本態性高血圧症における腎性降圧系の病態生理学的意義に関する研究 ―特に低レニン本態性高血圧患者の病因との関連について―
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The renal dopamine, kallikrein-kinin and prostaglandin systems are suppressed in essential hypertensives (EHT). The purpose of this study was to further clarify the pathophysiological role of the renal dopamine, kallikrein-kinin and prostaglandin systems in EHT. The effects of infused dopamine on these systems and renal sodium handling were investigated in EHT and compared to those in normotensives (NT). Urinary excretion of kallikrein, kinin and prostaglandin E2 (PGE2) in EHT was significantly lower than those in NT. Urinary kallikrein and kinin were more markedly suppressed in low renin patients than in normal renin patients, while no significant difference was observed in PGE2 between these subgroups. Kallikrein quantity (uKAL-Q), its activity (uKAL-A) and PGE2 were significantly increased in EHT by dopamine infusion. Following dopamine infusion, the significant difference in uKAL- Q and uKAL-A, which was cleary observed before the infusion, almost completely disappeared between NT and EHT. These increases of kallikrein and kinin by infused dopamine were significantly higher in the low renin group than in other groups, but that of PGE2 was not. Urine volume (UV), urinary sodium excretion (UNaV) and fractional excretions of sodium (FENa) and inorganic phosphorus (FEP) were all increased in both NT and EHT after the dopamine infusion. The increase of these was significantly greater in EHT than in NT, and greater in the low renin group than in the normal renin group in all cases of NT and EHT, significantly positive correlations were found between ΔUV and ΔuKAL-Q, and ΔPGE2 and AFENa or AFEP, and significantly negative correlations between changes in mean arterial pressure (AMAP) and AuKAL-Q, AuKAL-A or APGE2. From these studies, it was concluded that 1) a close relationship exists among these renal depressor systems (dopamine, kallikrein-kinin and prostaglandin systems), 2) the suppression of renal dopaminergic activity may contribute to the suppression of the renal kallikrein-kinin and prostaglandin systems, especially in low renin groups, and 3) the suppression of these renal depressor and natriuretic systems may play an important role in the pathophysiology of EHT, especially in low renin EHT mediated by volume and sodium retention.
- 札幌医科大学の論文
- 1988-12-01
札幌医科大学 | 論文
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