P-120: Reactive hyperaemia releases tissue plasminogen activator through a bradykinin-dependent mechanism in essential hypertensive men

Reactive hyperemia (RH) is a physiological vasodilator response mediated by endothelial-dependent and independent factors triggered by ischemia. Aim of the study was to evaluate whether RH releases tissue plaminogen activator (t-PA), the key fibrinolytic mechanism in man. We also tried to identify the underlying mechanisms by infusing adenosine (ADE), an endothelial-independent vasodilator, acetylcholine (ACH), a nitric oxide (NO)-releasing substance, and bradykinin (BK), an agonist acting also through release of an endothelium-derived hyperpolarizing factor (EDHF). A total of 39 uncomplicated essential hypertensive men (EH, age: 48±7yrs, 148±7/92±10 mmHg) were recruited. Forearm blood flow (FBF, venous plethysmography), arterial (A) and venous (V) t-Pa antigen concentrations (ELISA) to derive REL (V-AxFBF) were measured before and after RH induced by a 10-min inflation of a pressure cuff at mid systo-diastolic values (n=13). The same procedure was carried out before and after 10-min intraarterial infusions of ADE (5mg/dl tissuexmin-1, n=10), ACH (15μg/ dl tissuexmin-1, n=12) and BK (500 ng/ dl tissuexmin-1, n=4). Results (means±SD or medians[interquartile range]): 1 min after cuff release, FBF increased from 3.2±1.6 to 18±3 ml/minxdl-1 (p