Figure 2. Intracellular signaling within vascular smooth muscle following the activation of α₁‐adrenergic, vasopressin‐1, β₂‐adrenergic, and ATP‐sensitive potassium channel receptors.

Stimulation of the α₁‐adrenergic or vasopressin‐1 receptors causes activation of the Gq (G‐protein) subunit, resulting in downstream stimulation of the phospholipase C signaling pathway. Phospholipase C in turn activates inositol 1, 4, 5‐triphosphate (IP3) leading to Ca²⁺ release from the sarcoplasmic reticulum (SR), resulting in vasoconstriction. Conversely, β₂‐receptor stimulation activates the inhibitory G‐protein (Gi) subunit causing vasodilatation through increased cAMP (cyclic adenosine monophosphase) activation and resulting phospholamban‐mediated Ca²⁺ uptake into the SR. Similarly, activation of the ATP‐sensitive potassium channel causes potassium influx that hyperpolarizes voltage‐dependent Ca²⁺ channels, reducing intracellular Ca²⁺ and vasomotor tone. AMP indicates adenosine monophosphate; DAG, diacylglycerol; PDE3, phosphodiesterase 3; and PLB, phospholamban.