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Impact of high salt diet on Arylsulfatase B activity, glycosaminoglycans, kininogen, and bradykinin
Author(s) -
Bhattacharyya Sumit,
Kotlo Kumar,
Feferman Leonid,
Yang Bo,
Linhardt Robert J.,
Danziger Robert,
Tobacman Joanne K.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.829.2
Subject(s) - chemistry , bradykinin , kininogen , endocrinology , medicine , sulfotransferase , chondroitin sulfate , sulfation , glycosaminoglycan , high molecular weight kininogen , biochemistry , biology , receptor
Arylsulfatase B (ARSB; N‐acetylgalactosamine‐4‐sulfatase) removes sulfate groups from N‐acetylgalactosamine‐4‐sulfate residues at the non‐reducing end of chondroitin‐4‐sulfate (C4S). In this study, extending previous in vitro findings, we investigated the relationships among ARSB, C4S, kininogen, and bradykinin in Dahl salt‐sensitive (SS) rats exposed to high (SSH) and low salt (SSL) diets (total n=22). In renal tissue of SSH rats, ARSB activity was significantly less than in SSL rats, and C4S and total sulfated glycosaminoglycans were significantly greater. Disaccharide analysis confirmed marked increase in C4S disaccharides in the SSH renal tissue. In contrast, unsulfated, hyaluronan‐derived disaccharides were significantly increased in the SSL rats. In the SSH rats, with lower ARSB activity and higher C4S levels, cell‐bound, high‐molecular weight kininogen was significantly greater and urinary bradykinin was significantly lower (p<0.0001, unpaired t‐test, two‐tailed). ARSB activity in the SSH and SSL renal tissue and in normal rat kidney (NRK) cells declined with increasing exogenous sodium chloride concentration, but not with increased sodium acetate concentration. The effects of high chloride exposure in vivo on ARSB activity, chondroitin‐4‐sulfation, and kininogen‐C4S binding link dietary salt intake and regulation of bradykinin production from kininogen, although the mechanism whereby chloride regulates ARSB activity is not yet known.