Distension of urinary bladder induces exaggerated coronary constriction insmokers with early atherosclerosis

Distension of the urinary bladder causes an increase in efferent sympatheti c activity, which can precipitate myocardial ischemia. Smoking has been sho wn to modulate activities of afferent nerves from the distended urinary bla dder and to impair endothelial function in response to sympathetic activati on. To assess the effect of bladder distension on coronary dynamics in smok ers, we measured epicardial and microvascular responses in 24 patients with early atherosclerosis (< 50% diameter stenosis). Patients were classified into habitual smokers (group 1, n = 14) and nonsmokers (group 2, n = 10). H abitual smokers were randomized into two subgroups on the basis of the use of doxazosin, as follows: subgroup 1A (n = 7), without administration of do xazosin before catheterization; subgroup 1B (n = 7), with dosing doxazosin. In response to bladder distension (mean intravesical pressure 21.5 mmHg), bladder distension significantly decreased coronary diameter at the stenoti c segments, coronary blood flow, and increased coronary resistance compared with baseline values, in subgroup 1A patients. In subgroup 1B patients dur ing bladder distension, coronary diameter, coronary blood flow, and coronar y resistance did not show significant changes compared with baseline values . There were significant differences of coronary diameter at the stenotic s egments, coronary blood flow, and of changes of coronary vascular resistanc e between subgroup 1A and group 2 during bladder distension, despite simila r changes in rate-pressure product. The present study showed that urinary b ladder distension caused an abnormal vasomotor response of epicardial vasoc onstriction and a concomitant increased coronary resistance, which leads to reduction in coronary blood flow in patients with early atherosclerosis. S moking may further impair the response, implying that smoking has exaggerat ed response to sympathetic stimulation of conduit and resistance vessels. T he abnormal response was abolished by pretreated administration of doxazosi n, suggesting that the involved mechanisms are related to <alpha>(1)-adreno ceptors.