Aa. Houdi et al., CARDIOVASCULAR-RESPONSES TO CIGARETTE-SMOKE EXPOSURE IN RESTRAINED CONSCIOUS RATS, The Journal of pharmacology and experimental therapeutics, 275(2), 1995, pp. 646-653
The effect of exposure to cigarette smoke on cardiovascular function w
as examined in conscious, restrained Sprague-Dawley rats. Rats were ex
posed 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 contin
uously throughout the experimental period. Rats exposed previously to
cigarette smoke generated from either low-nicotine (0.16 mg/cig.) or h
igh-nicotine (2.45 mg/cig.) cigarettes showed a dose-related decrease
in HR in response to restraint stress. In addition, exposure to cigare
tte 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 antagoni
sts mecamylamine and hexamethonium and also with the ganglionic blocke
r chlorisondamine. Intra-arterial pretreatment with atropine methyl br
omide blocked the bradycardia in response to both restraint stress and
cigarette smoke. Furthermore, pretreatment with an arginine vasopress
in antagonist, d(CH2)(5)Tyr(Me)arginine vasopressin, significantly att
enuated the increase in mean arterial pressure and total peripheral re
sistance and the decrease in HR and cardiac output due to cigarette sm
oke. On the other hand, pretreatment with the opioid receptor antagoni
st naloxone had no effect on cardiovascular parameters in response to
cigarette smoke. These results implicate arginine vasopressin, in addi
tion to the activation of both sympathetic and parasympathetic systems
, in mediating cardiovascular responses to cigarette smoke.