Role of vasopressin in cardiovascular adaptation to sodium depletion in the conscious rat.

The hypothesis that vasopressin participates in cardiovascular adaptation to sodium depletion was examined in male Sprague-Dawley rats studied after 6 days (n = 28) or 4 weeks (n = 28) of low sodium diet. Blood pressure was similar on the two diets but heart rate, water intake and urine volume were all significantly greater at 4 weeks. Animals were randomly assigned to four acute treatment groups: controls, vasopressin pressor antagonist, d(CH2)5Tyr(Me)AVP (AVPA, 10 micrograms/kg); angiotensin converting enzyme (ACE) inhibitor, enalaprilic acid (150 micrograms/kg); combined ACE inhibitor and AVPA. Cardiac output and blood flow distribution were measured using labelled microspheres. Blood pressure, cardiac output and blood flow distribution were unchanged after AVPA alone. Angiotensin converting enzyme inhibition and ACE inhibitor plus AVPA produced similar falls in mean blood pressure at 6 days (-12 +/- 1, -14 +/- 3 mmHg) and 4 weeks (-11 +/- 2, -16 +/- 2 mmHg) due to parallel falls in peripheral resistance. Angiotensin converting enzyme inhibition was associated with selective increases in renal and mesenteric blood flow. Renal blood flow increased further after combined blockade at 6 days (ACE inhibitor 9.68 +/- 0.71; ACE inhibitor plus AVPA 11.92 +/- 0.73 ml/min per g, P < 0.05) but not at 4 weeks (ACE inhibitor 11.15 +/- 0.23; ACE inhibitor plus AVPA 10.76 +/- 0.78 ml/min per g). Vasopressin appears to contribute to early but not late cardiovascular adaptation to sodium depletion. A specific effect on the renal vascular bed is only revealed after removal of the dominant effect of angiotensin II (ANG II).