Abstract
The pressor mechanism of amezinium metilsulfate (Am), a new antihypotensive agent which stimulates the sympathetic nerve endings, was investigated in 21 patients on maintenance hemodialysis. Hemodynamic parameters were obtained using echocardiograms before and after the oral administration of Am, 10mg once a day, for 5 weeks. Three patients were excluded because of minor adverse effects (urinary retention and headache); these effects disappeared immediately after Am was discontinued. Mean blood pressure (MBP) at the onset of dialysis increased from 88.2±9.5 to 95.1±16.1mmHg (m±SD; p<0.05) and the trough MBP during dialysis increased from 60.1±11.7 to 69.7±14.2mmHg (p<0.01). No changes were observed in left ventricular diameter, heart rate or cardiac output. The total peripheral resistance index (TPRI) increased from 845±267 to 968±230×10-4dynes·sec/cm7 (p<0.05). The significant correlation between the increases in blood pressure and TPRI indicates that the increase in blood pressure with Am is caused by peripheral vascular constriction. Am demonstrated a weak but definite cardiac stimulatory effect in patients with a cardiac index of less than 4l/min/m2 before treatment. The finding that blood pressure increased more in the more hypotensive patients suggests that dialysis hypotension is mainly caused by a decrease in sympathetic nervous activity.
