(Hypertension. 1999;34:659-665.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Activation of AT2 Receptors by Endogenous Angiotensin II Is Involved in Flow-Induced Dilation in Rat Resistance Arteries
From the Institut National de la Santé et de la Recherche Médicale (INSERM) Unit 141 (K.M., L.L., B.I.L., D.H.) and Unit 127 (C.H.), IFR 6, Université Paris VII, France.
Correspondence to D. Henrion, PhD, INSERM Unit 141, Hopital Lariboisiere, 41 Blvd de la Chapelle, 75475 Paris, cedex 10, France. E-mail daniel.henrion{at}inserm.lrb.ap-hop-paris.fr
Abstract—Pressure-induced tone (myogenic, MT) and flow (shear stress)–induced dilation (FD) are potent modulators of resistance artery tone. We tested the hypothesis that locally produced angiotensin II interacts with MT and FD. Rat mesenteric resistance arteries were perfused in situ. Arterial diameter was measured by intravital microscopy after a bifurcation on 2 distal arterial branches equivalent in size (150 µm, n=7 per group). One was ligated distally and thus submitted to pressure only (MT, no FD). The second branch was submitted to flow and pressure (MT and FD). The difference in diameter between the 2 vessels was considered to be FD. Flow-diameter-pressure relationship was established in the absence and then in the presence of 1 of the following agents. In the nonligated segment (MT+FD), angiotensin II type 1 (AT1) receptor blockade (losartan) had no significant effect, whereas angiotensin II type 2 (AT2) receptor blockade (PD123319) or saralasin (AT1+AT2 blocker) decreased the diameter significantly, by 9±1 and 10±0.8 µm, respectively. Angiotensin II in the presence of losartan increased the diameter by 18±0.6 µm (inhibited by PD123319). PD123319 or saralasin had no effect after NO synthesis blockade or after endothelial disruption. In the arterial segment ligated distally (MT only), AT1 or AT2 receptor blockade had no significant effect. AT2-dependent dilation represented 20% to 39% of FD (shear stress from 22 to 37 dyn/cm2), and AT2-receptor mRNA was found in mesenteric resistance arteries. Thus, resistance arterial tone was modulated in situ by locally produced angiotensin II, which might participate in flow-induced dilation through endothelial AT2 receptor activation of NO release.
Key Words: blood vessels • myogenic • arteries • stress, mechanical • angiotensin II • bradykinin
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