Mueller S M, Cohen M L
Artery. 1985;12(6):337-45.
Vascular angiotensin converting enzyme could contribute to the elevated vascular resistance found in hypertension. The purpose of this study was to determine if angiotensin converting enzyme activity was present in the hindquarter vasculature of one model of hypertension, the spontaneously hypertensive rat (SHR) and its normotensive control, the Wistar-Kyoto rat (WKY). We evaluated the effect of a maximal blocking dose of captopril (0.5 mg) on the angiotensin I pressor response during the infusion of the hindquarter with an artificial perfusate. Angiotensin I (1000 ng/ml) produced a significant increase in peripheral vascular resistance (PVR) in both SHR and WKY, but the increase was greater in SHR. Captopril inhibited the elevation in PVR in both. A lower concentration of angiotensin I (250 ng/ml) produced a significant and similar pressor response in SHR (less than the pressor response to 1000 ng/ml) and WKY (same as the pressor response to 1000 ng/ml). Again, captopril prevented the elevation in PVR to A1 in both SHR and WKY. Because these studies were performed using an artificial perfusate, angiotensin converting enzyme must be present in the SHR and WKY hindquarter vasculature including resistance vessels.
血管紧张素转换酶可能导致高血压中出现的血管阻力升高。本研究的目的是确定在一种高血压模型——自发性高血压大鼠（SHR）及其血压正常的对照——Wistar-Kyoto大鼠（WKY）的后肢血管系统中是否存在血管紧张素转换酶活性。我们评估了最大阻断剂量的卡托普利（0.5毫克）在向后肢灌注人工灌注液期间对血管紧张素I升压反应的影响。血管紧张素I（1000纳克/毫升）在SHR和WKY中均使外周血管阻力（PVR）显著增加，但在SHR中增加幅度更大。卡托普利在两者中均抑制了PVR的升高。较低浓度的血管紧张素I（250纳克/毫升）在SHR（小于对1000纳克/毫升的升压反应）和WKY（与对1000纳克/毫升的升压反应相同）中产生了显著且相似的升压反应。同样，卡托普利在SHR和WKY中均阻止了PVR对A1的升高。由于这些研究是使用人工灌注液进行的，因此血管紧张素转换酶必定存在于SHR和WKY的后肢血管系统中，包括阻力血管。
