20±4 to 12±3 uEq/min (p<.05). CH2O and CH2O+CCI decreased from 8.5±1.0 to 4.7±1.3 and 8.9±1.0 to 4.4±1.5 ml/min/100 GFR respectively (p<.05), no changes were noted on the left. The data indicate that the renal sympathetic nerves increase sodium reabsorption in the proximal nephron during acute systemic vasodilation.
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Brouhard, B., Lagrone, L., Allen, W. et al. 1487 MECHANISM OF ANTINATRIURESIS AFTER SYSTEMIC VASODILATION. Pediatr Res 15 (Suppl 4), 691 (1981). https://doi.org/10.1203/00006450-198104001-01516
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DOI: https://doi.org/10.1203/00006450-198104001-01516