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Calcium-activated potassium channel-mediated arteriolar relaxation during endotoxic shock
J M Price1, C H Baker, R F Bond
1Department of Physiology and Biophysics, University of South Florida, College of Medicine, Tampa 33612, USA.
Shock (Augusta, Ga.)
|April 1, 1997
Summary
Calcium-activated potassium (KCa) channels significantly influence arteriole relaxation, with their role in acetylcholine-induced vasodilation shifting during endotoxin shock. Endotoxin shock did not significantly affect KCa channels in cremaster microvessels.
Area of Science:
- Physiology
- Pharmacology
- Cardiovascular Research
Background:
- Calcium-activated potassium (KCa) channels play a role in regulating vascular tone.
- Endotoxin shock can alter microvascular function and reactivity.
Purpose of the Study:
- To investigate the role of KCa channels in the in vivo relaxation of arterioles before and during endotoxin shock.
- To determine how endotoxin shock affects endothelium-dependent and independent vasodilation mediated by KCa channels.
Main Methods:
- Measurements of arteriole diameters (A2 and A3) in rat cremaster muscle using videomicroscopy.
- Administration of vasoactive agents: adenosine (ADO), acetylcholine (ACH), and sodium nitroprusside (SNP).
- Pharmacological blockade of KCa channels using tetraethylammonium chloride (TEA).
Main Results:
- ADO-induced arteriolar dilation was mediated by KCa channels both before and during endotoxin shock.
- Endothelium-dependent ACH-induced vasodilation shifted from a non-KCa channel mechanism to a KCa channel-mediated mechanism during endotoxin shock.
- Endotoxin shock did not significantly alter the contribution of vascular smooth muscle KCa channels to ADO-induced relaxation.
Conclusions:
- Vascular smooth muscle KCa channels are crucial for ADO-induced relaxation of cremaster microvessels and are unaffected by endotoxin shock.
- The mechanism of ACH-induced vasodilation in arterioles becomes dependent on KCa channels during endotoxin shock, indicating a shift in the regulatory pathway.