Role of paraventricular angiotensin AT1 receptors in salt-sensitive hypertension in mRen-2 transgenic rats.

Role of paraventricular angiotensin AT1 receptors in salt-sensitive hypertension in mRen-2 transgenic rats.
复制标题

室旁血管紧张素 AT1 受体在 mRen-2 转基因大鼠盐敏感性高血压中的作用。

DOI:
10.1152/ajpregu.1996.270.5.r1178
复制
发表时间:
1996
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Callahan,MF
Callahan,MF
中科院分区:
--
文献类型:
--
作者:
Li,P;Morris,M;Diz,DI;Ferrario,CM;Ganten,D;Callahan,MF

文献摘要

被引文献

相似文献

我们先前已经证明mRen-2转基因[Tg(+)]大鼠显示盐诱导的高血压恶化(Callaha,M.,P. Li,C. M. Ferrario,D. Ganten和M.莫里斯Hypertension达拉斯27:573-577,1996)。在这项研究中,我们研究了室旁(PVN)血管紧张素1型(AT 1)受体在该模型的盐敏感性的作用。雄性Tg(+)和Tg(-)大鼠用PVN插管进行脑内给药,颈动脉导管进行慢性心血管监测。用2%NaCl代替饮用水4天后,Tg(+)大鼠的平均动脉压(MAP)显著升高(23 mmHg),而Tg(-)大鼠则无此现象。室旁核注射AT 1受体反义寡核苷酸(ASODN)可使盐处理的Tg(+)大鼠的MAP迅速下降24 +/_ 8 mmHg,而不注射错配寡核苷酸(SCODN)。AT 1 ASODN或SCODN对盐负荷的Tg(-)大鼠或饮用自来水的Tg(+)大鼠的MAP没有影响。盐负荷显著增加Tg(+)大鼠穹窿下器官AT 1受体,而ASODN或SCODN无变化。与此相反,在Tg(+)大鼠中,在直接注射AT 1 ASODN的PVN后20 h,与SCODN相比,PVN AT 1受体减少40%。我们得出结论,PVN AT 1受体在mRen-2转基因大鼠的盐敏感性的表达是至关重要的。
We have previously demonstrated that mRen-2 transgenic [Tg(+)] rats show a salt-induced exacerbation of hypertension (Callaha, M., P. Li, C. M. Ferrario, D. Ganten, and M. Morris. Hypertension Dallas 27: 573-577, 1996). In this study, we examined the role of paraventricular (PVN) angiotensin type-1 (AT1) receptors in the salt sensitivity of this model. Male Tg(+) and Tg(-) rats were instrumented with PVN cannulas for intracerebral drug administration and carotid catheters for chronic cardiovascular monitoring. Substitution of 2% NaCl for drinking water for 4 days caused a significant elevation (23 mmHg) of mean arterial pressure (MAP) in Tg(+) rats but not in Tg(-) rats. PVN injection of AT1 receptor antisense oligodeoxynucleotides (ASODN), but not scrambled oligodeoxynucleotides (SCODN), produced a rapid decrease in MAP of 24 +/_ 8 mmHg in salt-treated Tg(+) rats. There was no effect of either AT1 ASODN or SCODN on MAP in salt-loaded Tg(-) rats or in Tg(+) rats consuming tap water. Salt loading significantly increased subfornical organ AT1 receptors in Tg(+) rats with no changes produced by ASODN or SCODN. In contrast, there was a 40% decrease in PVN AT1 receptors 20 h after direct PVN injection of AT1 ASODN injection, compared with SCODN in Tg(+) rats. We conclude that PVN AT1 receptors are critical in the expression of salt sensitivity in mRen-2 transgenic rats.