Vasopressin can cause bronchoconstriction through stimulation of which receptors on bronchial smooth muscle?

Vasopressin can cause bronchoconstriction through stimulation of which receptors on bronchial smooth muscle?

• A. V2 receptors
• B. V1 receptors
• C. Alpha-1 receptors
• D. Beta-2 receptors

Answer: (B)

Vasopressin can cause bronchoconstriction by acting on V1 receptors on bronchial smooth muscle. When these V1 receptors are stimulated, they couple to a Gq protein, which activates phospholipase C, leading to increased inositol triphosphate (IP3) and diacylglycerol (DAG). This raises intracellular calcium and promotes contraction of the airway smooth muscle, narrowing the airways. V2 receptors, in contrast, are mainly in the kidneys and regulate water reabsorption, not airway tone. Beta-2 receptors produce bronchodilation when stimulated, not constriction. Alpha-1 receptors are adrenergic and are not the receptors through which vasopressin acts to affect the bronchial smooth muscle in this context. So the bronchoconstrictive effect of vasopressin is best explained by stimulation of V1 receptors on bronchial smooth muscle.

Vasopressin can cause bronchoconstriction by acting on V1 receptors on bronchial smooth muscle. When these V1 receptors are stimulated, they couple to a Gq protein, which activates phospholipase C, leading to increased inositol triphosphate (IP3) and diacylglycerol (DAG). This raises intracellular calcium and promotes contraction of the airway smooth muscle, narrowing the airways.

V2 receptors, in contrast, are mainly in the kidneys and regulate water reabsorption, not airway tone. Beta-2 receptors produce bronchodilation when stimulated, not constriction. Alpha-1 receptors are adrenergic and are not the receptors through which vasopressin acts to affect the bronchial smooth muscle in this context.

So the bronchoconstrictive effect of vasopressin is best explained by stimulation of V1 receptors on bronchial smooth muscle.