Chronic administration of water soluble tobacco smoke extract or nicotine fails to influence porcine coronary artery reactivity.

To determine if tobacco smoke components directly influence coronary vascular reactivity, we evaluated the contractile effects of prostaglandin (PG)F2 alpha and hypertonic KCl in porcine isolated left anterior descending coronary arteries derived from animals chronically treated (18 weeks) with either water soluble tobacco smoke extract, nicotine alkaloid, or saline. Dosing protocols for the extract and for nicotine were designed to achieve blood levels of nicotine approximating those attained by consumption of 2 packs/day of University of Kentucky 2Rl reference cigarettes. Histochemical evaluation of the arteries indicated that both the extract and nicotine caused expected increases in the collagen content of the tunica media. Neither the water soluble extract nor pure nicotine significantly altered coronary vascular sensitivity (as expressed by the ED50) to KCl or PGF2 alpha. Similarly, neither treatment altered the maximum contractile responses (determined as the tension developed normalized to mg wet wt) evoked by KCl and PGF2 alpha. These results indicate that prolonged exposure to water soluble components of tobacco smoke, in doses sufficient to elevate the collagen content of the coronary vascular wall, do not have direct effects on coronary reactivity to selected vasoconstrictor stimuli.