Article: PDF OnlyDeering A. H.; Riddell, J. G.; Harron, D. W. G.; Shanks, R. G.Journal of Cardiovascular Pharmacology: March 1988 - p 284-290 Free Abstract Summary Several mechanisms have been suggested for the absence of reflex tachycardia in response to the hypotensive effect of the selective α1-adrenoceptor antagonist indoramin, including, in animals, membrane-stabilising activity, prolongation of repolarisation time, and reduction in baroreflex sensitivity. The present study investigated the effect of acute and chronic oral administration of indoramin (50 mg daily for 8 days) on baroreflex sensitivity in six healthy male volunteers. Baroreflex function was measured by determining the relationship between systolic blood pressure (SBP) and R–R interval following intravenous administration of phenylephrine. Indoramin shifted (p < 0.05) the phenylephrine dose-response curve to the right on days 1 and 8 compared with placebo. Baroreflex sensitivity [R–R (ms)/SBP (mm Hg)] was reduced (p < 0.05) by indoramin on day 1 compared with placebo (18.3 ± 1.3 vs. 11.2 ± 2.2 ms/mm Hg), and on day 8 compared with pretreatment values (18.3 ± 2.8 vs. 10.8 ± 1.8 ms/mm Hg). Acute but not chronic administration of indoramin caused (p < 0.05) sedation; tremor tended to increase with chronic administration. It is suggested that depression of baroreflex sensitivity by indoramin may explain, in part, the lack of reflex tachycardia associated with its antihypertensive effect. © Lippincott-Raven Publishers.