open access

Vol 2, No 3 (2014)
Original article
Published online: 2014-12-16
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Effect of acetylcholine on vascular smooth muscle contraction induced by phenylephrine, angiotensin II and mastoparan-7

Elżbieta Grześk, Wioleta Stolarek, Michał Wiciński, Katarzyna Szadujkis-Szadurska, Bartosz Malinowski, Barbara Tejza, Sylwia Kołtan, Małgorzata Gołębiewska, Andrzej Kołtan, Grzegorz Grześk
Folia Medica Copernicana 2014;2(3):98-101.

open access

Vol 2, No 3 (2014)
ORIGINAL ARTICLES
Published online: 2014-12-16

Abstract

Background. The reactivity of blood vessels depends on their structure and the presence of calcium ions. It is modulated by numerous factors which activate specific signalling pathways leading to contraction or relaxation of smooth muscle. The action of various vasodilatation substances may be altered under the influence of similar or quite different modulators.

Main aim of this study was to assess the role of acetylcholine and calcium ions in modulating the contraction induced by angiotensin II (ANG II), phenylephrine (PHE) and mastoparan-7, a direct activator of G-protein.

Material and methods. Experiments were performed on isolated and perfused tail arteries of Wistar rats. Contraction force in our model was measured by increased level of perfusion pressure with a constant flow.

Results. ANG II caused an increase in perfusion pressure in physiological salt solution (PSS) and calcium free PSS (FPSS).Under the influence of increasing concentrations of acetylcholine, a statistically significant reduction in perfusion pressure in both types of fluid was noted. In the presence of nitro-L-arginine (nitric oxide synthase inhibitor, L-NNA) in both solutions, no changes in contraction stimulated by ANG II or spasmolytic effect of acetylcholine were observed. PHE, in a similar manner to ANG II, caused contraction in FPSS and PSS, which was similarly modulated by acetylcholine. In the mastoparan-7 induced contraction, the pattern of tissue response was similar. For all groups, maximal perfusion pressure in PSS was higher than for FPSS.

Conclusions. The results of our experiments suggest that acetylcholine by activation of vascular endothelium is able to induce dose-dependent vasodilatation not only in contraction related to typical metabotropic receptor agonists, but also after direct stimulation of G-protein with mastoparan-7. This effect may be reversed in the presence of inhibitors of endothelial synthase of nitric oxide.

Abstract

Background. The reactivity of blood vessels depends on their structure and the presence of calcium ions. It is modulated by numerous factors which activate specific signalling pathways leading to contraction or relaxation of smooth muscle. The action of various vasodilatation substances may be altered under the influence of similar or quite different modulators.

Main aim of this study was to assess the role of acetylcholine and calcium ions in modulating the contraction induced by angiotensin II (ANG II), phenylephrine (PHE) and mastoparan-7, a direct activator of G-protein.

Material and methods. Experiments were performed on isolated and perfused tail arteries of Wistar rats. Contraction force in our model was measured by increased level of perfusion pressure with a constant flow.

Results. ANG II caused an increase in perfusion pressure in physiological salt solution (PSS) and calcium free PSS (FPSS).Under the influence of increasing concentrations of acetylcholine, a statistically significant reduction in perfusion pressure in both types of fluid was noted. In the presence of nitro-L-arginine (nitric oxide synthase inhibitor, L-NNA) in both solutions, no changes in contraction stimulated by ANG II or spasmolytic effect of acetylcholine were observed. PHE, in a similar manner to ANG II, caused contraction in FPSS and PSS, which was similarly modulated by acetylcholine. In the mastoparan-7 induced contraction, the pattern of tissue response was similar. For all groups, maximal perfusion pressure in PSS was higher than for FPSS.

Conclusions. The results of our experiments suggest that acetylcholine by activation of vascular endothelium is able to induce dose-dependent vasodilatation not only in contraction related to typical metabotropic receptor agonists, but also after direct stimulation of G-protein with mastoparan-7. This effect may be reversed in the presence of inhibitors of endothelial synthase of nitric oxide.

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Keywords

calcium ions, adrenoceptors, angiotensin II, mastoparan-7, acetylocholine

About this article
Title

Effect of acetylcholine on vascular smooth muscle contraction induced by phenylephrine, angiotensin II and mastoparan-7

Journal

Medical Research Journal

Issue

Vol 2, No 3 (2014)

Article type

Original article

Pages

98-101

Published online

2014-12-16

Page views

1083

Article views/downloads

6299

Bibliographic record

Folia Medica Copernicana 2014;2(3):98-101.

Keywords

calcium ions
adrenoceptors
angiotensin II
mastoparan-7
acetylocholine

Authors

Elżbieta Grześk
Wioleta Stolarek
Michał Wiciński
Katarzyna Szadujkis-Szadurska
Bartosz Malinowski
Barbara Tejza
Sylwia Kołtan
Małgorzata Gołębiewska
Andrzej Kołtan
Grzegorz Grześk

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