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首页> 外文期刊>American Journal of Physiology >ANG II in median preoptic nucleus and pressor responses to CSF sodium and high sodium intake in SHR.
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ANG II in median preoptic nucleus and pressor responses to CSF sodium and high sodium intake in SHR.

机译:SHR中视神经中枢前核中的ANG II和对CSF钠和高钠摄入的升压反应。

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Pressor responses to increases in cerebrospinal fluid (CSF) sodium in Wistar rats and to high salt intake in spontaneously hypertensive rats (SHR) involve both brain ouabainlike activity ("ouabain") and the brain renin-angiotensin system (RAS). Because some of the effects of "ouabain" are mediated by the median preoptic nucleus (MnPO) and this nucleus contains all elements of the RAS, the present study assessed possible interactions of "ouabain" and ANG II in this nucleus. In conscious Wistar rats, injection of ANG II into the MnPO significantly increased mean arterial pressure (MAP) and heart rate (HR). This response was not affected by pretreatment with a subpressor dose of ouabain. MAP and HR increases by ouabain in the MnPO were significantly attenuated by MnPO pretreatment with losartan. In Wistar rats, losartan in the MnPO also abolished pressor and HR responses to intracerebroventricular 0.3 M NaCl and attenuated MAP and HR responses to intracerebroventricular ouabain. Five weeks of a high-salt diet in SHRs resulted in exacerbation of hypertension and increased responses to air-jet stress and intracerebroventricular guanabenz. Losartan injected into the MnPO reversed the salt-sensitive component of the hypertension and normalized the depressor response to guanabenz but did not change responses to air-jet stress. We conclude that in the MnPO, ANG II via AT(1) receptors mediates cardiovascular responses to an acute increase in CSF sodium as well as the chronic pressor responses to high sodium intake in SHR.
机译:Wistar大鼠中脑脊液(CSF)钠的增加和自发性高血压大鼠(SHR)对高盐摄入的升压反应涉及脑哇巴因样活性(“ ouabain”)和脑肾素-血管紧张素系统(RAS)。因为“哇巴因”的某些作用是由中视前视核(MnPO)介导的,并且该核包含RAS的所有元素,所以本研究评估了“哇巴因”和ANG II在该核中的可能相互作用。在有意识的Wistar大鼠中,将ANG II注射到MnPO中会显着增加平均动脉压(MAP)和心率(HR)。用降压剂量的哇巴因预处理不影响该反应。氯沙坦对MnPO的预处理可显着减弱ouabain在MnPO中的MAP和HR升高。在Wistar大鼠中,MnPO中的氯沙坦也取消了对0.3 M NaCl脑室内的升压和HR反应,并减弱了对脑室内哇巴因的MAP和HR反应。 SHRs高盐饮食五周会加剧高血压,并增加对喷气压力和脑室内guanabenz的反应。注射到MnPO中的氯沙坦可以逆转高血压病的盐敏感性成分,并使降压药对胍阿宾斯的反应正常化,但不会改变对喷气压力的反应。我们得出的结论是,在MnPO中,ANG II通过AT(1)受体介导心血管对CSF钠急剧增加的反应以及对SHR高钠摄入量的慢性升压反应。

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