Which receptor mediates vasodilation of arterioles in the heart, lungs, and skeletal muscle?

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Multiple Choice

Which receptor mediates vasodilation of arterioles in the heart, lungs, and skeletal muscle?

Explanation:
Activation of beta-2 adrenergic receptors on vascular smooth muscle in arterioles of the heart, lungs, and skeletal muscle causes relaxation and vasodilation. Epinephrine binds to these receptors, raising cAMP inside smooth muscle cells, which leads to relaxation and increased blood flow to these tissues during times of demand. This effect fits with how the body shunts blood to muscles and the heart under stress or exercise. Alpha-1 receptors produce vasoconstriction, so they don’t account for this dilation, and beta-1 receptors mainly increase heart rate and contractility rather than causing arteriolar dilation. Dopaminergic receptors can cause vasodilation in some beds (like renal) at certain doses, but they’re not the primary mechanism for arteriolar dilation in heart, lungs, and skeletal muscle. So the beta-2 adrenergic receptor mediates this vasodilation.

Activation of beta-2 adrenergic receptors on vascular smooth muscle in arterioles of the heart, lungs, and skeletal muscle causes relaxation and vasodilation. Epinephrine binds to these receptors, raising cAMP inside smooth muscle cells, which leads to relaxation and increased blood flow to these tissues during times of demand. This effect fits with how the body shunts blood to muscles and the heart under stress or exercise. Alpha-1 receptors produce vasoconstriction, so they don’t account for this dilation, and beta-1 receptors mainly increase heart rate and contractility rather than causing arteriolar dilation. Dopaminergic receptors can cause vasodilation in some beds (like renal) at certain doses, but they’re not the primary mechanism for arteriolar dilation in heart, lungs, and skeletal muscle. So the beta-2 adrenergic receptor mediates this vasodilation.

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