Sympathoadrenal control by paraventricular hypothalamic beta-endorphin in hypertension.
Sympathoadrenal control by paraventricular hypothalamic beta-endorphin in hypertension.
复制标题
高血压中室旁下丘脑β-内啡肽的交感肾上腺控制。
DOI：
10.1161/01.hyp.18.4.503
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Rockhold,RW
中科院分区：
文献类型：
--
作者：
Jin,CB;Rockhold,RW
室旁下丘脑调节自主神经流出，并受β-内啡肽免疫反应神经末梢支配。本研究探讨了在约9周龄的清醒、无限制的自发性高血压大鼠（SHR）和Wistar-Kyoto（WKY）大鼠中，将β-内啡肽微量注射到室旁下丘脑对血压、心率、血浆儿茶酚胺和葡萄糖浓度的影响。室旁下丘脑注射[125 I] β-内啡肽（3.5 μ g）后30分钟，在冠状面、矢状面和水平面上，可在距离注射部位+/- 0.5 mm范围内检测到大部分回收的放射性。单侧脑室旁下丘脑注射β-内啡肽（1和0.1微克/0.1微升）增加血压和心率在两个菌株在剂量依赖性的方式与显着更大的增加SHR。在β-内啡肽注射后15、30和60分钟测量血浆儿茶酚胺和葡萄糖浓度。去甲肾上腺素浓度在WKY大鼠中没有显着改变，但在SHR中增加。肾上腺素的浓度增加，在这两个菌株显着增加SHR。儿茶酚胺浓度的增加与剂量无关。两种品系的葡萄糖浓度也增加，仅在较低剂量下SHR的增加幅度更大。神经节阻滞与喷托溴铵显着减少β-内啡肽诱导的升压和心动过速反应在SHR。用纳洛酮（1.1微克）预处理SHR室旁下丘脑，阻断了对β-内啡肽（0.1微克）的初始升压和心动过速反应，并减弱了肾上腺素和葡萄糖水平的升高。在清醒动物中研究后2-5天，当用α-氯醛糖麻醉动物时，注射β-内啡肽（0.1微克）后，不同品系之间的血压或心率没有差异。结果表明，清醒的SHR表现出增强的心血管和交感肾上腺皮质反应的β-内啡肽注射到室旁下丘脑，表明室旁下丘脑β-内啡肽系统的活动的改变可以调节SHR的高血压的发展。
The paraventricular hypothalamus regulates autonomic nerve outflow and is innervated with beta-endorphin-immunoreactive nerve terminals. This study examined the effects of beta-endorphin microinjected into the paraventricular hypothalamus on blood pressure, heart rate, and plasma catecholamine and glucose concentrations in conscious, unrestrained spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats at the age of about 9 weeks. Thirty minutes after paraventricular hypothalamic injection of [125I] beta-endorphin (3.5 micrograms), most of the recovered radioactivity was detectable within +/- 0.5 mm from the injection site in the coronal, sagittal, and horizontal planes. Unilateral paraventricular hypothalamic injections of beta-endorphin (1 and 0.1 microgram/0.1 microliter) increased blood pressure and heart rate in both strains in a dose-independent manner with significantly greater increases in SHR. Plasma catecholamine and glucose concentrations were measured 15, 30, and 60 minutes after beta-endorphin injection. Norepinephrine concentrations were not significantly altered in WKY rats but increased in SHR. Epinephrine concentrations increased in both strains with significantly greater increases in SHR. Increases in catecholamine concentrations were not dose-related. Glucose concentrations also increased in both strains with significantly greater increases in SHR only at the lower dose. Ganglionic blockade with pentolinium significantly reduced beta-endorphin-induced pressor and tachycardiac responses in SHR. Pretreatment of the paraventricular hypothalamus with naltrexone (1.1 micrograms) in SHR blocked the initial pressor and tachycardiac responses to beta-endorphin (0.1 microgram) and blunted increases in epinephrine and glucose levels. When the animals were anesthetized with alpha-chloralose 2-5 days after the study in conscious animals, there were no differences in blood pressure or heart rate between strains after beta-endorphin (0.1 microgram) injection. The results indicate that conscious SHR show enhanced cardiovascular and sympathoadrenal responses to beta-endorphin injected into the paraventricular hypothalamus, suggesting that alterations in the activity of the paraventricular hypothalamic beta-endorphin system can modulate the development of hypertension in SHR.