Figure 2.

Physiology of contraction and relaxation of vascular smooth muscle. Muscle contraction occurs in response to the activation of receptors present in the membrane, such as the alpha-1 adrenergic receptor (a1R), the vasopressin-1 receptor (V1R) and the angiotensin type-1 receptor (AT1R); their activation by the selective agonist promotes the phosphorylation of the Gq protein and with that, the signaling pathway starts. With this, there is the release of calcium by the endoplasmic reticulum through phosphatidylinositol-3 (IP3); the calcium released in the cytosol binds with calmodulin (CaM), forming the calcium-calmodulin complex that phosphorylates myosin and promotes contraction. On the other hand, the nitric oxide (NO) produced by the endothelium reaches the smooth muscle, converting GTP into cGMP. cGMP dephosphorylates myosin and promotes relaxation. In addition, NO activates ATP-sensitive potassium channels (KATP), leading to hyperpolarization and inhibition of vasoconstriction. Angiotensin II (AgII); norepinephrine (NE); arginine-vasopressin (AVP); cyclic guanosine monophosphate (cGMP); guanosine triphosphate (GTP); diacyl glycerol (DAG); phospholipase C (PLC); phosphatidylinositol-4,5-bisphosphate (PIP2); protein kinase C (PKC).