Studies on the Mechanism of Pinacidil-Induced Vasodilation
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Authors
Purohit, Surendar S.
Issue Date
1989
Type
Thesis
Language
en_US
Keywords
Alternative Title
Abstract
It has been shown that pinacidil has its vasodilatory
effects by increasing the K+ permeability of the smooth muscle
cell. Recent work with pinacidil has suggested the presence of
a K+ conductance-independent mechanism of action. The
purpose of this project was to further investigate pinacidil's K+
conductance-independent mechanism of action using isometric
contractions induced by norepinephrine (NE) or 8OmM K+.
Pinacidil was found to dose-dependently inhibit the phasic
component of HE-induced contractions in the rabbit thoracic
aortic artery (RAO) and in the rabbit mesenteric artery (RMA).
The action of ryanodine, a drug which some studies suggested
disrupts the sarcoplasmic reticulum (SR) function, was confirmed
in :this project. In addition, data in this study suggested that
ryanodine did not affect the influx of extracellular Ca+ in
contractions induced by NE or 8OmM K+. Pinacidil's K+
conductance-independent mechanism in RAO was also verified in
this study. It was found that the SR does not seem to play an
essential role in pinacidil's K+ conductance independent
mechanism of action. From the results, it appears that the K+
conductance-independent mechanism of action of pinacidil may
involve the extrusion of Ca+2 from the cell or a direct
inhibition of the Ca+2 sensitivity of contractile proteins in the
cell.
Description
vii, 47 p.
Citation
Publisher
Kalamazoo College
License
U.S. copyright laws protect this material. Commercial use or distribution of this material is not permitted without prior written permission of the copyright holder.