Prevention of genetic hypertension by early treatment of spontaneously hypertensive rats with the angiotensin converting enzyme inhibitor captopril.
Prevention of genetic hypertension by early treatment of spontaneously hypertensive rats with the angiotensin converting enzyme inhibitor captopril.
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DOI：
10.1161/01.hyp.22.2.139
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发表时间：
1993-08
期刊：
影响因子：
8.3
通讯作者：
J. N. Wu;K. Berecek
中科院分区：
文献类型：
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作者：
J. N. Wu;K. Berecek
我们的目的是评估是否早期治疗自发性高血压大鼠（SHR）血管紧张素转换酶抑制剂卡托普利可以永久改变高血压的过程。交配的SHR用卡托普利处理，它们的幼崽在实验前一直服用卡托普利。在2月龄时，一些接受卡托普利治疗的大鼠停止治疗，然后在3月龄时对其中一些大鼠进行交配。清醒的captopril治疗的大鼠，从治疗中删除的大鼠，从治疗中删除的大鼠的后代的平均动脉压显着小于对照组大鼠在4个月和9个月的年龄。与对照组大鼠相比，血管紧张素I或II的中央给药在卡托普利治疗的大鼠和从治疗中移除的大鼠中诱导了血压和饮酒的显著较小的增加。静脉注射血管紧张素I或II引起的血压升高在所有组中相似，除了卡托普利治疗的大鼠对血管紧张素I的升压反应较低。早期给予巯甲丙脯酸，即使在停止给药后，也能防止SHR随后发生高血压，并改变其后代发生高血压的过程。这种效应与对血管紧张素I和II的中枢反应降低有关。我们的数据表明，巯甲丙脯酸可能通过改变中枢肾素-血管紧张素系统永久性地改变SHR高血压的发展。
Our purpose was to evaluate whether early treatment of spontaneously hypertensive rats (SHR) with the angiotensin converting enzyme inhibitor captopril could permanently alter the course of hypertension. Mating pairs of SHR were treated with captopril, and their pups were maintained on captopril until experimentation. Some captopril-treated rats were taken off treatment at 2 months of age, and then some of these rats were mated at 3 months of age. The mean arterial pressures of conscious captopril-treated rats, the rats removed from therapy, and the offspring of the rats removed from therapy were significantly smaller than control rats at 4 and 9 months of age. Central administration of angiotensin I or II induced significantly smaller increases in blood pressure and drinking in captopril-treated rats and the rats removed from therapy compared with control rats. The increase in blood pressure in response to intravenous injection of angiotensin I or II was similar among all groups, with the exception that captopril-treated rats showed lesser pressor responses to angiotensin I. Early administration of captopril, even after administration was stopped, prevented the subsequent development of hypertension in SHR and altered the course of development of hypertension in their progeny. This effect was associated with decreased central responses to angiotensin I and II. Our data suggest that captopril may permanently alter the development of hypertension in SHR through an alteration in the central renin-angiotensin system.