Relaxation of dog renal arteries by angiotensin II and mesenteric arteries by histamine is markedly suppressed by endothelium removal, likely resulting from PGI2 release.
Does the endothelium mediate the relaxation induced by angiotensin II and histamine in isolated dog arteries?
The endothelium is a major, but not exclusive, site responsible for the release of PGI2 mediating relaxation induced by angiotensin II and histamine in dog arteries.
In helical strips of dog renal and mesenteric arteries pre-contracted with prostaglandin F2 alpha (PGF2 alpha), endothelium-dependent relaxations were investigated. Removal of the endothelium was shown histologically by staining with silver nitrate and functionally by testing the inability of acetylcholine to induce arterial relaxations. When the endothelium was removed, relaxation of renal arteries to angiotensin (Ang) II was markedly suppressed, whereas relaxations induced by PGI2 or isoprenaline were attenuated only slightly. Removal of the endothelium attenuated the relaxant response of mesenteric arteries to histamine but did not significantly alter the response to PGI2. Treatment with indomethacin caused an additional attenuation of the relaxant response to histamine or a reversal of the Ang II-induced relaxation to a contraction in the arterial strips, from which the endothelium had been removed. Relaxation of renal arteries induced by Ang II and of mesenteric arteries induced by histamine is postulated to result from PGI2 released from the arterial wall. Therefore, it appears that the endothelium is a major site but not the only site responsible for drug-induced release of PGI2.
Noboru Toda (1984) studied this question. Angiotensin II and histamine vs. Endothelium removal and indomethacin was evaluated on Arterial relaxation. Relaxation of dog renal arteries by angiotensin II and mesenteric arteries by histamine is markedly suppressed by endothelium removal, likely resulting from PGI2 release.