Volume 29, Issue 5 pp. 564-572

Functional subtypes of renal α1-adrenoceptor in diabetic and non-diabetic 2K1C Goldblatt renovascular hypertension

A ARMENIA

A ARMENIA

School of Pharmaceutical Sciences, Universiti Sains Malaysia, Penang 11800, Malaysia

Department of Pharmacy, Faculty of Mathematical and Natural Sciences, University of Andalas, Padang, West Sumatra 25163, Indonesia.

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Munavvar Abdul SATTAR

Corresponding Author

Munavvar Abdul SATTAR

School of Pharmaceutical Sciences, Universiti Sains Malaysia, Penang 11800, Malaysia

Correspondence to Dr Munavvar Abdul SATTAR. Phn 60-4653-2251 [email protected]; [email protected]Search for more papers by this author
Nor Azizan ABDULLAH

Nor Azizan ABDULLAH

Department of Pharmacology, Universiti Malaya, Kuala Lumpur 50603, Malaysia

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Md Abdul Hye KHAN

Md Abdul Hye KHAN

School of Pharmaceutical Sciences, Universiti Sains Malaysia, Penang 11800, Malaysia

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Edward James JOHNS

Edward James JOHNS

Department of Physiology, University College Cork, Cork, Ireland

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First published: 27 April 2008
Citations: 5

Abstract

Aim: This study investigates the subtypes of the α1-adrenoceptor mediating the adrenergically-induced renal vasoconstrictor responses in streptozotocin-induced diabetic and non-diabetic 2-kidney one clip (2K1C) Goldblatt hypertensive rats. Methods: The renal blood flow responses to renal nerve stimulation, noradrenaline, phenylephrine, and methoxamine were measured in the absence and presence of nitrendipine, 5-methylurapidil, chloroethylclonidine and BMY 7378. Results: The renal vasoconstrictor responses were markedly attenuated by nitrendipine and 5-methylurapidil in the diabetic rats (all P<0.05). In the non-diabetic rats, these responses were markedly attenuated by nitrendipine, 5-methylurapidil, and BMY 7378 (all P<0.05). In both experimental groups, chloroethylclonidine markedly accentuated the renal vasoconstrictions caused by all the adrenergic stimuli (all P<0.05). Conclusion: These observations indicate that α1A-adrenoceptor subtypes play a major role in mediating adrenergically-induced renal vasoconstriction in the diabetic 2K1C Goldblatt hypertensive rats. In the non-diabetic 2K1C Goldblatt hypertensive rats, contributions of α1A and α1D-adrenoceptor subtypes were proposed. Apart from post-synaptic α1-adrenoceptors, both in the diabetic and non-diabetic 2K1C Goldblatt hypertensive rats, the potential involvement of presynaptic α1-adrenoceptors is also suggested.

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