RELEASE OF ENDOTHELIUM-DERIVED NITRIC-OXIDE (NO) INTO THE CORONARY CIRCULATION OF NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATS - SIGNIFICANCE FOR CORONARY VASOMOTION

Endothelium-derived nitric oxide (NO) is an important modulator of coronary vascular tone. Long lasting hypertension leads to a reduction of coronary flow reserve paralleled by structural changes in the coronary microcirculation. The aim of the present study was to investigate whether or not endothelial NO release into the coronary microcirculation is altered in arterial hypertension. Isolated hearts from either normotensive (WKY) or spontaneously hypertensive rats (SHR) were perfused according to Langendorff. Aside from changes in coronary perfusion pressure (CPP), left ventricular pressure (LVP) and dp/dt the release of NO into the coronary venous effluent was quantified continously deriving a difference spectrum. CPP and LVP was significantly higher in SHR compared to WKY. Correspondingly to the elevated CPP the basal release of NO was almost 100% higher compared to that in WKY. Bradykinin elicited concentration-dependently a coronary vasodilation in both groups. In parallel the release of NO increased by more than 200 pmol/min. The rate of stimulated NO release normalized to heart weight was similiar in both groups. These results indicate, that under basal conditions the release of NO into the coronary circulation of hypertensive animals is significantly enhanced whereas stimulation of basal NO synthesis do not reveal any significant differences between both groups. An increase of basal NO release may represent a compensatory mechanism for structural alterations in the coronary circulation associated with arterial hypertension.