Arteriolenvasodilatation

Arteriolenvasodilatation is the widening of arterioles, the small resistance vessels that regulate blood flow to organs and tissues. By increasing the radius of these vessels, arterioles decrease vascular resistance and raise perfusion to the affected tissue, while potentially lowering systemic blood pressure if widespread.

The process is primarily regulated by the endothelium and local metabolic conditions. Endothelial cells release vasodilators such as nitric oxide (NO), prostacyclin (PGI2), and endothelium-derived hyperpolarizing factors, which relax smooth muscle through mechanisms involving cyclic GMP or cyclic AMP. Local factors that promote dilation include increased carbon dioxide, decreased oxygen, lower pH, adenosine, potassium, and temperature rise. Mechanical cues like shear stress also stimulate NO production. Autonomic nerves can influence arteriolar tone, but in many tissues local metabolic control dominates.

Regulation balances regional needs with overall hemodynamics. Arteriolar dilation in specific tissues increases regional blood flow, supporting metabolic activity, while systemic vasodilation can reduce afterload and influence blood pressure. In thermoregulation, skin arterioles dilate to dissipate heat. In exercise, arterioles in skeletal muscle dilate to meet increased demand.

Clinical and pharmacological relevance includes conditions with altered arteriolar tone. Physiological vasodilatation occurs normally; excessive or widespread arteriolar dilation is seen in septic shock and anaphylaxis, contributing to hypotension. Therapeutically, vasodilators targeting arterioles (such as NO donors or calcium-channel blockers) lower vascular resistance and can improve tissue perfusion in selected settings.