1982 年 46 巻 5 号 p. 494-502
Altered prostacyclin metabolism may underlie essential hypertension. In this study, responses of plasma 6-keto-prostaglandin F1α (6-keto-PGF1α: a stable metabolite of prostacyclin) to infused norepinephrine (NE) were compared in 14 normotensive subjects (NT) and 20 untreated patients with essential hypertension (EH). In addition, changes in systemic hemodynamics following NE-infusion were compared with changes in plasma 6-keto-PGF1α. The subjects were all hospitalized and placed on a diet containing 6-8 g of salt per day. Blood pressure was recorded directly through the brachial artery, cardiac output (CO) was determined with the dye-dilution technique using cuvette and total peripheral vascular resistance (TPR) was calculated before and 60 min after NE-infusion. Arterial plasma 6-keto-PGF1α was also determined before and after NE-infusion. The rate of NE-infusion was adjusted to elevate mean arterial pressure (MAP) by I 0-15%. Plasma 6-keto-PGF1α was radio-immunoassayed. Elevation of MAP was 13.0 1.2 (SE) in NTs and 11.7 1 .4% in EHs. After NE-infusion, CO and TPR both significantly increased in NTs, while only CO increased significantly in EHs. Changes in CO and TPR were both significantly different between the two groups (p < 0.01). Initial plasma 6-keto-PGF1 was reduced in EHs as compared with NTs (1 74 15 vs 295 41 pg/ml, p < 0.02). However, during NE-infusion, the increase in plasma 6-keto-PGF1 was greater in EHs than in NTs (p < 0.0 l). There was a significant negative correlation between changes in TPR and plasma PG (r = -0.36, p < 0.05). The results indicate that responses of systemic hemodynamics and plasma 6-keto-PGF1 to infused NE are different in the NT and EH groups, and that the absence of changes in TPR in EHs may be related to a marked increase in circulating prostacyclin. These findings, together with the reduced initial levels of plasma 6-keto-PGF1 in EHs, probably represent altered prostacyclin metabolism in essential hypertension.
