Keitaro Saito

Estimation of Urinary Kininogenase Activity Using Bovine Serum Low Molecular Weight Kininogen

Estimation of urinary kininogenase activity by radioimmunoassay of generated kinin was studied. Bovine serum low molecular weight kininogen was proved not to cross-react with kallidin antibody and also bradykinin antibody. This kininogen was used as substrate measuring urinary kininogenase activity. Separation of released kinin from the kininogen was not required in the present method. Urinary kallikrein activity was found to be significantly decreased in essential hypertension, in chronic glomerulonephritis and in patients who had received renal transplantation. On the contrary, an increase in urinary kallikrein was found in primary aldosteronism and in Bartters syndrome. The present method was very useful for measuring kininogenase activity.

STUDIES ON KALLIKREIN-KININ SYSTEM IN ESSENTIAL HYPERTENSION

尿kininと尿kallikreinの簡便なradioimmunoassay法を確立させ,これを用いて本態性高血圧症の病態生理と腎kallikrein-kinin系との関係を研究した.本態性高血圧症では尿中kinin排泄量と尿中kallikrein排泄量とが正常者のそれに比し明らかに減少していた. kallikrein-kininの尿中排泄量と血漿renin活性或いは血漿aldostorone濃度との間には有意の相関々係がみられた.減塩食やfurosemide立位のrenin分泌刺激負荷後には尿中kallikrein排泄量が増加し, angiotensinII阻害薬投与や抗aldosterone薬投与により尿中kallikrein排泄量が減少したことから, renin-angiotensin-aldosterone系が腎kallikreinの産生を調節していると考えられた.一方,尿中prostaglandin E排泄量はfurosemide立位負荷後に増加したが,減塩食摂取後には減少し,腎kallikrein産生能と腎prostaglandin E産生能との間に解離がみられた. renin-angiotensin-aldosterone系を作動させた際の腎kallikreinの産生遊離の反応性は,本態性高血圧症で正常者に比し明らかに低下していた.腎kallikrein-kinin系は腎性減圧系物質の一つであるので,本態性高血圧症では腎性減圧系の機能低下があると考えられた.