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Abstract

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<.001), and t-PA REL from 1.4 [1] to 49 [9] ng/mlxmin-1 (p<.01) respectively. ADE, ACH and BK increased (p<0.001) FBF to a similar extent (ADE: from 3.5±0.8 to 17.6±4, ACH: from 3.2±0.8 to 14.8±3.2: BK: from 3.1±0.8 to 16.3±2.1 ml/dlxmin-1) but only BK increased t-PA REL (ADE: from -0.4[1] to 0. [10]; ACH: from 0.2 [1] to -0.5[18], BK: from -0.4[0.9] to 19[38] ng/mlxmin-1] (p<0.04).

RH, a physiological vasodilator response to ischemia, releases t-PA in EH, showing a relationship between endothelial-mediated vasomotion and local fibrinolysis, and possibly implying that a reduced endothelial mediated vasomotion leads to defective fibrinolysis.Enhanced local t-PA REL by RH could not be explained by vasodilatation per se or direct effects of either ADE or NO produced in response to ACH stimulation. Rather, the selective t-PA releasing effect of BK may suggest a preferential involvement of EDHF.

reactive hyperemia, tissue plasminogen activator, bradykinin
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© American Journal of Hypertension, Ltd. 2001
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