Matsugi T, Chen Q, Anderson D R
Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami School of Medicine, Fla., USA.
Arch Ophthalmol. 1997 Oct;115(10):1281-5. doi: 10.1001/archopht.1997.01100160451011.
To document that angiotensin (ANG) II contracts cultured bovine retinal pericytes via saralasin-sensitive receptors if the cells are prerelaxed.
Changes in the contractile tone were quantified as the changes in the summed length of wrinkles induced by pericytes cultured on the silicone surface.
Angiotensin II (10(-5) mol/L) did not increase the contractile tone of cultured pericytes that were not prerelaxed. However, when the pericytes had been prerelaxed 41% with 10(-6)-mol/L sodium nitroprusside, ANG II at the range of 10(-7) to 10(-5) mol/L caused prompt, dose-related, significant (P<.01) contraction. It induced a maximum contraction (29.9%+/-5.2% [mean+/-SE]) at 10(-6) mol/L. This effect lasted at least 10 minutes. Angiotensin II receptor antagonist saralasin (10(-6) mol/L) abolished the contractile effect of ANG II (10(-6) mol/L), although by itself it did not affect the contractile tone.
Angiotensin II contracts cultured pericytes through saralasin-sensitive ANG II receptors. If ANG II affects the contractile tone of pericytes in vivo, it may affect capillary caliber, resistance, and blood flow.
证明如果细胞预先松弛，血管紧张素（ANG）II通过对沙拉新敏感的受体使培养的牛视网膜周细胞收缩。
收缩张力的变化通过在硅表面培养的周细胞诱导的皱纹总长度变化来定量。
血管紧张素II（10⁻⁵mol/L）不会增加未预先松弛的培养周细胞的收缩张力。然而，当周细胞用10⁻⁶mol/L硝普钠预先松弛41%后，10⁻⁷至10⁻⁵mol/L范围内的ANG II会引起迅速的、剂量相关的、显著的（P<0.01）收缩。它在10⁻⁶mol/L时诱导最大收缩（29.9%±5.2%[平均值±标准误]）。这种效应至少持续10分钟。血管紧张素II受体拮抗剂沙拉新（10⁻⁶mol/L）消除了ANG II（10⁻⁶mol/L）的收缩作用，尽管其本身不影响收缩张力。
血管紧张素II通过对沙拉新敏感的ANG II受体使培养的周细胞收缩。如果ANG II在体内影响周细胞的收缩张力，它可能会影响毛细血管口径、阻力和血流。
