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髓旁入球小动脉的压力介导性血管收缩涉及P2嘌呤受体激活。

Pressure-mediated vasoconstriction of juxtamedullary afferent arterioles involves P2-purinoceptor activation.

作者信息

Inscho E W, Cook A K, Navar L G

机构信息

Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana 70112, USA.

出版信息

Am J Physiol. 1996 Nov;271(5 Pt 2):F1077-85. doi: 10.1152/ajprenal.1996.271.5.F1077.

Abstract

This study was conducted to examine the hypothesis that P2 purinoceptors contribute to pressure-induced autoregulatory adjustments of afferent arteriolar caliber. Experiments were performed in vitro using the blood-perfused juxtamedullary nephron technique. Afferent arteriolar diameter averaged 19.2 +/- 0.6 microns (n = 51) at control perfusion pressure of 100 mmHg and decreased when perfusion pressure was increased. Desensitization of P2 purinoceptors abolished the alpha, beta-methylene ATP-mediated afferent vasoconstriction and prevented pressure-dependent autoregulatory adjustments in afferent diameter. P2-purinoceptor saturation significantly decreased afferent caliber and attenuated pressure-induced autoregulatory responses. To block P2 receptors, afferent arterioles were treated with the P2-purinoceptor antagonists, pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid or suramin. P2-receptor blockade prevented the afferent arteriolar vasoconstriction evoked by increasing perfusion pressure from 100 to 130 and 160 mmHg. These data demonstrate that inhibition of P2 purinoceptor-dependent responses through receptor desensitization, receptor saturation, or purinoceptor blockade impairs normal autoregulatory behavior in rat juxtamedullary afferent arterioles. The results are consistent with the hypothesis that P2 purinoceptors participate in mediating autoregulatory adjustments in afferent arteriolar diameter.

摘要

本研究旨在检验P2嘌呤受体参与压力诱导的传入小动脉口径自动调节性调整这一假说。实验采用血液灌注的近髓肾单位技术在体外进行。在100 mmHg的对照灌注压力下,传入小动脉直径平均为19.2±0.6微米(n = 51),当灌注压力升高时直径减小。P2嘌呤受体脱敏消除了α,β-亚甲基ATP介导的传入血管收缩,并阻止了传入直径的压力依赖性自动调节性调整。P2嘌呤受体饱和显著降低了传入口径,并减弱了压力诱导的自动调节反应。为了阻断P2受体,用P2嘌呤受体拮抗剂磷酸吡哆醛-6-偶氮苯-2',4'-二磺酸或苏拉明处理传入小动脉。P2受体阻断阻止了因灌注压力从100 mmHg升高至130 mmHg和160 mmHg所诱发的传入小动脉血管收缩。这些数据表明,通过受体脱敏、受体饱和或嘌呤受体阻断抑制P2嘌呤受体依赖性反应会损害大鼠近髓传入小动脉的正常自动调节行为。结果与P2嘌呤受体参与介导传入小动脉直径自动调节性调整这一假说一致。

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