| Autor: |
Khan, Md. Abdul Hye, Sattar, Munavvar Abdul, Abdullah, Nor Azizan, Abdulla, Mohammed H., Salman, Ibrahim M., Kazi, Raisa N., Swarup, K. R. L. Anand, Rathore, Hassaan A., Basri, Fathihah, Hussain, NurJannah M., Dewa, Aidiahmad, Johns, Edward James |
| Předmět: |
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| Zdroj: |
Kidney & Blood Pressure Research; 2009, Vol. 32 Issue 5, p349-359, 11p, 1 Black and White Photograph, 2 Charts, 4 Graphs |
| Abstrakt: |
Aim: This study investigated the impact of hypertension combined with diabetic nephropathy on rat renal α1-adrenoceptor subtype composition. Methods: In streptozotocin-induced diabetic spontaneously hypertensive rats (SHR), diabetic nephropathy developed as reflected by increased kidney index, plasma creatinine, albumin excretion, creatinine clearance and fractional excretion of Na+ (all p < 0.05). Renal vasoconstrictions caused by electrical stimulation of renal nerves and intrarenally administered noradrenaline (α-adrenoceptor agonist), phenylephrine (α1-adrenoceptor agonist) and methoxamine (α1A-adrenoceptor agonist) were determined in the presence and absence of intrarenally administered amlodipine (Ca2+ channel blocker), 5-methylurapidil (α1A-adrenoceptor antagonist), chloroethylclonidine (α1B-adrenoceptor antagonist) and BMY 7378 (α1D-adrenoceptor antagonist). Results: In diabetic nephropathy SHR, there was a significant (all p < 0.05) attenuation of all adrenergically induced vasoconstrictor responses in the antagonists, except chloroethylclonidine, which caused a significant (all p < 0.05) enhancement of the responses. Conclusion: The data demonstrated that there was a functional coexistence of α1A- and α1D-adrenoceptors in the renal vasculature of SHR irrespective of the presence of diabetic nephropathy. However, there was a minor contribution of pre-synaptic α-adrenoceptors to the adrenergically mediated vasoconstrictor responses in the diabetic nephropathy SHR. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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