ETA receptor blockade with BQ123 inhibited ET-1-induced increases in splanchnic (64% vs -1%, P<0.05) and renal vascular resistance, while ETB blockade increased basal resistance.
Absolute Event Rate: -1% vs 64%
p-value: p=<0.05
The contribution of the endothelin (ET) receptors ETA and ETB to basal vascular tone and ET-1-induced vasoconstriction in the renal and splanchnic vasculature was investigated in six healthy humans. ET-1 was infused alone and in combination with the selective ETA receptor antagonist BQ123 or the selective ETB receptor antagonist BQ788 on three different occasions. BQ123 did not affect basal arterial blood pressure, splanchnic vascular resistance (SplVR) or renal vascular resistance (RVR), but inhibited the increase in vascular resistance induced by ET-1 64±18 versus -1±7% in SplVR (P0.05); 36±6 versus 12±3% in RVR (P0.0001). BQ788 increased basal SplVR and RVR 38±16% (P = 0.01) and 21±5% (P0.0001) respectively, and potentiated the ET-1-induced vasoconstriction. Plasma ET-1 increased more after ETB blockade than under control conditions or after ETA blockade. These findings suggest that the ETA receptor mediates the splanchnic and renal vasoconstriction induced by ET-1 in healthy humans. The ETB receptor seems to function as a clearance receptor and may modulate vascular tone by altering the plasma concentration of ET-1.
Böhm et al. (2003) studied Healthy (n=6). BQ123 (ETA antagonist) and BQ788 (ETB antagonist) vs. ET-1 alone was evaluated on Increase in splanchnic vascular resistance (SplVR) induced by ET-1 (p=<0.05). ETA receptor blockade with BQ123 inhibited ET-1-induced increases in splanchnic (64% vs -1%, P<0.05) and renal vascular resistance, while ETB blockade increased basal resistance.