Bradykinin‐induced vasoconstriction of rat mesenteric arteries precontracted with noradrenaline

Abstract

1 Administration of bradykinin caused dose-dependent vasoconstriction in rat isolated perfused mesenteric arteries precontracted with noradrenaline.2 The vasoconstrictor response was not mediated by BK1-bradykinin receptors.3 Inhibition of cyclo-oxygenase with indomethacin, aspirin or meclofenamate abolished the vasoconstrictor effect of bradykinin, showing that a member of the arachidonic acid cascade may be involved. 4 Inhibitors of thromboxane synthesis (imidazole and UK 38485) did not affect or only reduced the bradykinin-induced vasoconstriction. 5 The endoperoxide H2/thromboxane A2 receptor antagonist SQ 29548 significantly reduced the vasoconstrictor effect of bradykinin, but did not affect the vasoconstrictor response to noradrenaline, adrenaline, vasopressin, 5-hydroxytryptamine or prostaglandins. 6 The eicosanoid(s) that mediate bradykinin-induced vasoconstriction appear to be synthesized outside the arterial endothelium. 7 The data suggest that the vasoconstrictor effect of bradykinin in the rat isolated mesenteric artery is mediated by vasoconstrictor arachidonic acid metabolites including the cyclic endoperoxides and/or the thromboxanes.

Kinin B2 receptor‐mediated contraction of tail arteries from normal or streptozotocin‐induced diabetic rats

“…It is generally acknowledged that the activation of B 1 receptors located on smooth muscle cells leads to the contraction of various types of vascular tissues, including rat mesenteric artery (Fasciolo et al, 1990) and rabbit mesenteric artery and aorta (Churchill & Ward, 1987;Levesque et al, 1993). The B 1 receptor-mediated vasoconstriction is endothelium independent and not mediated by prostaglandins (Regoli et al, 1982).…”

“…The mechanisms by which the activation of B 2 receptors contracts vascular tissues, however, are unclear yet. Knowing that the activation of B 1 receptors located on vascular smooth muscle cells also leads to vasoconstriction (Churchill & Ward, 1987;Fasciolo et al, 1990;Levesque et al, 1993), the previously reported BKinduced vasoconstriction may result from the activation of B 1 receptors, instead of B 2 receptors as suggested (Fasciolo et al, 1990;Regoli & Barabe, 1980). This hypothesis is supported by the observation that both B 1 and B 2 receptors may co-exist in the same vascular tissues .…”

“…This nonapeptide has been shown to relax large blood vessels via the activation of B 2 receptors located on vascular endothelial cells, from which endothelium-derived nitric oxide, prostacyclin, and a hyperpolarizing factor are likely to be released (Groves et al, 1995). On the other hand, the activation of B 2 receptors, assuming to be located on vascular smooth muscle cells (Field et al, 1994), has been reported to contract vascular tissues (Fasciolo et al, 1990;Regoli & Barabe, 1980). The mechanisms by which the activation of B 2 receptors contracts vascular tissues, however, are unclear yet.…”

Different Prostanoids Are Involved in Bradykinin-Induced Endothelium-Dependent and -Independent Vasoconstriction in Rat Mesenteric Resistance Arteries

“…Thus, this finding strongly suggests that PGH 2 is responsible for the bradykinin-induced endotheliumindependent vasoconstriction in the rat mesenteric artery. Bradykinin has been shown to cause vasoconstriction (10,24,25). The bradykinin-induced vasoconstrictor response has been reported to be endothelium-independent and indomethacin-sensitive or mediated by bradykinin B 2 receptors located in the vascular smooth-muscle layer (2,9).…”

“…To remove the vascular endothelium, preparations with resting tone were perfused with a 1.80 mg / mL solution of sodium deoxycholate (SD) in saline for 30 s. This caused a transient increase (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) in perfusion pressure. Then, the preparations were rinsed with SD-free Krebs solution for 40 min.…”