|The renin-angiotensin system does not contribute to the endothelial dysfunction and increased infarct size in rats exposed to second hand smoke.|
|PMID: 11984749 Owner: NLM Status: MEDLINE|
|INTRODUCTION: Both second hand smoke (SHS) and the renin-angiotensin system (RAS) contribute to endothelial dysfunction and increased infarct size in a rat ischaemia-reperfusion model. However, the potential interaction between SHS and the RAS is unknown. METHODS: Eighty-four rats were randomised into four groups: group C was a normal control; L was given 40 mg/kg/day of losartan in drinking water; SC and SL were exposed to SHS (smoking chamber) and given regular water or 40 mg/kg/day of losartan in drinking water, respectively. After six weeks of pre-treatment, rats were subjected to 17 minutes of left coronary artery occlusion and 2 hours of reperfusion with haemodynamic and ECG monitoring. RESULTS: Haemodynamics were not significantly different among the four groups. Losartan increased the threshold for ventricular fibrillation (p=0.0001) and reduced spontaneous ventricular arrhythmias (p=0.002) during ischaemia-reperfusion, while SHS did not (p=0.713, 0.110), and there was no interaction between losartan and SHS. The maximal endothelium-dependent vasorelaxation induced by a calcium ionophore (A23187) was increased by losartan (p=0.007). Myocardial infarct size was smaller in the losartan groups (p=0.032), larger in the SHS groups (p=0.0001), and there was no significant interaction. CONCLUSION: In conclusion, losartan decreased infarct size and increased endothelium-dependent vasorelaxation. SHS exposure impaired endothelial function and increased infarct size. The effects of losartan and SHS were consistently independent of each other. These results suggest that the RAS does not contribute to the adverse effects of SHS.|
|Bo-qing Zhu; Richard E Sievers; Amanda E M Browne; Robert T Hillman; Kamel Chair; Randall J Lee; Kanu Chatterjee; Stanton A Glantz; William W Parmley|
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|Type: Journal Article|
|Title: Journal of the renin-angiotensin-aldosterone system : JRAAS Volume: 3 ISSN: 1470-3203 ISO Abbreviation: J Renin Angiotensin Aldosterone Syst Publication Date: 2002 Mar|
|Created Date: 2002-05-01 Completed Date: 2002-09-24 Revised Date: 2007-11-15|
Medline Journal Info:
|Nlm Unique ID: 100971636 Medline TA: J Renin Angiotensin Aldosterone Syst Country: England|
|Languages: eng Pagination: 54-60 Citation Subset: IM|
|Department of Medicine, University of California, San Francisco 94143-0124, USA.|
|APA/MLA Format Download EndNote Download BibTex|
Antihypertensive Agents / pharmacology
Arrhythmias, Cardiac / physiopathology
Electrocardiography / drug effects
Endothelial Growth Factors / metabolism
Endothelium, Vascular / pathology, physiopathology*
Hemodynamics / physiology
Losartan / pharmacology
Lymphokines / metabolism
Muscle, Smooth, Vascular / drug effects, physiology
Myocardial Infarction / pathology, physiopathology*
Nicotine / blood
Refractory Period, Electrophysiological / drug effects
Renin / blood
Renin-Angiotensin System / drug effects, physiology*
Reperfusion Injury / physiopathology
Tobacco Smoke Pollution / adverse effects*
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
Ventricular Fibrillation / physiopathology
|0/Antihypertensive Agents; 0/Endothelial Growth Factors; 0/Lymphokines; 0/Tobacco Smoke Pollution; 0/Vascular Endothelial Growth Factor A; 0/Vascular Endothelial Growth Factors; 11128-99-7/Angiotensin II; 114798-26-4/Losartan; 54-11-5/Nicotine; EC 126.96.36.199/Renin|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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