Guidi E, Hollenberg N K
Hypertension. 1987 Jun;9(6):591-7. doi: 10.1161/01.hyp.9.6.591.
The suggestion has been made that the Okamoto strain of spontaneously hypertensive rats (SHR) shares some features with a subgroup of patients with essential hypertension, called nonmodulators. One feature of nonmodulators is a renal blood flow response to angiotensin II (ANG II) that is blunted on a high salt diet; the blunted renal vascular response is corrected by converting enzyme inhibition. Renal blood flow (electromagnetic flowmeter) and pressor responses to graded ANG II doses (5-300 ng) were assessed in 24 SHR and 24 Wistar-Kyoto rats (WKY) ingesting 1.6% Na. In comparison to WKY, blood pressure was higher in SHR (155 +/- 4 vs 106 +/- 2 mm Hg; p less than 0.001), renal blood flow was lower (6.9 +/- 0.5 vs 8.2 +/- 0.4 ml/min/g; p less than 0.05), and the pressor response to ANG II was enhanced, (p less than 0.0005) but the renal vascular response was blunted (p less than 0.005). Captopril (1-30 mg/kg) reduced blood pressure more in SHR than in WKY but increased renal blood flow similarly in both strains. The blunted renal vascular response to ANG II in SHR was reversed by captopril, but inhibition of converting enzyme in the kidney did not parallel systemic inhibition. Maximum blockade of converting enzyme in the kidney appears to require a larger captopril dose than is required for systemic inhibition. These results suggest that the renal blood supply in SHR also shares some of the characteristics of nonmodulators and that the action of captopril on the renal blood flow probably reflects reversal of inappropriate intrarenal ANG II formation.
有人提出，冈本自发性高血压大鼠（SHR）品系与原发性高血压患者的一个亚组（称为无反应调节者）具有一些共同特征。无反应调节者的一个特征是，在高盐饮食时，其对血管紧张素II（ANG II）的肾血流反应减弱；这种减弱的肾血管反应可通过转换酶抑制得到纠正。对24只摄入1.6%钠的SHR和24只Wistar-Kyoto大鼠（WKY），评估其肾血流（电磁流量计）和对不同剂量（5 - 300 ng）ANG II的升压反应。与WKY相比，SHR的血压更高（155±4 vs 106±2 mmHg；p<0.001），肾血流更低（6.9±0.5 vs 8.2±0.4 ml/min/g；p<0.05），对ANG II的升压反应增强（p<0.0005），但肾血管反应减弱（p<0.005）。卡托普利（1 - 30 mg/kg）使SHR的血压降低幅度大于WKY，但在两种品系中使肾血流增加的程度相似。卡托普利可逆转SHR对ANG II的肾血管反应减弱，但肾脏中转换酶的抑制与全身抑制并不平行。肾脏中转换酶的最大阻断似乎需要比全身抑制更大剂量的卡托普利。这些结果表明，SHR中的肾血液供应也具有一些无反应调节者的特征，并且卡托普利对肾血流的作用可能反映了肾内不适当的ANG II生成的逆转。
