α1B-Adrenoceptors mediate adrenergically-induced renal vasoconstrictions in rats with renal impairment

• 来源期刊: 中国药理学报（英文版）
• 关键词: α1B-adrenoceptor chloroethylclonidine re-nal resistance vessels rats
• 年，卷（期）: 2008,（2）
• 页码范围: 193-203
• 页数: 11页
• 语种: 英文
• DOI: 10.1111/j.1745-7254.2008.00727.x

摘要

Aim: This study examined whether α1B-adrenoceptors are involved in mediating adrenergically-induced renal vasoconstrictor responses in rats with pathophysi-ological and normal physiological states. Methods: Male Wistar Kyoto and spon-taneously hypertensive rats were induced with acute renal failure or experimental early diabetic nephropathy by cisplatin or streptozotocin, respectively. Cisplatin-induced renal failure was confirmed by impaired renal function and pronounced tubular damage. Experimental early diabetic nephropathy was confirmed by hyperglycemia, changes in physiological parameters, and renal function. The hemodynamic study was conducted on anesthetized rats after 7 d of cisplatin (renal failure) and 4 weeks of streptozotocin (experimental early diabetic nephropathy). Results: In the rats with renal failure and experimental early dia-betic nephropathy, there were marked reductions in their baseline renal blood flow (P<0.01). The baseline mean arterial blood pressure was either unaltered or lower (all P>0.05) in the renal failure and experimental early diabetic nephropathy rats, respectively, as compared to their non-renal failure and non-diabetic nephropathy controls. In the rats with renal impairment, chloroethylclonidine caused either accentuation or attenuation (all P<0.01) of the renal vasoconstrictor responses elicited by the adrenergic stimuli. However, in the non-renal failure and in the non-diabetic nephropathy rats, chloroethylclonidine did not cause any alteration in such responses (P>0.05). Conclusion: This study demonstrated the presence of functional α1B-adrenoceptors that mediated the adrenergically-induced renal vaso-constrictions in rats with renal impairment, but not in rats with normal renal function.