Endothelialdependent

Endothelialdependent, in scientific usage, refers to processes or responses that require the vascular endothelium to function or mediate their effects. In particular, endothelial-dependent mechanisms are those in which the endothelium releases signaling molecules that influence the underlying vascular smooth muscle and thereby regulate blood flow, vessel diameter, and tone.

A central example is endothelium-dependent vasodilation. This occurs when the endothelium releases relaxing factors such as nitric oxide (NO), prostacyclin (PGI2), and endothelium-derived hyperpolarizing factor (EDHF) in response to stimuli like increased shear stress or certain pharmacologic agents. Nitric oxide, produced by endothelial nitric oxide synthase (eNOS), diffuses to smooth muscle to induce relaxation. Acetylcholine, bradykinin, and other agonists typically produce endothelium-dependent responses, whereas some agents can cause vasodilation directly on smooth muscle without endothelium involvement, termed endothelium-independent.

Endothelialdependent processes are frequently assessed clinically and experimentally. Noninvasive tests of flow-mediated dilation (FMD) measure the arterial dilation response to shear stress and reflect endothelial function. Pharmacologic tests compare endothelium-dependent responses (e.g., acetylcholine) with endothelium-independent responses (e.g., nitroprusside).

Endothelial dysfunction denotes impaired endothelium-dependent responses and is associated with cardiovascular risk factors such as hypertension, diabetes, smoking, and hyperlipidemia. It contributes to reduced vasodilatory capacity, pro-inflammatory and pro-thrombotic states, and contributes to the progression of atherosclerosis. Understanding endothelialdependent mechanisms aids in assessing vascular health and guiding interventions aimed at restoring endothelial function.