Mechanism of effect of hypercapnic acidosis on renin secretion in the dog

Publisher Website
Google Scholar
Abstract
The effect of hypercapnic acidosis on renin secretion has not been clarified. Hypercapnic acidosis (PCO2 [partial pressure of carbon dioxide] 25-70 mmHg, P < 0.001; pH 7.43-7.04, P < 0.001) was induced in anesthetized dogs with constant renal perfusion pressure and 1 kidney denervated. Hypercapnic acidosis was associated with a rise in plasma renin activity (PRA) (from 5.9-16.3 ng .cntdot. ml-1 .cntdot. h-1, P < 0.001) and renin secretion in innervated kidneys. To determine if the fall in mean arterial pressure (from 145 to 129 mmHg, P < 0.001) associated with hypercapnic acidosis stimulated the observed neural renin secretion, hypercapnic acidosis was induced in animals in which norepinephrine maintained mean arterial pressure constant. In these animals, hypercapnic acidosis was associated with increases in PRA (from 10.7 to 25.3 ng ml-1 .cntdot. h-1, P < 0.001) and renin secretion in innervated kidneys. To further evaluate this neurogenic renin secretion, hypercapnic acidosis was induced in animals undergoing .beta.-adrenergic blockade with propranolol. In propranolol-treated animals, hypercapnia was not associated with a rise in either PRA (3.7 to 3.7 ng .cntdot. ml-1 .cntdot. h-1, NS [non-significant]) or renin secretion. To evaluate the role of prostaglandins [PG], hypercapnic acidosis was induced in animals treated with indomethacin. In these animals, hypercapnic acidosis resulted in increases in PRA (from 1.8 to 5.4 ng .cntdot. ml-1 .cntdot. h-1, P < 0.005) and renin secretion in innervated kidneys. Since anesthesia is associated with activation of the renin-angiotensin system, hypercapnic acidosis was induced in 6 conscious dogs and increases in PRA (from 0.8 to 1.8 ng .cntdot. ml-1 .cntdot. h-1, P < 0.05) were observed. Hypercapnic acidosis stimulates renin secretion independent of anesthesia, mechanical ventilation, mean arterial pressure, renal perfusion pressure and renal hemodynamics. This renin secretion is mediated by .beta.-adrenergic renal nerves and occurs independent of PG.