1988 年 52 巻 11 号 p. 1277-1285
It has been reported that salt loading induces a blood pressure rise in rats whose renal mass has been reduced .We examined the involvement of the peripheral sympathetic nervous system in the pathogenesis of hypertension in subtotally nephrectomized and salt-loaded rats. Male Wistar rats (200-240g) underwent subtotal nephrectomy (removal of 70-80% of the renal mass). After surgery, 1% saline was given ad libitum as drinking water in the experimental group (E), while tap water was given to the controls (C). On the 10th day after nephrectomy, blood pressure was determined, and plasma samples were collected. Deproteinized plasma samples were diluted with Ringer-Locke solution (1/40 v/v), and were perfused into isolated mesenteric artery-intestinal loop preparations of normotensive male Wistar rats. Pressor responses and norepinephrine overflow induced by electrical nerve stimulation, and the pressor responses to exogenous norepinephrine were assessed before and after the addition of deproteinized plasma to the perfusate. Systolic blood pressure was significantly elevated in the experimental group (E: 150 5 mmHg, C: 109 4 mmHg, p 0.01). When deproteinized plasma from the experimental group was perfused, pressor responses to electrical nerve stimulation were significantly increased (E: 167.2 13.7%, C: 91.1 6.4%; p 0.01), as was norepinephrine overflow (E: 117.3 6.4%, C: 90.7 5.9%; p 0.05), while responses to exogenous norepinephrine were only slightly augmented compared with the control group (E:120.0 2.7%, C: 105.5 9.0%; n.s.). Deproteinized plasma from the experimental rats highly inhibited Na-K ATPase (E: 24.7 3.8%, C: 2.4 1.1 %, p 0.01) and strongly cross-reacted with antidigoxin antibodies being much more active than deproteinized plasma from control rats. Moreover, there was a significant positive correlation between Na-K ATPase inhibition and blood pressure (p 0.01). These data indicate that plasma from reduced renal mass-salt hypertensive rats contains an augmenting factor for norepinephrine overflow from sympathetic nerve endings. This factor might be Na-K ATPase inhibitor.
