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Antagonism and supersensitivity to phenylephrine-induced chronotropic responses
Acta Physiologica Latino Americana
|January 1, 1983
Summary
Phenylephrine increases heart rate indirectly through beta-adrenoceptor stimulation and directly via alpha 1-adrenoceptor activation. Papaverine induces supersensitivity to phenylephrine, suggesting calcium influx plays a key role.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
Background:
- Phenylephrine is an agonist that affects heart rate.
- Adrenoceptors play a crucial role in regulating cardiovascular function.
Purpose of the Study:
- To investigate the mechanisms underlying phenylephrine-induced chronotropic responses in rat right atria.
- To elucidate the roles of beta-adrenoceptors and alpha 1-adrenoceptors in phenylephrine's effects.
- To explore the impact of papaverine on phenylephrine-induced supersensitivity.
Main Methods:
- Isolated rat right atria were used to assess chronotropic responses.
- Drug treatments included propranolol (beta-blocker), prazosin (alpha 1-blocker), phentolamine (non-selective alpha-blocker), and papaverine.
- Concentration-effect curves and antagonism studies were performed.
Main Results:
- Propranolol competitively antagonized phenylephrine, similar to reserpinized conditions, suggesting indirect beta-adrenoceptor stimulation via norepinephrine release.
- Prazosin, but not phentolamine, inhibited phenylephrine effects, indicating alpha 1-adrenoceptor involvement.
- Combined alpha and beta-blockade fully antagonized the response.
- Papaverine induced supersensitivity to phenylephrine, which was blocked by alpha or beta-antagonists.
Conclusions:
- Phenylephrine stimulates heart rate both indirectly via beta-adrenoceptor activation (norepinephrine release) and directly via alpha 1-adrenoceptor activation.
- Papaverine-induced supersensitivity likely involves enhanced calcium influx, not phosphodiesterase inhibition.
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