Norepinephrine-induced potentiation of arginine vasopressin reactivity in arterioles of the spontaneously hypertensive rat.
Norepinephrine-induced potentiation of arginine vasopressin reactivity in arterioles of the spontaneously hypertensive rat.
复制标题
去甲肾上腺素诱导自发性高血压大鼠小动脉中精氨酸加压素反应性的增强。
DOI：
10.1161/01.hyp.5.3.321
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Dusseau,JW
中科院分区：
文献类型：
--
作者：
Sueta,CA;Hutchins,PM;Dusseau,JW
我们研究了幼龄（6- 8周龄）自发性高血压大鼠（SHR）和正常Wistar-Kyoto （WKY）对照组的微血管对抗利尿激素单独和联合去甲肾上腺素的反应性。采用闭路电视显微镜定量观察小动脉（17 ~ 26 μ M）对动脉内单独注射抗利尿激素(1.25 × 10（-8) ~ 3.75 × 10(-7) M）和同时局部灌注阈下浓度的去甲肾上腺素在肌微循环中的体内直径反应。在30秒的时间内综合管径减少的百分比，得到对数浓度响应曲线。血管收缩剂对血管加压素的反应在两组中均呈浓度依赖性（p < 0.001）。与WKY血管相比，SHR小动脉对单抗利尿激素的反应性显著增加（p < 0.02）。SHR组最大缩窄比对照组高55% （p < 0.04）。SHR对抗利尿激素也表现出更高的敏感性（p < 0.02）。去甲肾上腺素可增强SHR中抗利尿激素诱导的血管收缩，单用抗利尿激素时SHR反应曲线显著上移和左移（p < 0.01）。最大应答率高38% （p < 0.02）。敏感性显著提高（p < 0.01）。此外，去甲肾上腺素的存在刺激完全闭合的发生率增加了三倍。与SHR结果相反，局部灌注去甲肾上腺素并没有显著改变WKY小动脉对抗利尿激素引起的收缩的反应性。我们的研究结果支持血管加压素在SHR高血压的发展阶段作为一种潜在的血管收缩剂的作用，这可能是由去甲肾上腺素调节的，因此有助于观察到的总外周阻力升高。
We have studied microvascular reactivity to vasopressin alone and in combination with norepinephrine in young (6- to 8-week-old) spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) controls. Closed-circuit TV microscopy was used to quantify the in vivo diameter responses of small arterioles (17 to 26 mu) to vasopressin (1.25 X 10(-8) to 3.75 X 10(-7) M) injected intraarterially alone and with simultaneous topical suffusion of a subthreshold concentration of norepinephrine in the cremaster muscle microcirculation. Percent decrease in luminal diameter was integrated over a 30-second period to obtain log concentration response curves. The vasoconstrictor response to vasopressin was concentration-dependent in both groups (p less than 0.001). A significant increase in reactivity to vasopressin alone was exhibited by the SHR arterioles compared to the WKY vessels (p less than 0.02). Maximum constriction was 55% higher in the SHR (p less than 0.04). The SHR also demonstrated a greater sensitivity to vasopressin (p less than 0.02). Vasopressin-induced vasoconstriction was potentiated by norepinephrine in the SHR, demonstrated by the significant shift of the curve up and to the left of the SHR response curve to vasopressin alone (p less than 0.01). The maximum response was 38% greater (p less than 0.02). Sensitivity was significantly enhanced (p less than 0.01). Additionally, the presence of norepinephrine stimulated a three-fold greater incidence of complete closure. In contrast to SHR results, topical suffusion of norepinephrine did not significantly alter the reactivity of the WKY arterioles to vasopressin-induced constriction. Our results support a role for vasopressin as a potential vasoconstrictor in the developing stage of SHR hypertension which may be modulated by norepinephrine and thus contribute to the elevated total peripheral resistance observed.