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Acute effects of doxazosin and atenolol on smoking-induced peripheral vasoconstriction in hypertensive habitual smokers.

The acute effects of selective alpha 1 inhibition with doxazosin (0.5-0.7 mg intravenously) and beta 1-blockade with atenolol (0.1 mg/kg body weight, intravenously) on smoking-induced peripheral vasoconstriction were investigated in 24 hypertensive habitual smokers. Forearm blood flow was measured by venous occlusion plethysmography and skin blood flow was estimated by thermography and laser doppler flowmetry. After the patients had smoked two cigarettes, plasma adrenaline elevations were similar under basal conditions and after drug administration; plasma noradrenaline remained unchanged. The smoking-induced increase in the heart rate was attenuated by atenolol compared with basal values. The smoking-induced increase in systolic blood pressure was more marked after atenolol and doxazosin (P less than 0.05) than before the drug administration. The smoking-induced increase in diastolic blood pressure was enhanced by atenolol (P less than 0.05) but unchanged by doxazosin. Smoking increased forearm vascular resistance under basal conditions (P less than 0.05) and after atenolol (P less than 0.01) but not after doxazosin. Similarly, skin temperature was significantly reduced by smoking under basal conditions and after the administration of atenolol (P less than 0.001) but not doxazosin. The smoking-induced reduction in skin blood flow was attenuated by doxazosin compared with atenolol (P less than 0.05). Thus, smoking-induced muscular and cutaneous vasoconstriction was inhibited by doxazosin as opposed to atenolol in hypertensive habitual smokers. This may reflect unmasked beta-adrenoceptor mediated vasodilation in addition to attenuated alpha 1-adrenoceptor mediated vasoconstriction.