Role of area postrema in transgene hypertension.

Role of area postrema in transgene hypertension.
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后区在转基因高血压中的作用。

DOI:
10.1161/01.hyp.27.3.591
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发表时间:
1996
期刊:
Hypertension (Dallas, Tex. : 1979)
影响因子:
--
通讯作者:
Ferrario,CM
Ferrario,CM
中科院分区:
--
文献类型:
--
作者:
Averill,DB;Matsumura,K;Ganten,D;Ferrario,CM

文献摘要

被引文献

相似文献

Transgenic [Tg(+)] rats carrying the mouseRen-2dgene [(mRen-2d)27] are a newly established monogenetic form of experimental hypertension. To determine whether the area postrema contributes to the development of hypertension in mRen-2 Tg(+) rats, this circumventricular organ in the fourth ventricle was removed from 5-week-old Tg(+) rats. From weeks 4 through 9, systolic blood pressure was measured weekly by tail-cuff plethysmography in area postrema–lesioned and sham-lesioned Tg(+) rats. Although systolic blood pressure rose markedly in sham-lesioned Tg(+) rats, the increase in systolic blood pressure was significantly attenuated in area postrema–lesioned Tg(+) rats. At 9 weeks of age, a femoral artery was cannulated for the measurement of arterial pressure in awake rats. Mean arterial pressure (MAP) in area postrema–lesioned Tg(+) rats was significantly (P<.01) lower than that in sham-lesioned rats: 171±7 and 132±5 mm Hg, respectively. Baroreceptor reflex was evaluated by intravenous infusion of sodium nitroprusside. There was no significant difference in baroreceptor reflex sensitivity between the two groups. Intravenous pentolinium (5 mg/kg), used to produce sympathetic ganglionic block, caused significant decreases in MAP in both groups. However, the reduction of MAP in the sham-lesioned group was significantly (P<.05) greater than that in the area postrema–lesioned group: −73±4 and −48±6 mm Hg, respectively. The ratio of left ventricular weight to body weight in sham-lesioned Tg(+) rats was significantly larger than that of area postrema–lesioned rats. These results suggest that ablation of the area postrema markedly attenuates the development of hypertension in mRen-2dTg(+) rats, and this attenuation may be attributed to decrease in sympathetic outflow.