Nitric oxide-mediated arteriolar dilation after endothelial deformation

Previously, we frequently observed dilation of arterioles after agonist-induced constrictions. We hypothesized that deformation of the endothelium during decreases in diameter of isolated arterioles elicits the release of nitric oxide (NO). In isolated arterioles of rat mesentery, phenylephrine (PE, 10−7 M)-, U-46619 (10−7 M)-, and KCl (50 mM)-induced constrictions were followed by potent dilations. Inhibition of NO synthase withN ω-nitro-l-arginine (l-NNA, 2 × 10−4 M) or removal of the endothelium significantly enhanced constriction and reduced the postconstriction dilation. In the presence of 80 mmHg of intraluminal pressure, an increase in extraluminal pressure (Pe) to 75 mmHg for 20 s and 1 and 2 min decreased vessel diameter. After release of Pe, arterioles dilated as a function of the duration of diameter reduction by Pe. Removal of the endothelium or administration of l-NNA significantly diminished the post-Pe dilations. In cultured mesenteric arteriolar endothelial cells (EC), PE, U-46619, or KCl ...