Hinojosa C, Haywood J R
Am J Physiol. 1986 Nov;251(5 Pt 2):H908-14. doi: 10.1152/ajpheart.1986.251.5.H908.
The hemodynamic changes associated with the onset of one-kidney, figure-8, renal-wrap hypertension were monitored in rats fed a high-sodium diet. In addition, the hemodynamic contributions of the sympathetic nervous system (SNS) and arginine vasopressin (AVP) were assessed during the 1st week of hypertension. Renal wrapping caused mean arterial pressure (MAP) to increase significantly from 108 +/- 4 to 140 +/- 4 mmHg on day 5 after renal surgery. The hypertension was associated with a significant bradycardia and no significant change in cardiac output (CO), as measured with an electromagnetic flow probe. Total peripheral resistance (TPR) was significantly elevated to 140% above control value on day 5 after renal surgery. Ganglionic blockade caused similar decreases in MAP and TPR in normotensive and hypertensive animals. Sympathetic blockade after pretreatment with a specific vascular antagonist of AVP, [1-beta-mercapto-beta, beta-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine]Arg8-vasopressin ([d(CH2)5Tyr(Me)]AVP), caused a greater depressor response in the renal-wrapped animals as compared with the effect of ganglionic blockade alone in these animals. The effect of [d(CH2)5Tyr(Me)]AVP alone on the hemodynamics was not different between the two groups of rats. After ganglionic blockade pretreatment, [d(CH2)5Tyr(Me)]AVP caused a significant decrease in MAP and TPR in the renal-wrapped animals. In addition, the difference in MAP and TPR between the two groups of rats was eliminated after combined blockade of AVP and the SNS. The results of this study indicated that the onset of hypertension was a result of an activation of neurohumoral mechanisms to increase TPR.(ABSTRACT TRUNCATED AT 250 WORDS)
在喂食高钠饮食的大鼠中监测了与单肾、8字形、肾包裹性高血压发作相关的血流动力学变化。此外,在高血压的第1周评估了交感神经系统(SNS)和精氨酸加压素(AVP)对血流动力学的影响。肾包裹导致肾手术后第5天平均动脉压(MAP)从108±4显著升至140±4 mmHg。高血压伴有显著的心动过缓,且用电磁流量探头测量的心输出量(CO)无显著变化。肾手术后第5天,总外周阻力(TPR)显著升高至对照值的140%。神经节阻断在正常血压和高血压动物中引起类似的MAP和TPR降低。在用AVP的特异性血管拮抗剂[1-β-巯基-β,β-环戊亚甲基丙酸),2-(O-甲基)酪氨酸]精氨酸加压素([d(CH2)5Tyr(Me)]AVP)预处理后进行交感神经阻断,与仅进行神经节阻断相比,肾包裹动物的降压反应更大。两组大鼠中单独使用[d(CH2)5Tyr(Me)]AVP对血流动力学的影响无差异。在神经节阻断预处理后,[d(CH2)5Tyr(Me)]AVP使肾包裹动物的MAP和TPR显著降低。此外,在AVP和SNS联合阻断后,两组大鼠之间的MAP和TPR差异消除。本研究结果表明,高血压的发作是神经体液机制激活以增加TPR的结果。(摘要截断于250字)