Acute Effects of Urinary Bladder Distention on the Coronary Circulation in Patients with Early Atherosclerosis

Abstract Objectives This study sought to examine whether distension of the urinary bladder, a physiological stimulus, could induce impaired coronary circulation in patients with early atherosclerosis. Background Distension of the urinary bladder reflexly causes an increase in sympathetic activity . The effect of such distension on the coronary circulation in patients with early atherosclerosis remains unknown. Methods To assess the effect of bladder distension on coronary dynamics, epicardial and microvascular responses were measured with intracoronary Doppler flow wire in 40 patients with early atherosclerosis (< 50% diameter stenosis ). Patients were randomized into two groups on the basis without (group 1, n = 20) or with (group 2, n = 20) pretreatment of 1 adrenergic receptor blocker (oral doxazosin 2 mg). Coronary flow velocity and quantitative coronary angiography were monitored at baseline, during urinary bladder distension, and after intracoronary nitroglycerin injection. Results In response to bladder distension, bladder distension significantly decreased coronary diameter at the stenotic segments (p < 0. 001), coronary blood flow (p < 0.001), and increased coronary resistance ( p < 0.001) compared with baseline values, in group 1 patients. In group 2 patients during bladder distension, angiographic variables did not show significant changes compared with baseline values. No significant differences were noted between the groups in the responses of angiographic variables after nitroglycerin administration . Conclusions The present study showed for the first time that urinary bladder distension caused vasoconstriction of coronary conduit and resistance vessels involved mechanisms related to 1-adrenoceptors. Pretreated administration of doxazosin had reversed the changes towards baseline. Vasoconstriction during bladder distension can be relieved after nitroglycerin administration, suggesting an unchanged responsiveness of vascular smooth muscle cells to such distension.