Nitric oxide‐dependent regulation of coronary vascular resistance in hypertension

Abstract

Hypertension is associated with impaired endothelium dependent relaxations in many vascular beds. Evidence from the coronary vasculature offers conflicting results. The current investigation examined the role of NO in regulating coronary vascular resistance (CVR) in spontaneously hypertensive rats (SHR) and their normotensive counterparts (WKY). Rats were anesthetized, the hearts were removed and the aorta was cannulated to allow for retrograde coronary perfusion using a constant flow Langendorff set‐up. Flow was assigned based on heart weight which was estimated from body weight. SHR had a greater baseline CVR than the WKY (6.72±0.34 vs 4.97±0.62 mmHg/ml/min, p<0.05). Following ET‐1 administration SHR had a greater resistance (9.82±0.75 vs 6.87±0.96 mmHg/ml/min, p<0.05) although the absolute change was not different. There were no differences in maximal reduction in CVR to bradykinin (BK) or sensitivity to BK. Treatment with LNAME caused an increase in resistance in both groups although the change in resistance was not different between the SHR and WKY (3.46±0.41 vs 3.02±0.69 p>0.05). LNAME completely abolished the BK induced reduction in CVR in both the SHR and WKY; the response to sodium nitroprusside was unchanged. Thus, the response to BK is NO dependent in both SHR and WKY. The CVR is elevated in the SHR and inhibition of eNOS increases CVR to a similar extent in both strains.Funded by NSERC & HSFO