Microsoft Word - NEF687BF

Kazuo Tsunoda, MD, PhD, Second Department of Internal Medicine, Tohoku University School of Medicine, Aobaku Seiryomachi 1-1, Sendai 980 (Japan) 4-, 1 Dear Sir, Hypertension in patients receiving maintenance hemodialysis usually can be controlled by ultrafiltration. However, in a small number hemodialysis fails to reduce the blood pressure despite the removal of salt and water. Such patients are defined as having dialysis-resistant hypertension. In these cases, the plasma volume and cardiac output are usually lower, and the total peripheral resistance is almost always higher than in the controllable cases [1]. Therefore, dialysis-resistant hypertension is mainly the result of an increase in total peripheral resistance. An increase in PRA [2], a circulating Na/K ATPase pump inhibitor [3], and inadvertent hypercalcemia [4] have been reported to be pathogenetic factors. However, the pathogenesis of vasoconstriction in dialysis-resistant hypertension remains a question. Endothelin (ET), a newly discovered peptide hormone released from the endothelium, exhibits potent vasoconstrictive activity [5]. Recently, an increased plasma immunoreactive ET (ir-ET) concentration has been reported in patients with myocardial infarction and those with subarachnoid hemorrhage, indicating an involvement of ET in the etiology of vasospastic disorders [6,7]. To investigate the involvement of ET in hemodialysis-resistant hypertension, we measured ir-ET-1 [1–21] concentration in plasma before and after hemodialysis in 11 patients with hemodialysis-resistant hypertension and in 22 with hemodialysis-con-trollable hypertension. All subjects were dialyzed three times weekly for periods of 4 h each. Blood was collected from the arterio-venous shunt and plasma ir-ET-1 was extracted using Sep-Pak C-18 cartridges (Waters Associates, Milford, Mass., USA). Plasma ir-ET-1 was measured by a previously described sandwich-enzyme immunoassay for ET-1 [8]. In brief, standard ET-1 or samples