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Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography

Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography

Published on: September 22, 2011

Ghrelin signaling in human mesenteric arteries.

D Z Dimitrova¹, S D Dimitrov, I Iliev

¹Institute of Biophysics, Bulgarian Academy of Sciences, Sofia, Bulgaria.

Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society

|September 4, 2010

Summary

Ghrelin enhances human mesenteric artery contraction via a novel pathway involving Src kinase, MEK, and thromboxane A2. This study identifies new mediators in the ghrelin signaling pathway.

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Area of Science:

Vascular Physiology
Molecular Signaling
Gastrointestinal Hormones

Background:

Ghrelin is known to influence vascular tone.
The precise signaling mechanisms of ghrelin in human mesenteric arteries remain incompletely understood.

Purpose of the Study:

To elucidate the novel signaling pathway and mediators involved in ghrelin-induced contraction of human mesenteric arteries.

Main Methods:

Isometric wire myography was used to measure arterial contractile force.
Whole-cell patch clamp electrophysiology was performed on isolated smooth muscle cells.
Pharmacological inhibitors and specific receptor antagonists were employed to dissect the signaling cascade.

Main Results:

Ghrelin (100 nmol) abolished outward potassium currents via iberiotoxin-sensitive calcium-activated potassium channels.
Ghrelin dose-dependently increased mesenteric artery contraction.
This effect was mediated by Src kinase, mitogen-activated protein kinase kinase (MEK), cyclooxygenase 1, and a T prostanoid receptor agonist, likely thromboxane A2.

Conclusions:

Ghrelin stimulates contraction in human mesenteric arteries through a novel signaling pathway.
Key components of this pathway include Src kinase, MEK, cyclooxygenase 1, and thromboxane A2.