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Hypoxia/reoxygenation selectively impairs alpha 1b-adrenoceptor function in small mesenteric arteries
H Gao1, R J Korthuis, J N Benoit
1Department of Physiology, Louisiana State University Medical Center, Shreveport 71130-3932, USA.
The American Journal of Physiology
|November 1, 1996
Summary
Hypoxia/reoxygenation impairs norepinephrine effectiveness in small arteries by disrupting alpha 1b-adrenoceptor function. Antioxidants prevented this dysfunction, highlighting the role of reactive oxygen metabolites in norepinephrine signaling.
Area of Science:
- Physiology
- Pharmacology
- Cardiovascular Research
Background:
- Hypoxia/reoxygenation (H/R) is a significant physiological stressor.
- Norepinephrine (NE) regulates vascular tone via alpha-adrenoceptors.
- The impact of H/R on specific alpha-adrenoceptor subtypes remains unclear.
Purpose of the Study:
- To investigate if H/R affects norepinephrine (NE) effectiveness in small arteries.
- To determine the role of alpha 1a- and alpha 1b-adrenoceptor subtypes in H/R-induced changes.
- To elucidate the involvement of reactive oxygen metabolites in this process.
Main Methods:
- Small mesenteric arteries from rats were studied using a small vessel myograph.
- Hypoxia was induced by N2/CO2 bubbling, followed by reoxygenation.
- Selective receptor blockade and antioxidant treatment (SOD/CAT) were employed.
Main Results:
- H/R significantly reduced NE effectiveness (pD2 decreased from 6.26 to 5.84).
- Antioxidants (SOD and CAT) abolished H/R-induced contractile dysfunction.
- H/R selectively attenuated alpha 1b-adrenoceptor responses, while alpha 1a-responses remained unaffected.
Conclusions:
- H/R-induced impairment of NE effectiveness in small arteries is mediated by alpha 1b-adrenoceptor dysfunction.
- Reactive oxygen metabolites play a crucial role in this H/R-induced signaling defect.
- Targeting alpha 1b-adrenoceptor pathways may offer therapeutic potential in conditions involving H/R injury.