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肾上腺去髓质术及肾上腺素对幼年自发性高血压大鼠高血压发展及血管反应性的影响

Effect of adrenal demedullation and adrenaline on hypertension development and vascular reactivity in young spontaneously hypertensive rats.

作者信息

Borkowski K R

机构信息

John P. Robarts Research Institute, London, Ontario, Canada.

出版信息

J Auton Pharmacol. 1991 Feb;11(1):1-14. doi: 10.1111/j.1474-8673.1991.tb00239.x.

Abstract
  1. The effects of adrenal demedullation and subcutaneous depots of adrenaline, on hypertension development and vascular reactivity, were determined in young spontaneously hypertensive rats (SHRs). 2. Plasma adrenaline, but not noradrenaline, was significantly lower in all 16-week-old demedullated SHRs, irrespective of the time of demedullation. However, hypertension development was attenuated only in SHRs demedullated at 6 weeks of age or younger. 3. Adrenaline depots restored hypertension development in SHRs demedullated at 4 weeks, irrespective of the time of depot implantation, but were without effect in sham-operated rats. 4. Pressor responses to exogenous noradrenaline, in isolated perfused mesenteric arteries from 16-week-old demedullated and sham-operated SHRs and those treated with adrenaline depots, did not differ significantly. Maximal neurogenic pressor responses were, however, reduced in mesenteries from all demedullated rats, including those treated with depot adrenaline. Adding adrenaline to the perfusate facilitated neurogenic responses only. 5. Thus, the adrenal medulla appears to be involved in modulating sympathetic neurogenic vasoconstriction. The nature of this sympathoadrenal interaction and its role in the early development of hypertension in the SHR is unclear and is not explicable simply in terms of a facilitation of sympathetic neurogenic responses by adrenaline.
摘要
  1. 在年轻的自发性高血压大鼠(SHRs)中,研究了肾上腺髓质切除和皮下注射肾上腺素对高血压发展及血管反应性的影响。2. 所有16周龄的去髓质SHRs的血浆肾上腺素水平显著降低,而去甲肾上腺素水平未降低,且与去髓质时间无关。然而,只有在6周龄及以下去髓质的SHRs中,高血压的发展才会减弱。3. 肾上腺素储存库可恢复4周龄去髓质SHRs的高血压发展,与储存库植入时间无关,但对假手术大鼠无效。4. 来自16周龄去髓质和假手术的SHRs以及用肾上腺素储存库处理的大鼠的离体灌注肠系膜动脉对外源性去甲肾上腺素的升压反应无显著差异。然而,所有去髓质大鼠(包括用储存库肾上腺素处理的大鼠)的肠系膜中最大神经源性升压反应均降低。仅向灌注液中添加肾上腺素可促进神经源性反应。5. 因此,肾上腺髓质似乎参与调节交感神经源性血管收缩。这种交感肾上腺相互作用的性质及其在SHRs高血压早期发展中的作用尚不清楚,不能简单地用肾上腺素促进交感神经源性反应来解释

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