This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Reinhart, G. A. Articles by Mizelle, H. L. Search for Related Content PubMed PubMed Citation Articles by Reinhart, G. A. Articles by Mizelle, H. L.

(Hypertension. 1997;29:199.)
© 1997 American Heart Association, Inc.

Arthur C. Corcoran Memorial Lecture

Temporal Influence of the Renal Nerves on Renal Excretory Function During Chronic Inhibition of Nitric Oxide Synthesis

Glenn A. Reinhart; Thomas E. Lohmeier; H. Leland Mizelle

From the University of Mississippi Medical Center, Department of Physiology and Biophysics, Jackson.

Reprint requests to Thomas E. Lohmeier, PhD, Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216-4505. E-mail tel{at}fiona.umsmed.edu

To determine whether the sympathetic nervous system contributes to the hypertension induced by long-term suppression of nitric oxide synthesis, we determined the neurally induced changes in renal excretory function during chronic administration of N^G-nitro-L-arginine methyl ester (L-NAME). Studies were carried out in six conscious chronically instrumented dogs subjected to unilateral renal denervation and surgical division of the urinary bladder into two hemibladders to allow separate 24-hour urine collection from denervated and innervated kidneys. Animals were studied during acute (100 minutes) and chronic (5 days) intravenous infusion of L-NAME at 37.1 nmol/kg per minute (10 µg/kg per minute). During the first 100 minutes of L-NAME, there were no significant changes in mean arterial pressure (control: 96±3 mm Hg), but heart rate fell from 66±6 to 55±7 beats per minute. Changes in glomerular filtration rate were not significant, but renal plasma flow and urinary sodium excretion decreased to 75% and 50% of control values, respectively; however, these changes were comparable in both kidneys. In association with these responses, plasma concentrations of norepinephrine (control: 887±130 pmol/L or 150±22 pg/mL) and epinephrine (control: 691±192 pmol/L or 108±30 pg/mL) tended to decrease. In contrast to the acute responses, mean arterial pressure increased from 92±3 to 106±3 mm Hg and heart rate decreased from 72±4 to 57±5 beats per minute by day 5 of L-NAME infusion, while renal plasma flow and glomerular filtration rate were not significantly different from control values. Most importantly, there were no significant differences in urinary sodium excretion between innervated (control: 31±2 mmol/d) and denervated (control 33±2 mmol/d) kidneys during chronic L-NAME infusion or during the recovery period. These results indicate that the renal sympathetic nerves do not play an important role in promoting sodium retention during either acute or chronic inhibition of nitric oxide synthesis in conscious dogs. Thus, increased renal sympathetic nerve activity does not contribute significantly to L-NAME-induced hypertension.

Key Words: nitric oxide • hypertension • renal nerves • sympathetic nervous system • L-NAME

Abbreviations: GFR = glomerular filtration rate • L-NAME = N^G-nitro-L-arginine methyl ester • MAP = mean arterial pressure • NO = nitric oxide • NOS = NO synthase • PRA = plasma renin activity • RPF = renal plasma flow

This article has been cited by other articles:

				R. Ramchandra, C. J. Barrett, S.-J. Guild, F. McBryde, and S. C. Malpas Role of renal sympathetic nerve activity in hypertension induced by chronic nitric oxide inhibition Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2007; 292(4): R1479 - R1485. [Abstract] [Full Text] [PDF]

				X.-H. Jin, H. E. McGrath, J. J. Gildea, H. M. Siragy, R. A. Felder, and R. M. Carey Renal Interstitial Guanosine Cyclic 3', 5'-Monophosphate Mediates Pressure-Natriuresis Via Protein Kinase G Hypertension, May 1, 2004; 43(5): 1133 - 1139. [Abstract] [Full Text] [PDF]

				N. Toda and T. Okamura The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels Pharmacol. Rev., June 1, 2003; 55(2): 271 - 324. [Abstract] [Full Text] [PDF]

				T. E. Lohmeier, J. R. Lohmeier, A. Haque, and D. A. Hildebrandt Baroreflexes prevent neurally induced sodium retention in angiotensin hypertension Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2000; 279(4): R1437 - R1448. [Abstract] [Full Text] [PDF]

				T. E. Lohmeier, D. A. Hildebrandt, and W. A. Hood Renal Nerves Promote Sodium Excretion During Long-Term Increases in Salt Intake Hypertension, January 1, 1999; 33(1): 487 - 492. [Abstract] [Full Text] [PDF]

				T. E. Lohmeier, G. A. Reinhart, H. L. Mizelle, M. Han, and M. M. Dean Renal denervation supersensitivity revisited Am J Physiol Regulatory Integrative Comp Physiol, October 1, 1998; 275(4): R1239 - R1246. [Abstract] [Full Text] [PDF]

				H. Takano, S. Manchikalapudi, X.-L. Tang, Y. Qiu, A. Rizvi, A. K. Jadoon, Q. Zhang, and R. Bolli Nitric Oxide Synthase Is the Mediator of Late Preconditioning Against Myocardial Infarction in Conscious Rabbits Circulation, August 4, 1998; 98(5): 441 - 449. [Abstract] [Full Text] [PDF]

				K. E. Scrogin, D. C. Hatton, Y. Chi, and F. C. Luft Chronic nitric oxide inhibition with L-NAME: effects on autonomic control of the cardiovascular system Am J Physiol Regulatory Integrative Comp Physiol, February 1, 1998; 274(2): R367 - R374. [Abstract] [Full Text] [PDF]

				A. Montanari, E. Tateo, E. Fasoli, A. Donatini, B. Cimolato, P. Perinotto, and P. Dall'Aglio Dopamine-2 Receptor Blockade Potentiates the Renal Effects of Nitric Oxide Inhibition in Humans Hypertension, January 1, 1998; 31(1): 277 - 282. [Abstract] [Full Text] [PDF]

				T. E. Lohmeier and D. A. Hildebrandt Renal Nerves Promote Sodium Excretion in Angiotensin-Induced Hypertension Hypertension, January 1, 1998; 31(1): 429 - 434. [Abstract] [Full Text] [PDF]

				R. Bolli, S. Manchikalapudi, X.-L. Tang, H. Takano, Y. Qiu, Y. Guo, Q. Zhang, and A. K. Jadoon The Protective Effect of Late Preconditioning Against Myocardial Stunning in Conscious Rabbits Is Mediated by Nitric Oxide Synthase : Evidence That Nitric Oxide Acts Both as a Trigger and as a Mediator of the Late Phase of Ischemic Preconditioning Circ. Res., December 19, 1997; 81(6): 1094 - 1107. [Abstract] [Full Text]

				Y. Qiu, A. Rizvi, X.-L. Tang, S. Manchikalapudi, H. Takano, A. K. Jadoon, W.-J. Wu, and R. Bolli Nitric oxide triggers late preconditioning against myocardial infarction in conscious rabbits Am J Physiol Heart Circ Physiol, December 1, 1997; 273(6): H2931 - H2936. [Abstract] [Full Text] [PDF]

				R. Bolli, Z. A. Bhatti, X.-L. Tang, Y. Qiu, Q. Zhang, Y. Guo, and A. K. Jadoon Evidence That Late Preconditioning Against Myocardial Stunning in Conscious Rabbits Is Triggered by the Generation of Nitric Oxide Circ. Res., July 19, 1997; 81(1): 42 - 52. [Abstract] [Full Text]