Effects of mastoparan on a vascular contractility in rabbit aorta

Abstract

Mastoparan is an amphiphilic tetradecapeptide derived from wasp venom which activates G-proteins. Several secondary effects have been attributed to this peptide, including activation of phospholipase and phosphatidylinositol kinase. The aim of the present study was to investigate the effects of mastoparan on vascular contractility. Rabbit aortic rings were cut and mounted on a force transducer to record isometric tension on a polygraph. The effects of mastoparan were then investigated on the contractile responses in the isolated rabbit aorta with or without endothelium. The results were summarized as follows; 1. Mastoparan caused biphasic response, a transient relaxation followed by a further contraction, in norepinephrine (NE)-precontracted ring with endothelium. These effects were not observed in the aorta in the absence of endothelium. 2. Mastoparan-induced transient relaxation was significantly inhibited by treatment with a N-omega-nitro-L-arginine or methylene blue. 3. When an inhibitor of phospholipase C, neomycin was added to the precontracted aortic ring with NE, the transient relaxation induced by mastoparan was inhibited, but sustained contraction was not inhibited. 4. When an inhibitor of phospholipase A2, quinacrine and inhibitor of the cyclooxygenase pathway, indomethacin, were added to a precontracted ring with NE, the transient relaxation induced by mastoparan was not inhibited, but sustained contraction was inhibited. 5. Mastoparan induced a contraction of the aorta either with or without endothelium. Indomethacin and nifedipine inhibited mastoparan-induced contraction. From the above results, we concluded that mastoparan acts on the endothelium and modifies the release of endothelium-derived relaxing factors such as nitric oxide and also endothelium-derived contracting factors such as metabolites of arachidonic acid.

The reaction products of sulfide and S-nitrosoglutathione are potent vasorelaxants

“…Since~90% of SSNO -was still present in the bath solution during the decay phase ( Figs 3A, 5A,B), we may assume that a product(s) within the 'SSNO -mix' other than NO must be responsible for the tachyphylaxis to the initial vasorelaxation observed. A similar reversal of the relaxation has been reported for other compounds (including nitroglycerine, mastoparan and exogenous NO) and suggested to involve different pathways in addition to sGC desensitization [31][32][33][34]. The relaxation was fitted by a simple exponential decay function, F = y0+a*exp(-b*x) (Fig.…”

Interleukin 6 augments mechanical strain-induced C-reactive protein synthesis via the stretch-activated channel–nuclear factor κ B signal pathway

“…Vessel rings stretched with a mechanical strain of 1.5−2 g as the rest tension are usually considered to have the best physiological status for most pharmacological and physiological experiments 20. Wendling et al 21 reported that 6.5 g of mechanical strain equals 80 mm Hg pressure in IMA according to the law of Laplace.…”

G protein‐independent stimulation of human myocardial phospholipase C by mastoparan

“…The PLCβ family comprises four members which are regulated by heterotrimeric G proteins. PLCβ 4 is the most distantly related isozyme and is expressed mainly in the retina and in neuronal tissues (Kim et al , 1993; Lee et al , 1993; 1995). In contrast, PLCβ 1–3 are more closely related with respect to their amino acid sequence and their sensitivity to stimulation by both G protein α‐ and βγ‐subunits amino acid sequence and their sensitivity to stimulation by both G protein α‐ and βγ‐subunits (Camps et al , 1992a, b; Katz et al , 1992; Park et al , 1993; Smrcka & Sternweis, 1993).…”