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Bradykinin induces concentration-dependent contractions across various human and animal smooth muscles primarily via activation of the constitutive B₂ kinin receptor. The mechanism involves elevation of intracellular calcium levels leading to activation/phosphorylation events that drive actomyosin interaction. Under inflammatory conditions or after tissue injury/sensitization, inducible B₁ kinin receptors may also contribute. Pharmacological modulation at multiple points along this pathway provides opportunities for therapeutic intervention against diseases characterized by abnormal smooth muscle tone.
Activation of B1 and B2 receptors leads to increased intracellular calcium, activation of myosin light chain kinase (MLCK), and subsequent actomyosin crossbridge cycling, resulting in smooth muscle contraction.
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