Vascular smooth muscle cell polyploidy and cardiomyocyte hypertrophy due to chronic NOS inhibition in vivo
| Autor: | Martin McIntyre, Allan R. McPhaden, Alison M. Devlin, Anna F. Dominiczak, M. Julia Brosnan, Carlene A. Hamilton, Delyth Graham, James J. Morton, John L. Reid |
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| Rok vydání: | 1998 |
| Předmět: |
Nitroprusside
medicine.medical_specialty Vascular smooth muscle Transcription Genetic Physiology Aorta Thoracic Cardiomegaly In Vitro Techniques Rats Inbred WKY Muscle Smooth Vascular Nitric oxide Muscle hypertrophy Polyploidy Renin-Angiotensin System Phenylephrine chemistry.chemical_compound In vivo Isometric Contraction Physiology (medical) Internal medicine Renin–angiotensin system medicine Animals Myocyte RNA Messenger Muscle Skeletal Aldosterone biology Vascular disease Myocardium Cell Cycle Heart DNA medicine.disease Actins Rats Nitric oxide synthase NG-Nitroarginine Methyl Ester Endocrinology chemistry Hypertension biology.protein Carbachol Nitric Oxide Synthase Cardiology and Cardiovascular Medicine |
| Zdroj: | Europe PubMed Central |
| ISSN: | 1522-1539 0363-6135 |
| DOI: | 10.1152/ajpheart.1998.274.1.h52 |
| Popis: | To assess the vascular and cardiac response to NO (nitric oxide) synthase (NOS) blockade in vivo, Wistar-Kyoto rats (WKY) were treated for 3 wk with N G-nitro-l-arginine methyl ester (l-NAME; 10 mg ⋅ kg−1 ⋅ day−1).l-NAME treatment induced hypertension that was associated with increased plasma renin activity. Flow cytometry cell cycle DNA analysis showed that aortic vascular smooth muscle cells (VSMC) froml-NAME-treated WKY had a significantly higher polyploid population compared with WKY controls. Using organ bath experiments, we have shown that aortic rings froml-NAME-treated WKY have an increased contractile response to phenylephrine and impaired relaxation to carbachol compared with control rings. NOS blockade in vivo caused a significant increase in cardiac and left ventricular hypertrophy. Northern mRNA analysis of the myocardium showed thatl-NAME treatment caused reexpression of the fetal skeletal α-actin isoform without alterations in collagen type I expression, a pattern indicating true hypertrophy of the cardiomyocytes. These studies provide further insight to confirm that NO deficiency in vivo results in the development of vascular and cardiac hypertrophy. |
| Databáze: | OpenAIRE |
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