Sasaki S, Takeda K, Takahashi H, Yoneda S, Okajima H, Iyoda I, Yoshimura M, Ijichi H
Jpn Circ J. 1984 Nov;48(11):1251-9. doi: 10.1253/jcj.48.1251.
Potassium supplementation attenuated the development of hypertension in DOCA-salt rats but did not affect blood pressure in control rats. However, it caused a decrease in body weight in both groups of rats. Sympathetic nerve and pressor responses either to electrical stimulation of the hypothalamus or to intracisternal injections of hypertonic NaCl were enhanced in DOCA-salt rats but were normalized by KCl supplementation. Since the pressor responses to injected norepinephrine or tyramine remained unaltered by KCl treatment, a peripheral inhibition of cardiovascular reactivity was considered unlikely. Pretreatment with methyclothiazide also attenuated the elevation in blood pressure but did not affect the responsiveness to hypothalamic stimulation; hence increased natriuresis or diuresis alone could not account for the effects induced by KCl. These findings are consistent with the conclusion that KCl supplementation attenuates the development of DOCA-salt hypertension in rats by acting on the central nervous system to reduce sympathetic output.
补钾可减轻去氧皮质酮盐(DOCA)-盐诱导的大鼠高血压的发展,但对对照大鼠的血压无影响。然而,它导致两组大鼠体重下降。去氧皮质酮盐大鼠对下丘脑电刺激或脑池内注射高渗氯化钠的交感神经和升压反应增强,但通过补充氯化钾可使其恢复正常。由于氯化钾处理对注射去甲肾上腺素或酪胺的升压反应无改变,因此不太可能存在心血管反应性的外周抑制。用甲基氯噻嗪预处理也可减轻血压升高,但不影响对下丘脑刺激的反应性;因此,仅增加尿钠排泄或利尿不能解释氯化钾诱导的效应。这些发现与以下结论一致,即补充氯化钾通过作用于中枢神经系统以减少交感神经输出,从而减轻大鼠去氧皮质酮盐高血压的发展。