Abstract

It is well known that the alternations on humoral homeostasis such as a decrease of pH, an elevation of PaCO2 and changes of electrolytes have been detected during respiratory acidosis. The author is of the opinion that the renin-angiotensin-aldosterone system might be related to these changes during respiratory acidosis. Recently, Fujii and Morita have reported that an increase in plasma renin activity appeared during acute respiratory acidosis. These reports prompted me to question whether the renin-angiotensin-aldosterone system was related to the pathophysiological evidence concerning the respiratory acidosis. It is generally accepted that plasma aldosterone concentration is controlled by (1) the renin-angiotensin system, (2) ACTH and (3) serum potassium. Therefore, the purpose of this experiment was to investigate the roles of the renin-angiotensin system and electrolyte metabolism on plasma aldosterone concentration during acute respiratory acidosis. I initiated acute respiratory acidosis with 10% CO2 inhalation in healthy mongrel dogs, and then plasma aldosterone concentration, plasma renin activity, electrolytes and cardiorenal hemodynamics were measured. The results were as follows: 1. The increase of plasma aldosterone concentration was delayed and blurred, in contrast with a significant increase of plasma renin activity, during the acute respiratory acidosis, due to delayed time course of angiotensin II stimulation and also the expected changes in the concentration of angiotensin II receptors on the zona glomerulosa in the adrenal cortex. 2. There was a possibility that the increase in the reabsorption of sodium and water in the proximal tubules, and the increase of ADH secretion during the acute respiratory acidosis, could be related to a decrease in excreted sodium and potassium as well as urine volume. These results suggest that the changes of plasma aldosterone concentration may be affected partially by renin-angiotensin system but not by serum potassium, and plasma aldosterone should be a minimal determinant on the electrolyte metabolism during respiratory acidosis with 10% CO2 inhalation.

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