RENIN AND VASOPRESSIN RESPONSES TO GRADED REDUCTIONS IN ATRIAL PRESSURE IN CONSCIOUS DOGS

Hypovolemia activates reflexes that stimulate secretion of renin and a rginine vasopressin (AVP). A large body of evidence, obtained mainly i n anesthetized preparations, supports the hypothesis that unloading ca rdiac receptors stimulates increases in plasma AVP and renin activity (PRA). We have observed significant increases in PRA before any change in either mean arterial pressure (MAP) or pulse pressure in conscious dogs undergoing continuous hemorrhage; however, plasma AVP did not ch ange until there was a significant fall in MAP. These results are comp atible with the hypothesis that cardiac receptors cause reflex stimula tion of renin but not AVP secretion. The aim of the present study was to test the hypothesis that a decrease in atrial pressure alone is suf ficient to stimulate an increase in plasma AVP and PRA. Graded thoraci c inferior vena caval constriction (TTVCC) was used to reduce atrial p ressure in four steps without altering MAP in conscious dogs. In a fif th step, TIVCC was increased to cause a fall in MAP. A reduction in le ft atrial pressure (LAP) of 4.2 +/- 0.9 mmHg was accompanied by a sign ificant (P < 0.05) increase in PRA from a control value of 0.4 +/- 0.1 ng angiotensin I (ANG I).ml(-1).3 h(-1) to 1.1 +/- 0.2 ng ANG I.ml(-1 ).3 h(-1) but no change in plasma AVP (from 1.0 +/- 0.1 to 1.2 +/- 0.2 pg/ml) or MAP (from 85 +/- 5 mmHg to 86 +/- 4 mmHg). Reducing LAP by 7.5 +/- 1.0 mmHg below control stimulated a further increase in PRA (1 .8 +/- 0.5 ng ANG I.ml(-l).3 h(-1)) but no change in plasma AVP (3.7 /- 1.7 pg/ml) or MAP (84 +/- 4 mmHg). Increasing TIVCC enough to cause a fall in MAP (25 +/- 4 mmHg below control) was accompanied by a sign ificant increase in plasma AVP (20 +/- 3 pg/ml above control). These r esults demonstrate that unloading cardiac receptors alone is sufficien t to stimulate an increase in renin but not AVP secretion in conscious dogs. The results suggest that arterial pressure is the critical vari able in the AVP response to acute hypovolemia.