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出生时用6-羟基多巴胺治疗的遗传性高血压大鼠的血压和血管阻力。

Blood pressure and vascular resistance in genetically hypertensive rats treated at birth with 6-hydroxydopamine.

作者信息

Clark D W, Jones D R, Phelan E L, Devine C E

出版信息

Circ Res. 1978 Aug;43(2):293-300. doi: 10.1161/01.res.43.2.293.

DOI:10.1161/01.res.43.2.293
PMID:668060
Abstract

Genetically hypertensive (GH) rats of the New Zealand strain and normotensive (N) rats were sympathectomized from birth with 6-hydroxydopamine (100 mg/kg,s.c, on alternate days, seven treatments). In adult treated rats from each strain (GHTr and NTr), blood pressure was lower than normal. Functional tests and electron microscopy showed that denervation was virtually complete in mesenteric and hindlimb arteries; the innervation of the renal artery was little affected. Ganglionic blockade still caused a large fall in blood pressure in treated rats. Vascular resistance was higher in blood-perfused hindlimbs and tails of GH rats than in those of N rats; in contrast, resistance was similar in limbs and tails of GHTr and NTr rats and was greater than that found in untreated N rats. Saline-perfused limb vessels had neither neurogenic nor myogenic tone and resistance was higher in GH limbs (whether these were from treated rats or not) than in untreated N limbs. In saline-perfused NTr limbs, there was a paradoxical structural adaptation (probably luminal narrowing) of the hindlimb blood vessels and resistance was higher than in untreated N rats. The resistance of saline-perfused GH and GHTr limbs was similar. A high peripheral resistance appears to be the main mechanism sustaining genetic hypertension, and the integrity of the vasomotor sympathetic nerves is necessary for the development of this form of experimental hypertension.

摘要

对新西兰品系的遗传性高血压(GH)大鼠和正常血压(N)大鼠自出生起用6-羟基多巴胺进行交感神经切除术(100mg/kg,皮下注射,隔日一次,共七次治疗)。在来自每个品系的成年治疗大鼠(GHTr和NTr)中,血压低于正常水平。功能测试和电子显微镜显示,肠系膜动脉和后肢动脉的去神经支配几乎完全;肾动脉的神经支配几乎未受影响。神经节阻断仍会导致治疗大鼠的血压大幅下降。GH大鼠血液灌注的后肢和尾巴的血管阻力高于N大鼠;相反,GHTr和NTr大鼠的肢体和尾巴的阻力相似,且大于未治疗的N大鼠。生理盐水灌注的肢体血管既无神经源性也无肌源性张力,GH肢体(无论是否来自治疗大鼠)的阻力高于未治疗的N肢体。在生理盐水灌注的NTr肢体中,后肢血管出现反常的结构适应性变化(可能是管腔狭窄),阻力高于未治疗的N大鼠。生理盐水灌注的GH和GHTr肢体的阻力相似。高外周阻力似乎是维持遗传性高血压的主要机制,血管运动交感神经的完整性对于这种实验性高血压的发展是必要的。

相似文献

1
Blood pressure and vascular resistance in genetically hypertensive rats treated at birth with 6-hydroxydopamine.出生时用6-羟基多巴胺治疗的遗传性高血压大鼠的血压和血管阻力。
Circ Res. 1978 Aug;43(2):293-300. doi: 10.1161/01.res.43.2.293.
2
Control of hindlimb vascular resistance in rats chronically sympathectomized with 6-hydroxydopamine.用6-羟基多巴胺对大鼠进行慢性交感神经切除术后后肢血管阻力的控制
Clin Exp Pharmacol Physiol. 1975 Nov-Dec;2(6):509-15. doi: 10.1111/j.1440-1681.1975.tb01856.x.
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Fluvastatin remodels resistance arteries in genetically hypertensive rats, even in the absence of any effect on blood pressure.氟伐他汀可重塑遗传性高血压大鼠的阻力动脉,即使对血压没有任何影响。
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Circ Res. 1976 Aug;39(2):191-9. doi: 10.1161/01.res.39.2.191.
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[Role of sympathetic nervous system in the pathogenesis of spontaneous hypertension in rats].[交感神经系统在大鼠自发性高血压发病机制中的作用]
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Pressure-independent increases in vascular resistance in hypertension: role of sympathoadrenergic influences.高血压中与压力无关的血管阻力增加:交感肾上腺素能影响的作用。
Hypertension. 1980 Nov-Dec;2(6):780-6. doi: 10.1161/01.hyp.2.6.780.

引用本文的文献

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Renal alpha-adrenergic receptors and genetic hypertension.肾α-肾上腺素能受体与遗传性高血压
Pediatr Nephrol. 1993 Dec;7(6):853-8. doi: 10.1007/BF01213373.
2
Arterial pressure, cardiac output and exercise hyperemia in chemically sympathectomized rats.
Pflugers Arch. 1981 Oct;391(4):324-6. doi: 10.1007/BF00581516.
3
Central noradrenergic neurons and vascular non-collagen protein in the initial phase of two-kidney, one-clip renovascular hypertension.两肾一夹肾血管性高血压初期的中枢去甲肾上腺素能神经元与血管非胶原蛋白
Int Urol Nephrol. 1988;20(4):439-47. doi: 10.1007/BF02549578.