Cardiovascular responses to cigarette smoke exposure in restrained conscious rats.

The effect of exposure to cigarette smoke on cardiovascular function was examined in conscious, restrained Sprague-Dawley rats. Rats were exposed to 3, 6 and 9 puffs of either air or cigarette smoke during the "break in" period and to 10 puffs on the day of the experiment (day 4). HR, cardiac output and mean arterial pressure were recorded continuously throughout the experimental period. Rats exposed previously to cigarette smoke generated from either low-nicotine (0.16 mg/cig.) or high-nicotine (2.45 mg/cig.) cigarettes showed a dose-related decrease in HR in response to restraint stress. In addition, exposure to cigarette smoke produced a further decrease in HR and cardiac output and an increase in mean arterial pressure. This effect by cigarette smoke was dose-dependent (dependent on the cigarette nicotine content) and was antagonized by intra-arterial pretreatment with the nicotinic antagonists mecamylamine and hexamethonium and also with the ganglionic blocker chlorisondamine. Intra-arterial pretreatment with atropine methyl bromide blocked the bradycardia in response to both restraint stress and cigarette smoke. Furthermore, pretreatment with an arginine vasopressin antagonist, d(CH2)5Tyr(Me)arginine vasopressin, significantly attenuated the increase in mean arterial pressure and total peripheral resistance and the decrease in HR and cardiac output due to cigarette smoke. On the other hand, pretreatment with the opioid receptor antagonist naloxone had no effect on cardiovascular parameters in response parameters in response to cigarette smoke. These results implicate arginine vasopressin, in addition to the activation of both sympathetic and parasympathetic systems, in mediating cardiovascular responses to cigarette smoke.