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Acidic media have been reported to inhibit the hydro-osmotic effect of vasopressin in toad bladders, probably through inhibition of the cyclic AMP system. However, the mechanism of inhibition of the cyclic AMP system is controversial. Therefore, that inhibitory mechanism was further investigated in rat kidneys. The antidiuretic response to vasopression was significantly inhibited in animals with metabolic acidosis. The inhibition of the antidiuretic response was associated with a smaller than normal increase of urinary excretion of cyclic AMP after the iv injection of vasopressin. In in vitro experiments, both the increase of cyclic AMP concentration in renal medullary slices and the activation of adenylate cyclase in medulla by vasopressin were significantly less in acidic than in control media. These findings suggest that medabolic acidosis inhibits the antidiuretic effect of vasopressin by inhibiting the vasopressin-dependent cyclic AMP system in the kidney. Acidic media also inhibited cyclic AMP-phosphodiesterase. These dual effects of acidosis on adenylate cyclase and cyclic AMP-phosphodiesterase may explain the conflicting findings observed in the experiments on toad bladders.
N Beck, and
Kim H-P
January 1987,
Renal physiology,
N Beck, and
Kim H-P
July 1975,
Endocrinology,
N Beck, and
Kim H-P
February 1980,
Biochimica et biophysica acta,
N Beck, and
Kim H-P
February 1989,
The American journal of physiology,
N Beck, and
Kim H-P
August 1980,
Japanese journal of pharmacology,
N Beck, and
Kim H-P
December 1997,
Molecular and cellular biochemistry,
N Beck, and
Kim H-P
June 1987,
Masui. The Japanese journal of anesthesiology,
N Beck, and
Kim H-P
May 1973,
FEBS letters,
N Beck, and
Kim H-P
March 1989,
Kidney international,
N Beck, and
Kim H-P
January 1982,
The Journal of laboratory and clinical medicine,
