Adenosine and metabolic regulation of coronary blood flow in dogs with renal hypertension.

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Abstract
It has been demonstrated that resting coronary vascular resistance is elevated with chronic hypertension and concomitant cardiac hypertrophy. The present study employed a model of 6-week, one-kidney, one wrapped Page hypertension to determine if the ability of the heart to match an increase in oxygen demand with an increase in oxygen supply (coronary blood flow) is impaired, and to determine if these vasoregulatory abnormalities are attributable to inadequate adenosine release. Studies were performed in a pentobarbital anesthetized, open-chest canine preparation using a pericardial infusate method to determine adenosine release. Results showed that dobutamine (a beta-receptor agonist) induced increases in myocardial oxygen consumption (MVO2) over a physiological range (8-30 ml O2 X min-1 X 100 g-1) that were accompanied by an increase in coronary blood flow (CBF) with no change in oxygen extraction. The relationship between MVO2 and CBF was not different between the normotensive (NTC) and hypertensive (RHT) animals. Pericardial infusate adenosine (PI ADO) concentrations were not different for the same MVO2 and CBF, and the relationships for MVO2 vs PI ADO as well as PI ADO vs CBF were unaltered by hypertension. However, the relationship between PI ADO and coronary vascular resistance (CVR) was altered in the RHT group such that a given PI ADO concentration was associated with a significantly higher CVR. These data suggest that, over the range of MVO2 studied, there are no limitations in metabolic regulation of the coronary circulation of RHT animals, and that the higher CVR encountered in the RHT group is not the result of a reduced release of the endogenous vasodilator, adenosine.