Impact of L-NAME on the cardiopulmonary reflex in cardiac hypertrophy

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology Vol. 301; no. 5; pp. R1549 - R1556
• Main Authors: Buckley, Maria M, Johns, Edward J
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.11.2011
• Subjects: Animals; Baroreflex - drug effects; Blood Pressure - drug effects; Blood Volume - drug effects; Caffeine; Cardiomegaly - chemically induced; Cardiomegaly - enzymology; Cardiomegaly - physiopathology; Cardiovascular disease; Disease Models, Animal; Diuresis - drug effects; Enzyme Inhibitors - pharmacology; Heart Rate - drug effects; Isoproterenol; Kidney - innervation; Kidneys; Male; NG-Nitroarginine Methyl Ester - pharmacology; Nitric oxide; Nitric Oxide - metabolism; Nitric Oxide Synthase - antagonists & inhibitors; Nitric Oxide Synthase - metabolism; Physiology; Rats; Rats, Wistar; Rodents; Sympathetic Nervous System - drug effects; Sympathetic Nervous System - metabolism; Sympathetic Nervous System - physiopathology; Thyroxine; Urodynamics - drug effects
• ISSN: 0363-6119; 1522-1490
• DOI: 10.1152/ajpregu.00307.2011

There is evidence that in cardiac failure, there is defective baroreceptor reflex control of sympathetic nerve activity. Often, cardiac failure is preceded by a state of cardiac hypertrophy in which there may be enhanced performance of the heart. This study investigated whether in two different models of cardiac hypertrophy, there was an increased contribution of nitric oxide (NO) to the low-pressure baroreceptor regulation of renal sympathetic nerve activity (RSNA) and nerve-dependent excretory function. Administration of a volume load, 0.25* body wt/min saline for 30 min, in normal rats decreased RSNA by 40* and increased urine flow by some 9-fold. Following nitro-L-arginine methyl ester (L-NAME) administration, 10 μg·kg(-1)·min(-1) for 60 min, which had no effect on blood pressure, heart rate, or RSNA, the volume load-induced renal sympathoinhibitory and excretory responses were markedly enhanced. In cardiac hypertrophy states induced by 2 wk of isoprenaline/caffeine or 1 wk thyroxine administration, the volume challenge failed to suppress RSNA, and there were blunted increases in urine flow in the innervated kidneys, but following L-NAME infusion, the volume load decreased RSNA by 30-40* and increased urine flow by some 20-fold in the innervated kidneys, roughly to the same extent as observed in normal rats. These findings suggest that the blunted renal sympathoinhibition and nerve-dependent diuresis to the volume load in cardiac hypertrophy are related to a heightened production or activity of NO within either the afferent or central arms of the reflex.