The molecule mechanisms of L‐arginine inhibit pulmonary hypertension
Abstract only L ‐arginine( L ‐arg) has been shown to attenuate pulmonary hypertension (PH). Monocrotaline can induce PH. To investigate the molecule mechanism by which L ‐arg attenuates PH, SD rats were injected intraperitoneally with Monocrotaline once with or without L ‐arg 3 for weeks. The right...
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| Published in: | The FASEB journal Vol. 23; no. S1 |
|---|---|
| Main Authors: | , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
01-04-2009
|
| Online Access: | Get full text |
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| Summary: | Abstract only
L
‐arginine(
L
‐arg) has been shown to attenuate pulmonary hypertension (PH). Monocrotaline can induce PH. To investigate the molecule mechanism by which
L
‐arg attenuates PH, SD rats were injected intraperitoneally with Monocrotaline once with or without
L
‐arg 3 for weeks. The right ventricular systolic pressure (RVSP) was measured. Nitric oxide (NO) concentration in plasma was assayed with chemical colorimetry. Superoxide anion (O
2▸
−
) generation in lung was determined by hydroethidine. Pulmonary arteries wall thickness was observed by histology. The expressions of endothial nitric oxide synthase (eNOS) and heat shock protein 90 (HSP90) and their association in lung were determined by immunoprecipitation and western blot. Monocrotaline increased RVSP and pulmonary arteries wall thickness with attenuating NO concentration in plasma, enhancing O
2▸
−
generation in lung, decreasing eNOS experssion and the association between eNOS and HSP90 in lung.
L
‐arg can partially decrease the RVSP, inhibit pulmonary arteries wall thickness, restore NO level in plasma, block O
2▸
−
generation in lung, restore eNOS expression and the association between eNOS and HSP90 in lung in Monocrotaline‐treated SD rats. Our findings illustrated part of molecular mechanisms of
L
‐arg preventing PH. Such findinds may provide an opportunity for exploring the pathogenesis and preventive and therapeutic measures for PH. |
|---|---|
| ISSN: | 0892-6638 1530-6860 |
| DOI: | 10.1096/fasebj.23.1_supplement.770.2 |