Electrical stimulation of afferent renal nerves and activation of intrarenal receptors increases plasma vasopressin concentration, but the role of afferent renal nerves in the control of vasopressin secretion is not clear. Recently, we reported that activation of renal mechanoreceptors stimulates the release of vasopressin. However, Intrapelvic pressure was increased to 50mmHg, and this increase is above the normal physiological range. Therefore, in the present study, we investigated the effect of moderately increased intrapelvic pressure on plasma vasopressin concentration in anesthetized rabbits. First, we measured renal tissue pressure while Intrapelvic pressure was increased stepwise in 10-mmHg increments. Basal renal tissue pressure was 17±2mmHg. Renal tissue pressure increased only when Intrapelvic pressure was higher than the basal tissue pressure of each animal. Usually, increases in intrapelvic pressure less than 20mmHg did not increase renal tissue pressure. This finding suggests that only increases in Intrapelvic pressure more than 20mmHg can activate renal mechanoreceptors. Based on this finding, the effects of moderate increases in intrapelvic pressure (15 and 30mmHg) were studied. With a 15-mmHg increase in intrapelvic pressure, plasma vasopressin concentration did not change significantly. However, when Intrapelvic pressure was increased to 30mmHg, plasma vasopressin concentration increased from 5.6±1.4 to 9.5±2.8pg/ml at 5min (p<0.05) and to 8.8±2.0pg/ml at 10mm (p< 0.05). Plasma renin activity and mean arterial pressure also increased when intrapelvic pressure was increased to 30mmHg. We conclude that moderate increases in intrapelvic pressure stimulate vasopressin secretion. This provides further evidence that the kidneys participate in the physiological control of vasopressin release by way of afferent renal nerves. (Hypertens Res 1995; 18: 197-202)