Chronic L-Arginine Administration Attenuates Cardiac Hypertrophy in Spontaneously Hypertensive Rats

• Published in: Hypertension (Dallas, Tex. 1979) Vol. 27; no. 1; pp. 14 - 18
• Main Authors: Matsuoka, Hidehiro, Nakata, Masashi, Kohno, Keisuke, Koga, Yoshinori, Nomura, Gakuji, Toshima, Hironori, Imaizumi, Tsutomu
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Heart Association, Inc 01.01.1996; Hagerstown, MD Lippincott
• Subjects: Actins - genetics; Animals; Arginine - pharmacology; Base Sequence; Biological and medical sciences; Blood Pressure - drug effects; Bone and Bones - metabolism; Cardiomegaly - pathology; Cardiovascular system; Cyclic GMP - metabolism; Hemodynamics - drug effects; Male; Medical sciences; Miscellaneous; Molecular Probes - genetics; Molecular Sequence Data; Myocardium - chemistry; Myocardium - metabolism; Nitric Oxide - metabolism; Norepinephrine - metabolism; Pharmacology. Drug treatments; Rats; Rats, Inbred SHR - physiology; Rats, Inbred WKY; RNA, Messenger - metabolism; Time Factors; Hypertension; Rat; Rodentia; Cardiovascular disease; Myocardial disease; Essential; Prevention; In vivo; Vertebrata; Chemotherapy; Mammalia; Treatment; Arginine; Heart disease; Aminoacid; Animal; Nitrogen monoxide; Hypertrophic cardiomyopathy
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/01.HYP.27.1.14

Nitric oxide inhibits proliferation and migration of vascular smooth muscle cells and contractility of cardiomyocytes in vitro. In spontaneously hypertensive rats (SHR), evidence suggests intrinsic abnormalities of the L-arginine-nitric oxide axis, such as low cGMP-dependent protein kinase in the heart and abnormal L-arginine metabolism. To investigate the in vivo effect of L-arginine on cardiac hypertrophy, 30 SHR and 30 Wistar-Kyoto rats (WKY) were randomly grouped to receive L-arginine (7.5 g/L in drinking water) or vehicle for 12 weeks. L-Arginine treatment did not affect body weight or arterial pressure in either strain. In vehicle-treated animals, the heart/body weight ratio was significantly higher in SHR than in WKY (P < .01). L-Arginine treatment decreased the heart/body weight ratio in SHR (P < .05) but did not affect it in WKY. Expression of skeletal alpha-actin mRNA, known to be expressed in the hypertrophied myocardium, was attenuated in L-arginine-treated SHR compared with vehicle-treated SHR. Cardiac cGMP content and nitrate/nitrite content were less in SHR than WKY. L-Arginine treatment increased these levels only in SHR, suggesting enhanced nitric oxide production. Thus, chronic L-arginine administration attenuated cardiac hypertrophy independently of blood pressure and increased myocardial content of cGMP and nitrate/nitrite. Our results suggest that abnormality of the cardiac L-arginine-nitric oxide axis may play an important role in the pathogenesis of cardiac hypertrophy in SHR. (Hypertension. 1996;27:14-18.)