[The effect of inhibition of angiotensin II synthesis on the response of plasma antidiuretic hormone (ADH) to the osmotic and volume-dependent stimuli in uremic patients (author's transl)].
The effect of inhibition of angiotensin II synthesis by captopril on the response of plasma ADH to the osmotic and volume-dependent stimuli has been studied in 15 uremic patients. Captopril administration had no effect either on basal plasma ADH or on plasma ADH response to the osmotic stimulus. Time-course of plasma ADH following hypertonic saline administration and sensitivity of the response (increase of plasma ADH related to increase of plasma sodium) were not modified. On the contrary, the response of plasma ADH to the volume-dependent stimulus induced by hemofiltration was markedly blunted by captopril administration. The sensitivity estimated from the slope of the regression line relating plasma ADH to the cumulated lost volume was clearly diminished. These results suggest that angiotensin II mediates ADH response only to the volume-dependent stimulus.
D000328:Adult; D000368:Aged; D000804:Angiotensin II / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D001769:Blood; D002216:Captopril / Q000494:pharmacology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009994:Osmolar Concentration; D012964:Sodium / Q000097:blood; D013997:Time Factors; D014462:Ultrafiltration; D014511:Uremia / Q000503:physiopathology*; D014667:Vasopressins / Q000097:blood*
D014667:Vasopressins; D000804:Angiotensin II; D002216:Captopril; D012964:Sodium
Effet de l'inhibition de la synthèse de l'angiotensine II sur la sécrétion de l'hormone antidiurétique chez l'urémique en réponse aux stimuli osmotique et volumique.