title: The pathophysiological role of renal dopamine, kallikrein kinin and prostaglandin systems in essential hypertension.
abstract: In order to clarify the relationship and the pathophysiological role of renal dopamine, kallikrein-kinin and prostaglandin systems in essential hypertensives, the effects of dopamine on these systems and renal sodium handling were investigated. Basal levels of kallikrein, kinin and prostaglandin E2 in essential hypertensives were significantly lower than those in normotensives. Those of kallikrein and kinin were obviously more suppressed in the low renin group than in the normal renin group, but no significant difference in prostaglandin E2 was found in either subgroup. Urinary dopamine excretion was significantly lower in the low renin essential hypertensives, while no significant difference was found between normotensives and normal renin essential hypertensives. Kallikrein activity and prostaglandin E2 were significantly increased in essential hypertensives by dopamine infusion, and no significant difference was found in kallikrein-quantity and kinin between normotensives and essential hypertensives after the infusion. These increases of kallikrein and kinin were significantly higher in the low renin group than in normal renin group, but those of prostaglandin E2 were not. Urine volume, urinary sodium excretion and fractional excretions of sodium and inorganic phosphorus were all increased in both normotensives and essential hypertensives after dopamine infusion. The increases of these were significantly greater in essential hypertensives than in normotensives, and greater in the low renin group than the normal renin group. From these results, it was suggested that the dopamine, kallikrein-kinin and prostaglandin E2 system have a close relationship with each other, and the suppression of these systems may contribute to the pathophysiology of essential hypertension, especially in the low renin group.
authors.affiliation: Second Department of Internal Medicine, Sapporo Medical College, Japan.
authors.forename: O
authors.initials: O
authors.lastname: Iimura
authors.forename: K
authors.initials: K
authors.lastname: Shimamoto
authors.forename: N
authors.initials: N
authors.lastname: Ura
authors.forename: M
authors.initials: M
authors.lastname: Nakagawa
authors.forename: T
authors.initials: T
authors.lastname: Nishimiya
authors.forename: T
authors.initials: T
authors.lastname: Ando
authors.forename: Y
authors.initials: Y
authors.lastname: Yamaguchi
authors.forename: A
authors.initials: A
authors.lastname: Masuda
authors.forename: H
authors.initials: H
authors.lastname: Ogata
authors.forename: S
authors.initials: S
authors.lastname: Saito
mesh_terms: D015232:Dinoprostone; D004231:Diuresis / Q000187:drug effects; D004298:Dopamine / Q000494:pharmacology / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007610:Kallikreins / Q000652:urine; D007668:Kidney / Q000187:drug effects / Q000503:physiopathology*; D007705:Kinins / Q000652:urine; D009318:Natriuresis / Q000187:drug effects; D011458:Prostaglandins E / Q000652:urine; D012083:Renin / Q000172:deficiency
chemical_list: D007705:Kinins; D011458:Prostaglandins E; D007610:Kallikreins; D012083:Renin; D015232:Dinoprostone; D004298:Dopamine