Mosqueda-Garcia R, Tseng C J, Appalsamy M, Robertson D
Department of Medicine, Vanderbilt University, Nashville, Tennessee 37232.
J Pharmacol Exp Ther. 1990 Oct;255(1):374-81.
The cardiovascular effects of microinjection of angiotensin II (AII) into the area postrema (AP), nucleus of the solitary tract (NTS) and rostroventrolateral medulla were studied in urethane anesthetized sham-normotensive (NT) and two-kidney, one-clip renal hypertensive rats. Microinjection of AII (2-2000 ng) in the AP of renal hypertensive rats elicited a dose-dependent decrease in blood pressure, heart rate and renal sympathetic nerve activity. Similar effects were observed in the NTS. In the NT rats, low doses of AII (2 and 20 ng), either in the AP or NTS, were also depressor. High doses of AII (200-2000 ng) were needed to observe a modest pressor effect in the NT animals. A decrease in heart rate and renal sympathetic activity was observed with the pressor effect. The AII-antagonist, [Sar1,Val5,Ala8]-AII, into the NTS or AP increased blood pressure and heart rate and inhibited the cardiovascular effects of low doses of AII in both group of rats. In contrast, [Sar1,Val5,Ala8]AII did not affect the pressor action of high doses of AII in the NT group. While the microinjection of AII into the rostroventrolateral medulla did not produce any significant cardiovascular effect in the renal hypertensive group, it resulted in a modest pressor effect in the NT rats. These results indicate that acute activation of AII receptors in the AP or NTS does not contribute to the pressor effect of AII in renal hypertensive rats.
在氨基甲酸乙酯麻醉的假正常血压(NT)大鼠以及两肾一夹肾性高血压大鼠中,研究了向最后区(AP)、孤束核(NTS)和延髓头端腹外侧区微量注射血管紧张素II(AII)后的心血管效应。在肾性高血压大鼠的AP中微量注射AII(2 - 2000 ng)可引起血压、心率和肾交感神经活动呈剂量依赖性降低。在NTS中也观察到类似效应。在NT大鼠中,无论是在AP还是NTS中,低剂量的AII(2和20 ng)也有降压作用。需要高剂量的AII(200 - 2000 ng)才能在NT动物中观察到适度的升压效应。升压效应出现时,心率和肾交感神经活动降低。向NTS或AP中注射AII拮抗剂[Sar1,Val5,Ala8]-AII可升高血压和心率,并抑制两组大鼠中低剂量AII的心血管效应。相比之下,[Sar1,Val5,Ala8]AII对NT组中高剂量AII的升压作用没有影响。虽然向延髓头端腹外侧区微量注射AII在肾性高血压组中未产生任何显著的心血管效应,但在NT大鼠中却导致了适度的升压效应。这些结果表明,AP或NTS中AII受体的急性激活对肾性高血压大鼠中AII的升压效应没有作用。