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Postsynaptic alpha 1- and alpha 2-adrenergic mechanisms in coronary vasoconstriction
D G Chen1, X Z Dai, B G Zimmerman
1Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.
Journal of Cardiovascular Pharmacology
|January 1, 1988
Summary
Postsynaptic alpha 2-adrenoceptors are the primary mediators of coronary vasoconstriction in dogs, even though both alpha 1 and alpha 2 stimulation can cause this effect. This finding is crucial for understanding cardiac adrenergic signaling.
Area of Science:
- Cardiovascular Physiology
- Adrenergic Pharmacology
Background:
- Adrenergic receptors play a key role in regulating coronary blood flow.
- The specific roles of postsynaptic alpha-1 and alpha-2 adrenoceptors in coronary vasoconstriction require further elucidation.
Purpose of the Study:
- To determine the relative importance of postsynaptic alpha-1 and alpha-2 adrenoceptors in mediating coronary vasoconstriction.
- To investigate the specific adrenoceptor subtypes responsible for vasoconstrictive responses to norepinephrine and epinephrine.
Main Methods:
- Open-chest dog model with constant coronary artery perfusion.
- Surgical transection of vagus nerves and stellate ganglia.
- Pharmacological blockade using alpha-1 (prazosin) and alpha-2 (yohimbine, idazoxan) antagonists.
- Intra-arterial administration of alpha-1 (phenylephrine) and alpha-2 (BHT 933) agonists, as well as norepinephrine and epinephrine.
- Regional myocardial blood flow assessment using radioactive microspheres.
Main Results:
- Both phenylephrine (alpha-1 agonist) and BHT 933 (alpha-2 agonist) induced coronary vasoconstriction.
- Prazosin partially blocked phenylephrine response; yohimbine nearly eliminated it.
- Yohimbine almost completely blocked BHT 933 response, which was resistant to prazosin.
- Norepinephrine-induced vasoconstriction was blunted by alpha-2 blockade (yohimbine, idazoxan) but resistant to prazosin.
- Epinephrine-induced vasoconstriction was markedly attenuated by yohimbine.
- No transmural redistribution of myocardial perfusion was observed during vasoconstriction.
Conclusions:
- Both postsynaptic alpha-1 and alpha-2 adrenoceptors can mediate coronary vasoconstriction.
- However, vasoconstriction induced by norepinephrine and epinephrine is primarily mediated by postsynaptic alpha-2 adrenoceptors.
- These findings highlight the dominant role of alpha-2 adrenoceptors in sympathetic-mediated coronary vasoconstriction.