Published online before print January 5, 2004, doi: 10.1161/01.HYP.0000113047.47711.fa
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Hypertension. 2004;43:147.)
© 2004 American Heart Association, Inc.
Hypertension Highlights |
The Sympathetic Nervous System and Hypertension
Recent Developments
From Departments of Internal Medicine and Physiology & Biophysics, University of Iowa Carver College of Medicine and Veterans Administration Medical Center, Iowa City.
Correspondence to Dr Gerald F. DiBona, Department of Internal Medicine University of Iowa College of Medicine 200 Hawkins Drive Iowa City, IA 52252. E-mail gerald-dibona@uiowa.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Arterial Baroreflex Control of Renal Sympathetic Nerve Activity and the Renal Body Fluid Feedback Mechanism— A Revisionist View
A major hypothesisfor the development of hypertension is that abnormal renal excretory function is critical for the initiation, development, and maintenance of primary hypertension.1 The renal body fluid feedback mechanism couples the long-term regulation of arterial pressure to extracellular volume (sodium and water) homeostasis via pressure natriuresis, whereby the kidneys respond to changes in arterial pressure by altering urinary sodium and water excretion. The obligatory requirement for maintenance of sodium and water balance by the kidneys is believed to be primary in the long-term control of arterial pressure. An increase in arterial pressure (via increases in total peripheral resistance or cardiac output or both) leads to an increased urinary sodium and water excretion via the pressure natriuresis mechanism, with consequent reduction in blood volume until arterial pressure is returned to normal. Thus, factors that decrease renal excretory function and disrupt the maintenance of sodium and water balance by the kidneys lead to an increase in arterial pressure, which is required to reestablish and maintain sodium and water balance. Based on computer modeling studies, a long-term increase in arterial pressure can only occur if there is a chronic and sustained decrease in renal excretory function.
Increased renal sympathetic nerve activity (RSNA) is known to be a factor capable of decreasing renal excretory function.2,3 The renal effects of increased RSNA include increased renal tubular sodium reabsorption leading to renal sodium retention; decreased renal blood flow and glomerular filtration rate with renal vasoconstriction and increased renal vascular resistance; and increased renin release leading
This article has been cited by other articles:
 |
|
 |
|
  M. P. Schlaich, P. A. Sobotka, H. Krum, R. Whitbourn, A. Walton, and M. D. Esler Renal Denervation as a Therapeutic Approach for Hypertension: Novel Implications for an Old Concept Hypertension, December 1, 2009; 54(6): 1195 - 1201. [Full Text] [PDF]
|
|
|
|
|
|
P. Mathieu, P. Poirier, P. Pibarot, I. Lemieux, and J.-P. Despres Visceral Obesity: The Link Among Inflammation, Hypertension, and Cardiovascular Disease Hypertension, April 1, 2009; 53(4): 577 - 584. [Full Text] [PDF]
|
|
|
|
 |
|
 N. A. Lutaif, E. M. Rocha, L. A.Veloso, L. M. Bento, and J. A. R. Gontijo Renal contribution to thermolability in rats: role of renal nerves Nephrol. Dial. Transplant., December 1, 2008; 23(12): 3798 - 3805. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Ren, Z. Mi, and E. K. Jackson Assessment of Nerve Stimulation-Induced Release of Purines from Mouse Kidneys by Tandem Mass Spectrometry J. Pharmacol. Exp. Ther., June 1, 2008; 325(3): 920 - 926. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A L Markel, O E Redina, M A Gilinsky, G M Dymshits, E V Kalashnikova, Y. V Khvorostova, L A Fedoseeva, and G S Jacobson Neuroendocrine profiling in inherited stress-induced arterial hypertension rat strain with stress-sensitive arterial hypertension J. Endocrinol., December 1, 2007; 195(3): 439 - 450. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. W. Rajapakse, G. A. Eppel, R. E. Widdop, and R. G. Evans ANG II type 2 receptors and neural control of intrarenal blood flow Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2006; 291(6): R1669 - R1676. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Song, C. K. Kost Jr., and D. S. Martin Androgens augment renal vascular responses to ANG II in New Zealand genetically hypertensive rats Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2006; 290(6): R1608 - R1615. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Rahmouni, D. A. Morgan, G. M. Morgan, A. L. Mark, and W. G. Haynes Role of Selective Leptin Resistance in Diet-Induced Obesity Hypertension Diabetes, July 1, 2005; 54(7): 2012 - 2018. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Klein, M. Daschner, M. Vogel, J. Oh, T. J. Feuerstein, and F. Schaefer Impaired Autofeedback Regulation of Hypothalamic Norepinephrine Release in Experimental Uremia J. Am. Soc. Nephrol., July 1, 2005; 16(7): 2081 - 2087. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Ohkita, Y. Wang, N. D. T. Nguyen, Y.-H. Tsai, S. C. Williams, R. C. Wiseman, P. D. Killen, S. Li, M. Yanagisawa, and C. E. Gariepy Extrarenal ETB Plays a Significant Role in Controlling Cardiovascular Responses to High Dietary Sodium in Rats Hypertension, May 1, 2005; 45(5): 940 - 946. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Vitela, M. Herrera-Rosales, J. R. Haywood, and S. W. Mifflin Baroreflex regulation of renal sympathetic nerve activity and heart rate in renal wrap hypertensive rats Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2005; 288(4): R856 - R862. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Sharma Is There a Rationale for Angiotensin Blockade in the Management of Obesity Hypertension? Hypertension, July 1, 2004; 44(1): 12 - 19. [Abstract] [Full Text] [PDF]
|
|