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首页> 外文期刊>American Journal of Physiology >Brain sodium channels and ouabainlike compounds mediate central aldosterone-induced hypertension.
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Brain sodium channels and ouabainlike compounds mediate central aldosterone-induced hypertension.

机译：脑钠通道和哇巴因样化合物介导醛固酮诱导的高血压。

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Central nervous system (CNS) effects of mineralocorticoids participate in the development of salt-sensitive hypertension. In the brain, mineralocorticoids activate amiloride-sensitive sodium channels, and we hypothesized that this would lead to increased release of ouabainlike compounds (OLC) and thereby sympathetic hyperactivity and hypertension. In conscious Wistar rats, intracerebroventricular infusion of aldosterone at 300 or 900 ng/h in artificial cerebrospinal fluid (aCSF) with 0.145 M Na+ for 2 h did not change baseline mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), or heart rate (HR). Intracerebroventricular infusion of aCSF containing 0.16 M Na+ (versus 0.145 M Na+ in regular aCSF) did not change MAP or RSNA, but significant increases in MAP, RSNA, and HR were observed after intracerebroventricular infusion of aldosterone at 300 ng/h for 2 h. Intracerebroventricular infusion of aCSF containing 0.3 M Na+ increased MAP, RSNA, and HR significantly more after intracerebroventricular infusion of aldosterone versus vehicle. After intracerebroventricular infusion of aldosterone, the MAP, RSNA, and HR responses to intracerebroventricular infusion of aCSF containing 0.16 M Na+ were blocked by blockade of brain OLC with intracerebroventricular infusion of Fab fragments or of brain sodium channels with intracerebroventricular benzamil. Chronic intracerebroventricular infusion of aldosterone at 25 ng/h in aCSF with 0.15 M Na+ for 2 wk increased MAP by 15-20 mmHg and increased hypothalamic OLC by 30% and pituitary OLC by 60%. Benzamil blocked all these responses to aldosterone. These findings indicate that in the brain, mineralocorticoids activate brain sodium channels, with small increases in CSF Na+ leading to increases in brain OLC, sympathetic outflow, and blood pressure.
机译：盐皮质激素的中枢神经系统（CNS）效应参与了盐敏感性高血压的发展。在大脑中，盐皮质激素激活阿米洛利敏感的钠通道，我们假设这会导致哇巴因样化合物（OLC）释放增加，从而引起交感神经亢进和高血压。在有意识的Wistar大鼠中，以0.145 M Na +的人工脑脊液（aCSF）在300或900 ng / h的脑室内脑内输注醛固酮2 h不会改变基线平均动脉压（MAP），肾交感神经活性（RSNA）或心率（HR）。脑室内注入0.16 M Na +的aCSF（常规aCSF中为0.145 M Na +）并没有改变MAP或RSNA，但脑室注入300 ng / h醛固酮2 h后，MAP，RSNA和HR显着增加。脑室内输注含有0.3 M Na +的aCSF与醛固酮相比，脑室内输注醛固酮后，MAP，RSNA和HR明显增加。脑室内输注醛固酮后，脑内OLC阻断脑室内注入Fab片段或脑钠通道与脑室内苯并苯甲酰氨基苯甲酸酯，阻断MAP，RSNA和HR对脑室内注入含0.16 M Na +的aCSF的反应。长期脑室内以25 ng / h的速率在0.15 M Na +的aCSF中连续2周灌输醛固酮可使MAP升高15-20 mmHg，下丘脑OLC增加30％，垂体OLC增加60％。 Benzamil阻断了所有对醛固酮的反应。这些发现表明，在大脑中，盐皮质激素激活了脑钠通道，CSF Na +的增加很小，导致脑中的OLC，交感神经流出和血压增加。

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