Response of collateral-dependent myocardium to vasopressin release during prolonged intense exercise
Symons, J.D.; Longhurst, J.C.; Stebbins, C.L.
American Journal of Physiology 264(5 Pt 2): H1644-H1652
1993
ISSN/ISBN: 0002-9513 PMID: 7684576 Document Number: 406269
We hypothesized that vasopressin concentrations during exercise attenuate the increase in collateral-dependent blood flow leading to left ventricular dysfunction in Ameroid-occluded miniswine. An Ameroid occluder was placed around the proximal left circumflex coronary artery (LCX) of 19 miniswine. Ten weeks later V-1 receptor blockade with the use of (d(CH-2)-5Tyr-(Me))arginine vasopressin (10-12 mu-g/kg iv) increased resting transmural flow (radioactive microspheres) in the LCX region, indicating the presence of V-1 receptors. Neither injection of lysine vasopressin (125 pmol/kg) after V-1 receptor blockade nor injection of two specific V-2 receptor agonists caused changes in mean arterial pressure, heart rate, or left anterior descending coronary arterial flow velocity, indicating that V-2 receptors mediate no appreciable vasodilation in the swine coronary circulation. Next the ratio of collateral to noncollateral flow and regional systolic wall thickening (sonomicrometer dimension gauges) were measured at rest and after 20 min of prolonged, intense treadmill exercise (85-90% of heart rate reserve) in the presence and absence of V-1 receptor antagonism. This degree of exertion increased plasma lysine vasopressin from 6.2 +- 1.0 at rest to 21.0 +- 7.0 pg/ml (P lt 0.05) during the unblocked run. However, the decrease in transmural blood flow ratio (collateral to noncollateral flow) from rest was similar during exercise before and after V-1 receptor blockade (0.78 +- 0.07 and 0.80 +- 0.05, respectively; P lt 0.05 vs. rest). Likewise, percent systolic wall thickening in the collateral-dependent region decreased from rest to exercise in the absence and presence of V-1 receptor antagonism (35.9 +- 4.5 and 39.5 +- 3.8%, respectively; P lt 0.05 vs. rest). Because V-1 receptor blockade caused a significant reduction in mean and diastolic pressure during treadmill running, six pigs performed the same two exercise protocols except that dextran was infused during the V-1 receptor blockade run to match blood pressures to those obtained during the unblocked run. Similar transmural blood flow ratios and systolic wall thickening responses were still observed before and after blockade. We conclude that coronary vasodilatory metabolites released during prolonged, intense exercise predominate over the potential vasoconstrictor effects of vasopressin.