beta-Adrenoceptor blockade spares chemoreceptor responsiveness to hypoxia.

Abstract

The effect of beta-adrenoceptor blockade on the carotid body chemoreceptor response to hypoxia was assessed in anesthetized and paralyzed cats. Propranolol, atenolol and ICI 118,551 each abolished the enhancement of chemoreceptor activity produced by i.v. infusion of exogenous isoproterenol; however, the blocking drugs did not significantly diminish the increase in chemoreceptor neural discharge induced by hypoxia. These results do not support the hypothesis that beta-adrenergic receptors play an essential role in the chemoreceptor response to oxygen deprivation.

• Authors: S F Gonsalves, E J Smith, W F Nolan, R E Dutton
• Journal: Brain research (Brain Res) Vol. 324 Issue 2 Pg. 349-53 (Dec 24 1984) ISSN: 0006-8993 [Print] Netherlands
• PMID: 6099205 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Propanolamines
• Receptors, Adrenergic, beta
• ICI 118551
• Atenolol
• Propranolol

Topics

• Animals
• Atenolol (pharmacology)
• Carotid Body (drug effects, physiopathology)
• Cats
• Female
• Hypoxia (physiopathology)
• Male
• Propanolamines (pharmacology)
• Propranolol (pharmacology)
• Receptors, Adrenergic, beta (physiology)