Aldosterone secretion during acute respiratory acidosis and NH4CI-induced metabolic acidosis in the goat

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Abstract
Acute respiratory acidosis was induced in goats by inhalation of 6% or 8% CO2 in air for 30 min. The lower CO2 concentration caused a significant rise in plasma cortisol (PC), but had no appreciable influence upon plasma aldosterone (PA), and did not affect the arterial blood pressure (aBP). A more pronounced PC response was observed in association with the inhalation of 8% CO2, but also here without concomitant increase in PA. However, the aBP became elevated by about 30% during the CO2 exposure with a simultaneous increase in glomerular filtration rate and a water diuresis, suggesting that the release of arginine vasopressin temporarily became inhibited. It was confirmed that metabolic acidosis induced by duodenal NH4Cl administration is preceded by a transient rise in PA. Dexamethasone-induced feedback inhibition of the ACTH secretion blocked the PA response, which possibly reflects NH4 ion stimulation of the ACTH release. The combined results of the CO2 and NH4Cl experiments seem to justify the conclusion that increases in PA seen in conjunction with acidosis do not reflect a direct hydrogen ion stimulation of the adrenal glomerulosa cells.