Details

Autor(en) / Beteiligte

• Emond, C
• Bascands, J. L
• Rakotoarivony, J
• Praddaude, F
• Bompart, G
• Pecher, C
• Ader, J. L
• Girolami, J. P

Titel

Glomerular B2-kinin-binding sites in two-kidney, one-clip hypertensive rats

Ist Teil von

• American journal of physiology. Renal physiology, 1991-05, Vol.260 (5), p.626-F634

Ort / Verlag

United States

Erscheinungsjahr

1991

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• C. Emond, J. L. Bascands, J. Rakotoarivony, F. Praddaude, G. Bompart, C. Pecher, J. L. Ader and J. P. Girolami Institut National de la Sante et de la Recherche Medicale, Faculte de Medecine Rangueil, Toulouse, France. To extend our recent observations of the possible downregulation of glomerular B2-kinin-binding sites, we investigated density (Bmax) of bradykinin (BK)-binding sites in glomerular membranes of both the clipped (C) and nonclipped (NC) kidneys of two-kidney, one-clip (2K-1C) Goldblatt hypertensive rats, in relation to tissue kallikrein activity and glomerular three-dimensional structure. Compared with the Bmax of sham-operated (SO) kidney (31.8 +/- 7 fmol/mg protein), a significant increase in Bmax was observed in glomeruli of both kidneys in hypertensive rats, the Bmax being higher in glomeruli of NC than in C kidneys (98 +/- 11 vs. 59 +/- 12 fmol/mg protein). NC kidney compensatory hypertrophy was expressed by an increase in glomerular diameter, surface area, and volume. When expressed per unit of area or volume, Bmax in NC kidneys remained significantly higher than in both C and SO kidneys. Increased Bmax in both kidneys of 2K-1C rats was associated with a decreased intrarenal level of kallikrein. We also examined prostaglandin (PG) E2 release by isolated glomeruli from SO, C, and NC kidneys as a possible biological effect induced by BK. Whereas C kidney released more PGE2 than NC kidney under basal conditions, addition of BK (10 nM) induced greater PGE2 production in NC kidney consistent with the difference in Bmax between C and NC kidneys. These results suggest a possible downregulation of glomerular B2-binding sites by bradykinin, which may explain the difference between SO and C kidneys.