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Original Article
131 (
6
); 786-792
doi:
10.25259/IJMR_20101316_786

Role of norepinephrine & angiotensin II in the neural control of renal sodium & water handling in spontaneously hypertensive rats

Department of Cardiovascular & Renal Physiology & Pharmacology, School of Pharmaceutical Sciences, Universiti Sains Malaysia, Penang, Malaysia
Department of Pharmacology, Faculty of Medicine, Universiti Malaya, Kuala Lumpur, Malaysia
College of Pharmacy, University of Baghdad, Baghdad, Iraq
Department of Physiology, Tulane Hypertension & Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, Louisiana, USA
Department of Physiology, University College Cork, Cork, Ireland

Reprint requests: Dr Ibrahim M. Salman, Department of Cardiovascular & Renal Physiology & Pharmacology School of Pharmaceutical Sciences, Universiti Sains Malaysia, 11800 Minden, Penang, Malaysia e-mail: ibraheem_muhammed@yahoo.com

Licence
This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background & objectives:

A wealth of information concerning the essential role of renal sympathetic nerve activity (RSNA) in the regulation of renal function and mean arterial blood pressure homeostasis has been established. However, many important parameters with which RSNA interacts are yet to be explicitly characterized. Therefore, the present study aimed to investigate the impact of acute renal denervation (ARD) on sodium and water excretory responses to intravenous (iv) infusions of either norepinephrine (NE) or angiotensin II (Ang II) in anaesthetized spontaneously hypertensive rats (SHR).

Methods:

Anaesthetized SHR were acutely denervated and a continuous iv infusion of NE (200 ng/min/kg) or Ang II (50 ng/min/kg) was instigated for 1 h. Three 20-min urine clearances were subsequently collected to measure urine flow rate (UV) and absolute sodium excretion (UNaV).

Results:

Higher UV and UNaV (P<0.05) were observed in denervated control SHR as compared to innervated counterparts. The administration of NE or Ang II to innervated SHR produced lower UV and UNaV (P<0.05 vs. innervated control SHR). Lower diuresis/natriuresis response to ARD was observed in NE-treated SHR compared to denervated control SHR (P<0.05). Salt and water excretions in denervated NE-treated SHR, however, were significantly higher (P<0.05) relative to the excretion levels in control denervated SHR. Conversely, there was a higher (all P<0.05) diuresis/natriuresis response to ARD when Ang II was administered to SHR compared to denervated control or innervated Ang II-treated SHR.

Interpretation & conclusions:

NE retains its characteristic antidiuretic/antinatriuretic action following ARD in SHR. Typical action of Ang II on salt and water excretions necessitates the presence of an intact renal innervation. Ang II is likely to facilitate the release of NE from renal sympathetic nerve terminals through a presynaptic site of action. Moreover, there is a lack of an immediate enhancement in the renal sensitivity to the actions of NE and Ang II following ARD in a rat model of essential hypertension.

Keywords

Acute renal denervation
angiotensin II
diuresis
natriuresis
norepinephrine
spontaneously hypertensive rats

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