Which receptor mediates detrusor relaxation during bladder filling?

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Multiple Choice

Which receptor mediates detrusor relaxation during bladder filling?

Explanation:
During bladder filling, the detrusor smooth muscle must relax to enlarge the bladder and store urine. This relaxation is driven primarily by sympathetic signaling through beta-3 adrenergic receptors on the detrusor. When these receptors are activated, cAMP levels rise, activating protein kinase A and reducing calcium sensitivity, which leads to smooth muscle relaxation and increased bladder capacity. In contrast, acetylcholine acting on muscarinic M3 receptors promotes detrusor contraction, which is the action needed for voiding, not filling. Alpha-1 adrenergic receptors help maintain continence by tightening the internal urethral sphincter rather than relaxing the detrusor. Beta-1 receptors aren’t the main players in detrusor tone. Clinical note: beta-3 agonists (like mirabegron) are used to treat overactive bladder by promoting detrusor relaxation and increasing storage capacity.

During bladder filling, the detrusor smooth muscle must relax to enlarge the bladder and store urine. This relaxation is driven primarily by sympathetic signaling through beta-3 adrenergic receptors on the detrusor. When these receptors are activated, cAMP levels rise, activating protein kinase A and reducing calcium sensitivity, which leads to smooth muscle relaxation and increased bladder capacity.

In contrast, acetylcholine acting on muscarinic M3 receptors promotes detrusor contraction, which is the action needed for voiding, not filling. Alpha-1 adrenergic receptors help maintain continence by tightening the internal urethral sphincter rather than relaxing the detrusor. Beta-1 receptors aren’t the main players in detrusor tone.

Clinical note: beta-3 agonists (like mirabegron) are used to treat overactive bladder by promoting detrusor relaxation and increasing storage capacity.

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