Coronary vascular ATP-sensitive potassium channels are activated to a greater extent in spontaneously hypertensive rats than in Wistar-Kyoto rats

Objective To determine whether opening of coronary vascular adenosine 5'-triphosphate (ATP)-sensitive potassium (K(ATP)) channels is involved in the maintenance of resting coronary flow in hypertrophied hearts. Methods We examined the effects of glibenclamide, a selective inhibitor of K(ATP) channels, on basal coronary vascular tone in Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs). Using a Langendorff system, the hearts from WKY rats and SHRs were isolated and perfused with oxygenated Krebs-Henseleit solution at a constant perfusion pressure of 60 and 100 mmHg respectively. Results Basal coronary flow and myocardial oxygen consumption (MVo₂) were similar in SHRs and WKY rats. The percentage decreases in coronary flow with glibenclamide at graded doses were greater (P < 0.01) in SHRs than in WKY rats (n = 8), whereas the percentage decreases in MVo₂ with glibenclamide were similar in the two groups. The decreases in coronary flow caused by U46619 (a thromboxane A₂-mimetic agent) were similar in SHRs and WKY rats (n = 4). The increase in coronary flow caused by pinacidil (a K(ATP) opener) was greater in SHRs than in WKY rats; glibenclamide prevented the pinacidil-induced increase in coronary flow in both SHRs and WKY rats. There was a significant positive correlation between the glibenclamide-induced decrease in coronary flow and the degree of left ventricular hypertrophy (r = 0.54, P < 0.05). Conclusion Our results suggest that the basal opening state of coronary vascular K(ATP) channels is activated to a greater extent in SHRs than WKY rats, which may contribute to the maintenance of basal myocardial perfusion in hypertrophied hearts.