Which receptor subtype increases heart rate during sympathetic stimulation?

Study for the Ivy Tech Anatomy and Physiology II Heart Test. Access flashcards and multiple choice questions, each with helpful hints and explanations. Prepare effectively for your exam and bolster your understanding of heart anatomy and physiology!

Multiple Choice

Which receptor subtype increases heart rate during sympathetic stimulation?

Explanation:
Sympathetic control of heart rate comes mainly through beta-1 adrenergic receptors in the heart. When sympathetic nerves release norepinephrine (and circulating epinephrine can act on these receptors), beta-1 receptors activate Gs proteins, which stimulate adenylyl cyclase to raise cAMP. The increased cAMP activates protein kinase A, which enhances the activity of channels and calcium handling in pacemaker cells. This steepens the slope of phase 4 depolarization in the sinoatrial node, causing the SA node to fire more quickly and the heart rate to rise, with concurrent speeding of conduction through the AV node. Alpha-1 receptors drive vascular smooth muscle contraction and don’t primarily increase heart rate. Beta-2 receptors can contribute to some cardiac effects but are not the main drivers of heart rate in sympathetic stimulation. Muscarinic M2 receptors mediate parasympathetic slowing of the heart, opposite to the sympathetic effect. Thus, the receptor subtype responsible for increasing heart rate during sympathetic activation is the beta-1 adrenergic receptor.

Sympathetic control of heart rate comes mainly through beta-1 adrenergic receptors in the heart. When sympathetic nerves release norepinephrine (and circulating epinephrine can act on these receptors), beta-1 receptors activate Gs proteins, which stimulate adenylyl cyclase to raise cAMP. The increased cAMP activates protein kinase A, which enhances the activity of channels and calcium handling in pacemaker cells. This steepens the slope of phase 4 depolarization in the sinoatrial node, causing the SA node to fire more quickly and the heart rate to rise, with concurrent speeding of conduction through the AV node. Alpha-1 receptors drive vascular smooth muscle contraction and don’t primarily increase heart rate. Beta-2 receptors can contribute to some cardiac effects but are not the main drivers of heart rate in sympathetic stimulation. Muscarinic M2 receptors mediate parasympathetic slowing of the heart, opposite to the sympathetic effect. Thus, the receptor subtype responsible for increasing heart rate during sympathetic activation is the beta-1 adrenergic receptor.

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