Aorta and Skeletal Muscle NO Synthase Expression in Experimental Heart Failure

• Published in: Journal of molecular and cellular cardiology 1996-11, Vol.28 (11), p.2241-2248
• Main Authors: Comini, Laura, Bachetti, Tiziana, Gaia, Giuseppina, Pasini, Evasio, Agnoletti, Laura, Pepi, Patrizia, Ceconi, Claudio, Curello, Salvatore, Ferrari, Roberto
• Format: Article
• Language: English
• Subjects: Animals; Aorta - enzymology; Ascites; Body Weight; Congestive heart failure; Endothelium, Vascular - enzymology; Female; Heart Failure - chemically induced; Heart Failure - enzymology; Heart Failure - pathology; Monocrotaline - pharmacology; Muscle, Skeletal - enzymology; Muscle, Smooth, Vascular - enzymology; Nitric Oxide Synthase - biosynthesis; NO synthase; Organ Size; Pleural Effusion; Rats; Rats, Sprague-Dawley
• ISSN: 0022-2828; 1095-8584
• DOI: 10.1006/jmcc.1996.0216

Nitric oxide (NO), the free radical that accounts for the biological activity of endothelium-derived relaxing factor, is synthesized from L-arginine by NO synthase (NOS). There is evidence that NO availability is reduced in the peripheral vasculature of patients with congestive heart failure (CHF). The aim of this study was to investigate the expression of NOS in the descending aorta and in the skeletal muscles of rats subjected to heart failure. The alkaloid, monocrotaline, was used to induce pulmonary hypertension and cardiac failure in rats. The expression of both the constitutive (ecNOS) and the inducible (iNOS) isoforms of the enzyme was assessed by Western blot analysis. In CHF animals, the ecNOS location in the aorta is altered: the endothelial protein expression is substantially reduced (from 0.083±0.012 to 0.003±0.004 OD/ μg total proteins, P