血浆儿茶酚胺对自发性高血压大鼠中β-肾上腺素能受体拮抗剂所致血管减压反应的响应。

The response of plasma catecholamines to the vasodepression caused by beta-adrenoceptor antagonists in the spontaneously hypertensive rat.

作者信息

Keeton T K

出版信息

J Hypertens Suppl. 1986 Oct;4(3):S197-9.

Abstract

The 15-20% decrease in mean arterial pressure (MAP) seen in conscious spontaneously hypertensive rats (SHR) after the administration of a single dose of the beta-adrenoceptor antagonists atenolol, betaxolol, oxprenolol, pindolol, propranolol or sotalol was not accompanied by an increase in plasma norepinephrine (NE) concentration. In marked contrast, plasma NE concentration increased by 50-75% when MAP was lowered at the same rate, and to the same extent with the vasodilator minoxidil. Atenolol, betaxolol and propranolol significantly suppressed plasma renin activity (PRA), whereas oxprenolol, pindolol and sotalol did not alter PRA significantly. Based on these observations, I conclude that beta-adrenoceptor antagonists impair the normal baroreflexly-mediated increase in plasma NE concentration which occurs in response to a decrease in MAP and this sympatho-inhibitory effect does not require the suppression of renin release.

摘要

给清醒的自发性高血压大鼠（SHR）单次注射β-肾上腺素能受体拮抗剂阿替洛尔、倍他洛尔、氧烯洛尔、吲哚洛尔、普萘洛尔或索他洛尔后，平均动脉压（MAP）下降了15% - 20%，但血浆去甲肾上腺素（NE）浓度并未升高。与之形成显著对比的是，当用血管扩张剂米诺地尔以相同速率和相同程度降低MAP时，血浆NE浓度升高了50% - 75%。阿替洛尔、倍他洛尔和普萘洛尔显著抑制血浆肾素活性（PRA），而氧烯洛尔、吲哚洛尔和索他洛尔对PRA无显著影响。基于这些观察结果，我得出结论：β-肾上腺素能受体拮抗剂损害了正常的压力反射介导的血浆NE浓度升高，这种升高是对MAP降低的反应，并且这种交感神经抑制作用不需要抑制肾素释放。