Potentiated adrenaline vasoconstrictor response by subthreshold concentrations of serotonin, endothelin-1 or U-46619 in human umbilical vein (HUV): evaluation of receptors involved.

ERRASTI A, LUCIANI L, TRAMONTANO J, BARD J, BOVERIS D, ROTHLIN U, PUGLIESE M, ROTHLIN R.

San Luis, Argentina

Congreso; XXXV Reunión anual de la Asociación Argentina de Farmacología Experimental.; 2003

Asociación Argentina de Farmacología Experimental (SAFE)

Serotonin (5-HT), endothelin-1 (ET-1) and thromboxane A2 mimetic, U-46619 (U), not only act directly on blood vessels but also may amplify adrenaline-mediated responses. The aim  of this study was to asses whether subthreshold concentrations of mentioned agonists potentiate adrenaline-induced contraction in HUV rings and determine the receptor subtypes involved. Rings were mounted in isolated organ baths suspended in Krebs solution, 37ºC, pH 7,4. After 2 hs equilibration period rings were pretreated with 5-HT (1.7 nM), ET-1 (0.1 nM) or U (0.3 nM) during 10 min in the absence and presence (30 min) of the following antagonists: ketanserine 10 nM (5-HT2A) and SB-216641 10nM (5-HT1B), FR-139317 10mM (ETA and ETB) or SQ-30741  100 nM (TP). Then, concentration responses curves (CRC) to adrenaline were constructed. 5-HT, ET-1 and U produced a leftward shift of CRC to adrenaline (p<0.05). The antagonists ketanserine, FR-139317 and SQ-30741 abolished potentiation whereas SB-216641 had no effect. We conclude that potenciated adrenaline vasoconstrictor effects of 5-HT, ET-1 and U are mediated by estimulation of 5-HT2A, a mix population of ETA and ETB and TP receptors, respectively in HUV.