Interactions between coronary occlusion and the renin-angiotensin system in the dog.

Studies were carried out in 39 barbiturate-anesthetized dogs to determine whether the renin-angiotensin system is important in control of hemodynamics and coronary flow during myocardial ischemia. Plasma renin activity (PRA) was 2.2 +/- 0.4 ng x ml-l x hr-1 immediately before coronary artery occlusion (CAO) and increased to 3.8 +/- 0.5 (p less than .005) 15 minutes after CAO. In nephrectomized dogs, PRA was 0.76 +/- 0.14 ng x ml-l x hr-1 two hours after nephrectomy and remained unchanged after CAO. In contrast, hemodynamic changes following CAO were similar between nephrectomized and intact dogs: mean arterial pressure fell from 126 +/- 4 pre CAO to 116 +/- 4 mm Hg post CAO (p less than 0.005) in nephrectomized dogs and from 130 +/- 11 to 120 +/- 11 mm Hg (p less than 0.005) in intact dogs. Left atrial pressure rose from 5.4 +/- 0.9 pre CAO to 7.7 +/- 0.9 mm Hg (p less than 0.005) post CAO in nephrectomized from 5.4 +/- 0.9 pre CAO to 7.7 +/- 0.9 mm Hg (p less than 0.005) post CAO in nephrectomized dogs and 6.3 +/- 1.3 to 9.0 +/- 1.8 mm Hg (p less than 0.005) in intact dogs. Heart rate remained unchanged in both groups. In sham-operated dogs without CAO, neither the angiotensin II blocker Saralasin nor the converting enzyme inhibitor Captopril had significant effects on systemic (SVR) and coronary (CVR) vascular resistances. In contrast, in dogs with CAO, these drugs reduced CVR from 1.28 +/- 0.13 mm Hg x ml-1 x min x 100 g heart weight (resistance units = RU) to 0.85 +/- 0.08 RU (p less than 0.05) (Saralasin) 15 minutes after treatment and from 1.17 +/- 0.09 to 0.88 +/- 0.08 RU (p less than 0.025), (Captopril) respectively. However, only Captopril reduced SVR, from 10.7 +/- 1.13 to 8.2 +/- 0.8 RU (p less than 0.025). Both Captopril and Saralasin induced a significant increase in collateral blood flow. Nephrectomy, two hours prior to CAO, significant increase in collateral blood flow. Nephrectomy, two hours prior to CAO, significantly reduced the effect of Captopril on CVR and collateral blood flow while the effect on SVR persisted. Thus the reduction in CVR appears to be an effect of inhibition of the renin-angiotensin system; this system participates in control of CVR during CAO and may limit coronary collateral blood flow.