日本内分泌学会雑誌
本態性高血圧症における水・電解質代謝異常とオキシトシンとの関連
小野 美明
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63 巻 (1987) 2 号 p. 143-163

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A possible involvement of oxytocin (OT) has been indicated in regulation of water and electrolyte metabolism, based on findings that the secretion of OT is increased by either water deprivation or sodium loading. However, to date, no informations have yet been obtained about the role of OT in hypertension. The present study was therefore undertaken to elucidate the role of OT for abnormalities of fluid and electrolyte metabolism in essential hypertension (EH) in comparison with normotensive subjects (NT).
The major results were as follows.
1) Plasma level of OT was 3.7 ± 2.1 pg/ml (mean ± SD) in EH, not significantly higher than that in NT (3.2 ± 1.7 pg/ml). Plasma OT in low-renin EH (4.8 ± 2.5 pg/ml) was significantly different from that in high-renin EH (2.9 ± 1.4 pg/ml, p<0.05) and NT (p<0.05), but not in normal-renin EH (3.8 ± 2.0 pg/ml).
2) Plasma OT was inversely correlated with plasma renin activity (PRA) in EH (r =- 0.384, p<0.01), but not in NT (r = 0.102).
3) No significant correlation was found between plasma OT and plasma aldosterone concentration (PAC), plasma concentration of antidiuretic hormone (ADH), serum sodium and potassium, blood pressure and renal function in either EH or NT.
4) I.m. injection of OT (0.04 IU/kg) increased significantly urinary excretions of sodium and potassium in EH and NT. However, the increment in sodium excretion was greater in low-renin EH than that in normal-renin EH (0.05<p<0.10), high-renin EH (p<0.05) and NT (p<0.05). PRA, PAC and ADH were significantly decreased after OT injection, but blood pressure, serum sodium and potassium were not altered in both EH and NT. 5) I.v. administration of OT (0.1-0.2 IU/min) suppressed angiotensin II-induced in crease of PAC and elevation of blood pressure in both EH and NT. The decrease in PAC by the OT administration was the greatest in low-renin EH. The reduction of blood pressure was significantly greater in EH than in NT (p<0.05).
6) I.v. administration of hypertonic saline (5%) resulted in a significant increase of plasma OT in EH and NT, and the increment in OT was the greatest in low-renin EH. Serum sodium concentration was increased by the infusion, positively correlated with plasma OT in both EH (r = 0.458, p<0.05) and NT (r = 0.830, p<0.05).
7) High sodium intake (340 mEq/day for 5 days) increased plasma OT in EH and NT. The increment of plasma OT was significantly correlated with that of serum sodium concentration in EH (r = 0.497, p<0.02) and NT (r = 0.831, p<0.05). By contrast, low sodium intake (50 mEq/day for 5 days) caused reduction of plasma OT in EH and NT with high plasma OT level more than 5.5 pg/ml.
8) Water deprivation (15 h) resulted in a significant increase of plasma OT in EH and NT. The magnitude of increase in plasma OT, which was significantly greater in EH than in NT (p<0.05), was correlated with increment of serum sodium concentration (r = 0.529, p<0.05 for EH; r = 0.745, 0.05<p<0.10 for NT) and also plasma osmolarity (r = 0.479, p<0.05 for EH; r = 0.742, 0.05<p<0.10 for NT).
In conclusion, the secretion of OT is stimulated by a high circulating sodium level to display natriuretic effect on the kidney. Also, OT seems to be related, in part at least, to water and electrolyte metabolism in low-renin EH presumably with predisposition of fluid retention, through its natriuretic action and suppression to the renin-angiotensin-aldosterone activity.

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