Renin and vasopressin responses to graded reductions in atrial pressure in conscious dogs
O'Donnell, C.P.; Thompson, C.J.; Keil, L.C.; Thrasher, T.N.
American Journal of Physiology 266(3 Pt 2): R714-R721
1994
ISSN/ISBN: 0002-9513 PMID: 8160864 Document Number: 433327
Hypovolemia activates reflexes that stimulate secretion of renin and arginine vasopressin (AVP). A large body of evidence, obtained mainly in anesthetized preparations, supports the hypothesis that unloading cardiac 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 change until there was a significant fall in MAP. These results are compatible with the hypothesis that cardiac receptors cause reflex stimulation 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 sufficient to stimulate an increase in plasma AVP and PRA. Graded thoracic inferior vena caval constriction (TIVCC) was used to reduce atrial pressure in four steps without altering MAP in conscious dogs. In a fifth step, TIVCC was increased to cause a fall in MAP. A reduction in left atria) pressure (LAP) of 4.2 +- 0.9 mmHg was accompanied by a significant (P lt 0.05) increase in PRA from a control value of 0.4 +- 0.1 ng angiotensin I (ANG I) cntdot ml-1 cntdot 3 h-1 to 1.1 +- 0.2 ng ANG I cntdot ml-1 cntdot 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 cntdot ml-1 - 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 significant increase in plasma AVP (20 +- 3 pg/ml above control). These results demonstrate that unloading cardiac receptors alone is sufficient to stimulate an increase in renin but not AVP secretion in conscious dogs. The results suggest that arterial pressure is the critical variable in the AVP response to acute hypovolemia.