Vascular capacitance is reduced by endothelin-1 (ET-1) in DOCA-salt rats. This may contribute to hypertension development. Because the splanchnic blood vessels (especially veins) are important in determining vascular capacitance, we tested the hypothesis that ET-1 levels in the splanchnic vasculature are elevated in hypertensive DOCA-salt compared to normotensive rats. Tissue ET-1 content was measured using an ELISA method in aorta, vena cava, superior mesenteric artery and vein, and small mesenteric arteries and veins from normotensive sham-operated (sham) and four-week DOCA-salt hypertensive rats. We also determined ET-1 concentration in aortic and portal venous blood (draining the nonhepatic splanchnic organs) in anesthetized and conscious sham and DOCA-salt rats before and after acute blockade of ET receptor mediated plasma clearance of ET-1. Results showed that veins had a higher ET-1 content than did arteries of similar size. However, ET-1 content was similar in vessels from sham and DOCA-salt rats, except in the aorta and superior mesenteric artery (greater in DOCA-salt). ET-1 concentration was significantly higher in portal venous than in aortic blood, indicating net non-hepatic splanchnic release (nNHSR) of ET-1. However, nNHSR of ET-1 was similar in sham and DOCA-salt rats. Although nNHSR of ET-1 increased significantly after ETB receptor blockade in sham rats, it was completely unchanged in DOCA-salt rats. These data suggest that despite the absence of ET receptor mediated plasma clearance of ET-1, neither the venous peptide content nor the net release of ET-1 is increased in the splanchnic vasculature of hypertensive DOCA-salt rats. These results argue against the hypothesis that increased venomotor tone in DOCA-salt hypertension is caused by increased ET-1 concentration around splanchnic venous smooth muscle cells.