Peer-Reviewed Journal Details
Mandatory Fields
Buckley, MM,Johns, EJ
2011
January
American Journal of Physiology
Impact of L-NAME on the cardiopulmonary reflex in cardiac hypertrophy
Validated
()
Optional Fields
renal sympathetic nerve activity urine flow nitric oxide SYMPATHETIC-NERVE ACTIVITY NITRIC-OXIDE SYNTHASE HEART-FAILURE PARAVENTRICULAR NUCLEUS ANGIOTENSIN-II ANESTHETIZED RATS BLOOD-PRESSURE RENAL-FUNCTION GENE-TRANSFER OUTFLOW
301
1549
1556
Buckley MM, Johns EJ. Impact of L-NAME on the cardiopulmonary reflex in cardiac hypertrophy. Am J Physiol Regul Integr Comp Physiol 301: R1549-R1556, 2011. First published August 24, 2011; 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 mu g.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.
DOI 10.1152/ajpregu.00307.2011
Grant Details