Endothelium‐dependent relaxation induced by angiotensin II and histamine in isolated arteries of dog

Abstract

1In helical strips of dog renal and mesenteric arteries pre-contracted with prostaglandin F2X (PGF2<,), 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. 2 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 PGI2.3 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. 4 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.

Effects of Angiotensin II on Nitric Oxide Generation in Proliferating and Quiescent Rat Coronary Microvascular Endothelial Cells

“…Contrary to these findings, Ang II itself has been associated with significant induction of NOS activity in ECs and subsequent increases in cGMP production in VSMC. Several studies have shown that the endothelium can modulate Ang II-induced contraction or vasodilatation of blood vessels in some vascular beds under certain circumstances (36,37).…”

Methylene Blue for Distributive Shock: A Potential New Use of an Old Antidote

“…Early experiments demonstrate that histamine-induced vasodilation is dependent on intact endothelium containing eNOS which suggests that histamine's action is at least partly mediated through nitric oxide [51,52]. Further evidence to support the role of the NO-cGMP pathway in anaphylaxis is demonstrated by the finding that increased histamine results in upregulation of eNOS gene expression with increased production of NO leading to vasodilation through increased activity of GC.…”

Local modulation of adrenergic responses in the hindlimb vasculature of the intact conscious rat.

“…There was a significant treatment-by-dose interaction, suggesting receptor-stimulated dose-dependent release of a vasodilator PG. Other vasoconstrictors such as angiotensin II also release a vasodilator PG (Toda, 1984). Endothelial cells are known to respond to changes (Rubanyi, 1991;Davies & Tripathi, 1993) (Miller, 1991).…”