Examples and Individual Mechanisms
Vasodilation is the result of relaxation in smooth muscle surrounding the blood vessels. This relaxation, in turn, relies on removing the stimulus for contraction, which depends on intracellular calcium ion concentrations and, consequently, phosphorylation of the light chain of the contractile protein myosin. Thus, vasodilation mainly works either by lowering intracellular calcium concentration or the dephosphorylation of myosin. This includes stimulation of myosin light chain phosphatase and induction of calcium symporters and antiporters that pump calcium ions out of the intracellular compartment. This is accomplished through reuptake of ions into the sarcoplasmic reticulum via exchangers and expulsion across the plasma membrane. There are three main intracellular stimuli that can result in the vasodilation of blood vessels. The specific mechanisms to accomplish these effects vary from vasodilator to vasodilator.
| Class | Description | Example |
|---|---|---|
| Hyperpolarization mediated (Calcium channel blocker) | Changes in the resting membrane potential of the cell affects the level of intracellular calcium through modulation of voltage sensitive calcium channels in the plasma membrane. | adenosine |
| cAMP mediated | Adrenergic stimulation results in elevated levels of cAMP and protein kinase A, which results in increasing calcium removal from the cytoplasm. | prostacyclin |
| cGMP mediated (Nitrovasodilator) | Through stimulation of protein kinase G. | nitric oxide |
PDE5 inhibitors and potassium channel openers can also have similar results.
Compounds that mediate the above mechanisms may be grouped as endogenous and exogenous.
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