[Modification of the smoking-induced hemodynamic effect by nifedipine]

Effects of nifedipine, a Ca(++)-channel blocker, on smoking-induced hemodynamic changes were studied in 35 habitual male smokers. They were divided into three groups: 20 healthy persons (G1), 11 patients with essential hypertension (G2) who were under nifedipine treatment, and 4 patients (G3) with essential hypertension but who were receiving no medication. After abstaining from smoking for more than 12 hours, they smoked, within 10 minutes, two filtered cigarettes each containing 2 mg of nicotine. Hemodynamic parameters were measured and blood samples were taken before and 5, 10, and 30 minutes after beginning to smoke. In each group, smoking produced significant increases in blood pressure, heart rate and cardiac output. Plasma adrenaline increased significantly in 3 groups, and tended to be highest in G2. Plasma noradrenaline was the highest in G2 predominantly, but did not change after smoking. These results indicate that a smoking-induced hyperdynamic state including vasoconstriction due to catecholamine release might not depend on the calcium channel which is blocked by nifedipine, and the reflex activation of the sympathetic nerve system would develop in the presence of nifedipine.