The effects of cyclopiazonic acid on intracellular Ca in aortic smooth muscle cells from DOCA-hypertensive rats
Brazilian Journal of Medical and Biological Research, ISSN: 0100-879X, Vol: 30, Issue: 2, Page: 257-267
1997
- 12Citations
- 8,508Usage
- 14Captures
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Metrics Details
- Citations12
- Citation Indexes12
- 12
- CrossRef9
- Usage8,508
- Full Text Views8,473
- 8,473
- Abstract Views35
- 35
- Captures14
- Readers14
- 14
Article Description
We tested the hypothesis that cyclopiazonic acid (CPA), an inhibitor of the sarcoplasmic reticulum (SR) Ca-ATPaSe, increases intracellular Ca concentration ([Ca]) in aortic myocytes and that the increase in [Ca] is higher in aortic cells from deoxycorticosterone acetate (DOCA)-hypertensive rats. Male Sprague-Dawley rats, 250-300 g, underwent uninephrectomy, received a silastic implant containing DOCA (200 mg/kg) and had free access to water supplemented with 1.0% NaCl and 0.2% KCI. Control rats were also uninephrectomized, received normal tap water, but no implant. Intracellular Ca measurements were performed in aortic myocytes isolated from normotensive (Systolic blood pressure = 120 ± 3 mmHg; body weight = 478 ± 7 g, N = 7) and DOCA-hypertensive rats (195 ± 10 mmHg; 358 ± 16 g, N = 7). The effects of CPA on resting [Ca] and on caffeine-induced increase in [Ca] after [Ca] depletion and reloading were compared in aortic cells from DOCA and normotensive rats. The phasic increase in [Ca] induced by 20 mM caffeine in Ca-free buffer was significantly higher in DOCA aortic cells (329 ± 36 nM, N = 5) compared to that in normotensive cells (249 ± 16 nM, N = 7, P<0.05). CPA (3 μM) inhibited caffeine-induced increases in [Ca] in both groups. When the cells were placed in normal buffer (1.6 mM Ca, loading period), after treatment with Ca-free buffer (depletion period), an increase in [Ca] was observed in DOCA aortic cells (45 ± 11 nM, N = 5) while no changes were observed in normotensive cells. CPA (3 μM) potentiated the increase in [Ca] (122 ± 30 nM, N = 5) observed in DOCA cells during the loading period while only a modest increase in [Ca] (23 ± 10 nM, N = 5) was observed in normotensive cells. CPA-induced increase in [Ca] did not occur in the absence of extracellular Ca or in the presence of nifedipine. These data show that CPA induces Ca influx in aorta from both normotensive and DOCA-hypertensive rats. However, the increase in [Ca] is higher in DOCA aortic cells possibly due to an impairment in the mechanisms that control [Ca]. The large increase in [Ca] in response to caffeine in DOCA cells probably reflects a greater storage Of Ca in the SR.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0030992378&origin=inward; http://dx.doi.org/10.1590/s0100-879x1997000200016; http://www.ncbi.nlm.nih.gov/pubmed/9239314; http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1997000200016&lng=en&tlng=en; http://www.scielo.br/pdf/bjmbr/v30n2/2661c.pdf; http://www.scielo.br/scielo.php?script=sci_abstract&pid=S0100-879X1997000200016&lng=en&tlng=en; http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1997000200016; http://www.scielo.br/scielo.php?script=sci_abstract&pid=S0100-879X1997000200016; https://dx.doi.org/10.1590/s0100-879x1997000200016; https://www.scielo.br/j/bjmbr/a/b7FRbHwKcWpyFMH6VWJJJYD/?lang=en
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