Mechanisms of enhanced renin secretion during CO2 retention in dogs

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Abstract
Arterial renin activity and renal renin secretion were studied during CO2 inhalation (constant minute ventilation) in chloralose-anesthetized dogs. In 8 dogs with both renal nerves and adrenals intact, successive 30 min periods of 4, 8 and 12% CO2 inhalation resulted in a dose-dependent and reversible increase in arterial renin activity. Ten dogs with intact adrenals were studied 3-4 days after denervation of 1 kidney. Measurement of the simultaneous rate of renin secretion from the denervated kidney and from the contralateral innervated kidney indicated that both increased their rate of renin secretion after 10 min of 12% CO2 inhalation. In 6 adrenalectomized dogs with 1 kidney denervated, the denervated kidney failed to respond to an identical hypercapnic stimulus while the contralateral innervated kidney doubled its rate of renin secretion. Comparable hypercapnemia was produced in 6 intact dogs, but concomitant acidemia was prevented by infusion of tris(hydroxymethyl)aminomethane (Tris; 0.5 mM.cntdot.kg-1.cntdot.min-1, i.v.). Plasma renin activity (PRA) increased significantly despite the maintenance of a relatively constant arterial pH. In contrast, PRA did not change in 6 dogs when pH was lowered by lactic acid infusion (0.33 mM.cntdot.kg-1.cntdot.min-1 i.v.) but PaCO2 was maintained relatively constant (controlled minute ventilation). Acute respiratory acidosis stimulates renin release via adrenal medullary and renal nerve activation. The response is dependent upon elevation of PaCO2 rather than production of arterial pH per se.

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