CARDIOVASCULAR-RESPONSES TO CIGARETTE-SMOKE EXPOSURE IN RESTRAINED CONSCIOUS RATS

Citation
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
Citations number
43
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00223565
Volume
275
Issue
2
Year of publication
1995
Pages
646 - 653
Database
ISI
SICI code
0022-3565(1995)275:2<646:CTCEIR>2.0.ZU;2-3
Abstract
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.