Spence C D, Coghlan J P, Denton D A, Mills E H, Nelson M A, Whitworth J A, Scoggins B A
Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Australia.
Can J Physiol Pharmacol. 1987 Aug;65(8):1739-51. doi: 10.1139/y87-273.
The roles of the autonomic nervous system, renin-angiotensin system, and arginine vasopressin (AVP) during the onset of ACTH-induced hypertension were investigated in conscious sheep. Autonomic ganglion blockade or combined adrenergic and cholinergic receptor blockade demonstrated that an intact sympathetic nervous system was not essential for the development or maintenance of the hypertension. Autonomic blockade augmented the pressor response to ACTH, indicating that baroreceptor-mediated reflexes normally operate to suppress the degree of hypertension produced by ACTH. Evidence was obtained suggesting that the renin-angiotensin system and AVP may partially contribute to the maintenance of ACTH hypertension in the presence of autonomic blockade. However, the precise mechanism by which ACTH raises arterial pressure remains to be elucidated.
在清醒绵羊中研究了自主神经系统、肾素-血管紧张素系统和精氨酸加压素（AVP）在促肾上腺皮质激素（ACTH）诱导的高血压发作过程中的作用。自主神经节阻断或联合肾上腺素能和胆碱能受体阻断表明，完整的交感神经系统对于高血压的发生或维持并非必不可少。自主神经阻断增强了对ACTH的升压反应，表明压力感受器介导的反射通常起到抑制ACTH产生的高血压程度的作用。有证据表明，在存在自主神经阻断的情况下，肾素-血管紧张素系统和AVP可能部分有助于维持ACTH高血压。然而，ACTH升高动脉血压的确切机制仍有待阐明。
