The role of α1B-ARs in regulating renal hemodynamic and renal functions in hypertensive rats; impact of high dietary sodium intake | OMICS International | Abstract
ISSN: 2161-0479

Journal of Autacoids and Hormones
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Research Article

The role of α1B-ARs in regulating renal hemodynamic and renal functions in hypertensive rats; impact of high dietary sodium intake

Raisa N Kazi1*, Munavvar A Sattar2, Nor A Abdullah3, Md A Hye Khan4 and Edward J Johns5
1College of Applied Medical Science, Salman Bin Abdul-Aziz University, Saudi Arabia
2School of Pharmaceutical Sciences, University Sains Malaysia, 11800, Penang, Malaysia
3Department of Pharmacology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
4Department of Pharmacology and Toxicology, Medical College of Wisconsin, Wisconsin, USA
5Department of Physiology, Aras Windle, University College Cork, College Road, Cork, Ireland
Corresponding Author : Dr. Raisa N Kazi
College of Applied Medical Science
Salman Bin Abdul-Aziz University, Saudi Arabia
E-mail: [email protected]
Received March 26, 2012; Accepted June 11, 2012; Published June 14, 2012
Citation:Kazi RN, Sattar MA, Abdullah NA, Khan MA, Johns EJ (2012) The role of a1b-ARs in regulating renal hemodynamic and renal functions in hypertensive rats; impact of high dietary sodium intake. J Autacoids 1:101. doi: 10.4172/2161-0479.1000101
Copyright: © 2012 Kazi RN, et al. 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 author and source are credited.
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Background: Renal α1B-adrenoreceptors (α1-ARs) contributes to the pathogenesis of hypertension in spontaneously hypertensive rats (SHR). The present study examined the role of α1B-ARs in renal hemodynamic and tubular functions in SHR subjected to high-salt diet (SHRHNa) for 6 weeks. Methods: Renal cortical vasoconstriction to noradrenaline (NA), phenylephrine (PE), and methoxamine (ME) in presence and absence of chloroethylclonidine (CEC) was measured in SHRHNa and SHR on normal sodium diet (SHRNNa). Renal tubular functional responses to PE and CEC were assessed as a measure of insulin clearance. Results: SHRHNa showed no significant change in the mean arterial pressure (MAP) as compared to SHRNNa. SHRHNa expressed enhanced renal cortical vascular sensitivity to NA, PE, and ME. Furthermore, renal vasoconstrictor response to NA, PE and ME was accentuated in the presence of CEC in SHRNNa. On the other hand in SHRHNa, renal cortical vasoconstriction to NA and ME was inhibited by CEC. However tubular response to PE was inhibited by CEC in SHRNNa and remains unaffected in SHRHNa. Conclusion: Thus it is concluded that, augmented α1-adrenergic response to adrenergic stimuli contribute to salt-related increase in renal vascular sensitivity in SHRHNa and these changes were independent of any further increase in MAP in SHRHNa. Irrespective of dietary sodium changes, α1-ARs are involved in mediation of tubular functions like antinatriuresis and antidiuresis of SHR. In addition, α1B-ARs are the functional subtypes that mediate renal cortical vasoconstriction in SHRHNa and tubular function in SHRNNa, while high sodium in SHR did not influence the functionality of α1B-ARs in mediating tubular functions.