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Hindi Research Article
The role of Îñ1B-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: raisakolhar@yahoo.co.in |
|
| 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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Abstract
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.
