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PROMOTION OF NITRIC OXIDE FORMATION BY HEPARIN IN CULTURED AORTIC ENDOTHELIAL CELLS FROM SPONTANEOUSLY HYPERTENSIVE RATS
Author(s) -
Minami M.,
Yokokawa K.,
Kohno M.,
Ikeda M.,
Horio T.,
Kano H.,
Hanehira T.,
Yasunari K.,
Takeda T.
Publication year - 1995
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1995.tb02857.x
Subject(s) - heparin , nitric oxide , chemistry , endocrinology , bradykinin , medicine , cyclic guanosine monophosphate , radioimmunoassay , endothelin 1 , biochemistry , receptor
Summary 1. The present study examined the effect of heparin on nitric oxide (NO) formation and cyclic guanosine 3′, 5′‐monophos‐phate (cGMP) levels in cultured aortic endothelial cells (EC) from spontaneously hypertensive rats (SHR) and normoten‐sive Wistar‐Kyoto (WKY) rats. 2. Bradykinin (BK), adenosine diphosphate (ADP), Ca 2+ ionophore A23187 (Io) and endothelin‐3 (ET‐3) stimulated the production of NO and cGMP. No significant difference was observed in both NO and cGMP production in EC between WKY and SHR. 3. Heparin enhanced BK‐, ADP‐, Io‐ and ET‐3–stimulated NO and cGMP production. These enhancements by heparin in EC were significantly greater in SHR than in WKY. 4. Both NO formation and cGMP production stimulated by the agonists and/or heparin were blocked in the presence of N G ‐monomethyl‐L‐arginine (LNMMA, 10 ‐5 mol/L). 5. Increased sulphur level was observed on heparin‐treated SHR EC surface compared with that on control SHR EC or on heparin‐treated WKY EC surface. 6. These results suggest that heparin promotes agonist‐induced NO‐cGMP response in cultured EC from SHR.