Effects of quinidine on vascular resistance and sympathetic nerve activity in humans

Abstract Objectives . The purpose of the present study was to test the hypothesis that intravenous quinidine, unlike procainamide, causes direct vasodilation and reflexly mediated increases in sympathetic nerve activity. Background . Intravenous quinidine can cause significant hypotension. Animal ejsprimente have suggested that quinidine blocks alpha-receptors and also refers vascular smootSi muscle by a nonadrenergic mechanism. In a recent study we showed that intravenous procainamide causes peripheral vasodilstion, hypotension and inhibition of sympathetic nerve activity in humans. Intraarterial procainamide, however, did not cause vasodilation. Methods . Postganglionie muscle sympathetic nerve traffic was recorded from the peroneal nerve at the fibular head with tungsten microeiectrodes, and forearm blood flow was measured with venous occlusion plethysmography. Central venous pressure was measured directly. The direct effects of quinidine on vascular resistance were determined with brachial artery quinidine infusions and messurement of ipsilateral forearm blood flow. Results . In eight normal subjects intravenous quinidine (8 mg/kg body weight infused for 27 min) decreased mean arterial pressure from 87 ± 3 (mean ± SE) to 83 ± 3 mm Hg, central venous pressure from 6.3 ± 0.6 to 5.0 ± 0.7 mm Hg and forearm vascular resistance from 32.2 ± 5.5 to 25.3 ± 4.7 U (all p Conclusions . These data show that quinidine, unlike procainamide, causes vasodilation directly and, when given intravenously, is associated with barorefles-mediated increases in sympathetic nerve activity.