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.

Keywords:
α1-Adrenoceptor, Rat renal α1-adrenoceptor, Diabetic nephropathy, Renal vasculature
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© 2009 S. Karger AG, Basel
2009
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