ArticleMolecular and cellular biochemistry2003
Oxidant-induced pHi/Ca2+ changes in rat aortic smooth muscle cells. The role of atrial natriuretic peptide.
Article in Molecular and cellular biochemistry, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 14 citations in OpenAlex.
- Treatment with brain natriuretic peptide prevents the development of cardiac dysfunction in obese diabetic db/db mice.Diabetologia · 2014Article
- Oxytocin: Old Hormone, New Drug.Pharmaceuticals (Basel, Switzerland) · 2009Review
- NPRA-mediated suppression of AngII-induced ROS production contribute to the antiproliferative effects of B-type natriuretic peptide in VSMC.Molecular and cellular biochemistry · 2009Article
- Role of atrial natriuretic peptide in the suppression of lysophosphatydic acid-induced rat aortic smooth muscle (RASM) cell growth.Molecular and cellular biochemistry · 2005Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to investigate the effects of oxidative stress on PLD activity, [Ca2+]i and pHi levels and the possible relationship among them. Moreover, since atrial natriuretic peptide (ANP) protects against oxidant-induced injury, we investigated the potential protective role of the hormone in rat aortic smooth muscle (RASM) cells exposed to oxidative stress. Water-soluble 2,2'-Azobis (2-amidinopropane) dihydrochloride (AAPH) was used as free radical generating system, since it generates peroxyl radicals with defined reaction and the half time of peroxyl radicals is longer than other ROS. A significant increase of PLD activity was related to a significant decrease in pHi, while [Ca2+]i levels showed an increase followed by a decrease after cell exposure to AAPH. [Ca2+]i changes and pHi fall induced by AAPH were prevented by cadmium which inhibits a plasma membrane Ca2+ ATPase coupled to Ca2+/H+ exchanger, that operates the efflux of Ca2+ coupled to H+ influx. The involvement of PLD in pHi and [Ca2+]i changes was confirmed by calphostin-c treatment, a potent inhibitor of PLD, which abolished all AAPH-induced effects. Pretreatment of RASM cells with pharmacological concentrations of ANP attenuated the AAPH effects on PLD activity as well as [Ca2+]i and pHi changes, while no effects were observed with physiological ANP concentrations, suggesting a possible role of the hormone as defensive effector against early events of the oxidative stress.
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