Guidi E, Hollenberg N K
Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA.
J Hypertens Suppl. 1986 Dec;4(6):S480-2.
We assessed renal blood flow and pressor responses to graded angiotensin II doses in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats ingesting a diet containing 1.6% sodium basally and after acute and chronic angiotensin converting enzyme (ACE) inhibition with captopril. In the basal state the pressor response to angiotensin II was enhanced (P<0.0005) and the renal vascular response was blunted (P<0.005) in SHR compared with WKY rats. After acute captopril administration the pressor response was enhanced in both strains, and the difference between them was maintained, while the renal vascular response was enhanced in both, but more in SHR, so that the renal vascular response in the SHR became larger than in WKY (P<0.0001). Chronic captopril treatment blunted both pressor and renal responses in WKY rats, but only the pressor response in SHR. The renal vessels of SHR seem to be different from those of WKY rats in reaction to exogenous angiotensin II, and in response to both acute administration of captopril (probably acting through blockade of angiotensin II production) and chronic administration of captopril (probably acting mainly through accumulation of kinin or production of prostaglandins).
我们评估了自发性高血压大鼠（SHR）和Wistar-Kyoto大鼠（WKY）在基础状态下以及急性和慢性用卡托普利抑制血管紧张素转换酶（ACE）后，对不同剂量血管紧张素II的肾血流量和升压反应。在基础状态下，与WKY大鼠相比，SHR对血管紧张素II的升压反应增强（P<0.0005），肾血管反应减弱（P<0.005）。急性给予卡托普利后，两种品系的升压反应均增强，且它们之间的差异持续存在，而肾血管反应在两者中均增强，但在SHR中增强得更多，以至于SHR的肾血管反应变得比WKY大鼠更大（P<0.0001）。慢性卡托普利治疗使WKY大鼠的升压反应和肾反应均减弱，但仅使SHR的升压反应减弱。SHR的肾血管对外源性血管紧张素II的反应，以及对急性给予卡托普利（可能通过阻断血管紧张素II的产生起作用）和慢性给予卡托普利（可能主要通过激肽积累或前列腺素产生起作用）的反应，似乎与WKY大鼠不同。
