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Glibenclamide does not reverse attenuated vasoreactivity to acute or chronic hypoxia
M R Eichinger1, T C Resta, D S Balderrama
1Department of Physiology, University of New Mexico School of Medicine, Albuquerque 87131, USA.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|October 1, 1995
Summary
Hypoxia reduces blood vessel responses in rats. Blocking adenosine triphosphate-sensitive potassium channels (KATP channels) did not alter these effects, suggesting KATP channels are not involved in hypoxia-induced vasoreactivity changes.
Area of Science:
- Cardiovascular Physiology
- Respiratory Physiology
- Pharmacology
Background:
- Acute and chronic hypoxia are known to attenuate systemic vasoreactivity.
- Adenosine triphosphate-sensitive potassium channels (KATP channels) play a role in vascular tone regulation.
Purpose of the Study:
- To investigate the role of KATP channels in modulating pressor and vasoconstrictor responses to phenylephrine (PE) during acute and chronic hypoxia in conscious rats.
- To determine if KATP channel blockade affects attenuated vasoreactivity induced by hypoxia.
Main Methods:
- Conscious instrumented rats were exposed to acute hypoxia (12% O2) or chronic hypoxic conditions.
- Phenylephrine (PE) infusions were used to assess mean arterial pressure, cardiac output, and total peripheral resistance.
- Glibenclamide, a KATP channel blocker, was administered to assess its effect on vasoreactivity.
Main Results:
- Acute hypoxia attenuated pressor and constrictor responses to PE in control rats.
- Chronic hypoxia did not restore pressor and constrictor responses upon return to normoxia.
- Glibenclamide administration did not alter PE-induced pressor or vasoconstrictor responses in normoxic or hypoxic conditions.
Conclusions:
- The opening of KATP channels is not implicated in the attenuated vasoreactivity observed during acute and chronic hypoxia in conscious rats.
- Hypoxia-induced alterations in vasoreactivity are mediated by mechanisms independent of KATP channel activity.