Behavioral stress alters coronary vascular reactivity in borderline hypertensive rats

Background Behavioral stress has been proposed to contribute to the occurrence of myocardial ischemia, Objective To investigate the effect of chronic exposure to behavioral stress on the function and structure of the coronary artery of borderline hypertensive rats (BHR), Design BHR were either exposed to an air-jet stress for 2 h/day for 10 days or kept in their cage for 10 days. Methods After 10 days, hemodynamic measurements in conscious animals were recorded, and their hearts were removed for isolation of a left ventricular coronary artery for functional studies or for fixation by retrograde perfusion for study with scanning electron microscopy, Vascular reactivity was measured in isolated coronary arteries (approximate to 250 mu m) maintained at an intraluminal diameter of 40 mmHg while the intraluminal diameter was recorded continuously. Results The resting mean arterial pressure and heart rate in conscious, unrestrained BHR were not altered significantly by exposure to 10 days of 2 h/day air-jet stress, Coronary artery relaxation in response to the endothelium-dependent vasodilator acetylcholine was impaired in rats exposed to the air-jet stress compared with that in controls, An attenuated response to exogenous nitric oxide in coronary arteries from stressed BHR was confirmed by the finding of a reduced sensitivity to nitroprusside, which releases nitric oxide independently from the endothelium. However, relaxation of coronary arteries in response to isoproterenol, which acts independently from nitric oxide, was not altered, Coronary artery contraction in response to endothelin-l and phenylephrine was not altered in vessels taken from BHR exposed to behavioral stress compared with that in vessels from control rats, Scanning electron microscopy of the endothelial surface of the septal coronary artery showed no difference between vessels from control and stressed BHR, Conclusion These results indicate that behavioral stress impairs endothelium-dependent and nitric oxide-mediated coronary relaxation, but does not alter alpha(1)-adrenoceptor or endothelin-l-mediated contraction. By impairing coronary artery vascular relaxation, chronic exposure to behavioral stress may contribute to myocardial ischemia.