Endogenous prostaglandins limit angiotensin-II induced regional vasoconstriction in conscious rats

In conscious rats, we tested the hypothesis that prostaglandins attenuate regional vasoconstriction caused by acute infusion of angiotensin II. Mean arterial pressure, regional blood flow, and vascular conductance in response to 2-minute infusions of 0.05 or 1 μg/kg/min Ang II were assessed before and during indomethacin treatment (5 mg/kg). Effects of the lower dose of Ang II (n = 8) on regional blood flow were not altered by indomethacin, but conductance in the kidney (2.98 ± 0.35 vs. 2.19 ± 0.32), stomach (1.15 ± 0.13 vs. 0.83 ± 0.13), and white gastrocnemius muscle (0.11 ± 0.02 vs. 0.07 ± 0.01 mL/min/100g/mm Hg) were reduced. Changes in conductance were not seen in the pancreas or spleen. In response to the higher dose of Ang II (n = 7), indomethacin reduced blood flow in the kidney, red and white gastrocnemius, and soleus muscles. Reductions in conductance were found in the kidney, stomach and small intestine, and in the red and white gastrocnemius, and soleus muscles (2.27 ± 0.9 vs. 1.79 ± 0.14, 0.44 ± 0.07 vs. 0.27 ± 0.03, 0.68 ± 0.11 vs. 0.60 ± 0.07, 0.43 ± 0.08 vs. 0.16 ± 0.03, 0.10 ± 0.02 vs. 0.05 ± 0.01, and 0.26 ± 0.03 vs. 0.15 ± 0.02 mL/min/100g, respectively). No changes occurred in the pancreas and spleen. Indomethacin had no effect on baseline blood flow or conductance in any of these organs. These results suggest that prostaglandins attenuate vasoconstriction caused by Ang II in a manner that is organ-specific and dependent on the dose of Ang II. Consequently, prostaglandins may limit vasoconstriction and potential ischemia caused by elevated levels of this hormone.