@article{oai:sapmed.repo.nii.ac.jp:00014783,
 author = {斎藤, 重幸 and 島本, 和明 and Oscar, A.  Carretero},
 issue = {2},
 journal = {札幌医学雑誌 = The Sapporo medical journal, The Sapporo medical journal},
 month = {Apr},
 note = {Recent findings have suggested that the endogenous renal kallikrein-kinin system acts on the renal water-sodium metabolism at the distal nephron as a paracrine hormone system. The present study was designed to determine the acting site, and secondarily, to evaluate the role of the kallikrein-kinin system on renal hemodynamics and prostaglandin E? （PGE?） production. IgG （anti-KAL-IgG） and Fab fragment （anti-KAL-Fab） were isolated from monoclonal antibody against rat glandular kallikrein ; both anti-KAL-IgG and anti-KAL-Fab were found to inhibit glandular kallikrein activity in vitro. Next, purified IgG （anti-ricin-IgG） and Fab fragment （anti-ricin-Fab） from monoclonal antibody to ricin, which is a vegetable protein and does not exist in mammals, were tested ; neither anti-ricin-IgG nor anti-ricin-Fab blocked kallkrein activity in vitro. The anti-KAL-Fab were observed to pass through the glomeruli and reach the luminal site of the distal nephron, but anti-KAL-IgG did not pass through the glomerulus. In this study, both anti-KAL-Fab and anti- KAL-IgG were administered to unanesthetized normotensive rats. When 1.0 mg anti-KAL-Fab was administered, urinary kallikrein activity （kininogenase activity） and the excretion of immunoreactive kinin were significantly decreased （-73.4±4.3% and -84.2± 5.3% change from control values, respectively）. At the same time, the urine volume and urinary sodium excretion significantly decreased by 27.0±7.1% and 21.4±6.1%, respectively. In the rats receiving anti-ricin-IgG or anti-ricin-Fab, the renal function revealed no change. Bolus injection of 2.0 mg anti-KAL-Fab caused antidiuretic and antinatriuretic actions without change in GFR, renal blood flow or mean blood pressure. On the other hand, urinary PGE? fell by 39.4±18.4% following the injection of 2.0mg anti-KAL-Fab. Anti-ricin-Fab demonstrated no change in any of these parameters. The change in PGE? correlated significantly with that of urine volume （r=0.73 ; p< 0.001） and urinary sodium excretion （r=0.61 ; p<0.01）. Thus, these findings show that 1） anti-KAL-Fab probably suppresses the renal kallikrein activity in the luminal site of the nephron ; 2） inhibition of kinin generation causes decreases in the water and sodium excretions in normotensive conscious rats ; 3） these renal changes are not dependent on renal hemodynamic alteration ; and 4） luminal kinin partially controls PGE? formation in the kid- neys. From these results, it was concluded that kinin on the luminal site of the distal nephron plays a role in the regulation of water and sodium excretion acting as a paracrine hormone, either directly or via PGE?.},
 pages = {75--85},
 title = {非麻酔下正常血圧ラットにおける腎Kallikrein-Kinin系抑制時の腎水・ナトリウム代謝},
 volume = {62},
 year = {1993}
}