The effects of cyclopiazonic acid on intracellular Ca2+ in aortic smooth muscle cells from DOCA-hypertensive rats

Tostes, Rita C.; Wilde, Dixon W.; Bendhack, Lusiane Maria; Webb, R. Clinton

doi:10.1590/s0100-879x1997000200016

Cited by 14 publications

(6 citation statements)

References 34 publications

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“…Smooth muscle cells and isolated vascular tissue from SHR and DOCA-salt rats have been shown to have greater basal and agonist-induced intracellular calcium concentrations, as well as heightened sensitivity to the calcium channel agonist Bay K 8644, possibly mediated by an increased activity of voltage gated Ca ++ channels [27][28][29]. An increased response to depolarization stimuli (potassium chloride) in isolated tissue also supports the role of altered Ca ++ channels in hypertension.…”

Section: Increased Vasoconstrictor Sensitivity In Hypertensionmentioning

confidence: 84%

RhoA/Rho-kinase, vascular changes, and hypertension

Chitaley

Weber

Webb

2001

Current Science Inc

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Hypertension, the result of a sustained increase in vascular peripheral resistance, is partly due to vascular remodeling and increased vasoconstrictor sensitivity. Stimulation of heterotrimeric G-protein-coupled receptors by various contractile agonists activates intracellular signaling molecules to result in an increase in cytosolic Ca++ and the subsequent phosphorylation of myosin light chain by Ca++/calmodulin-dependent myosin light chain kinase. Additionally, a portion of alpha-adrenergic, serotonergic, and endothelin-1-induced contraction is partially mediated by the calcium-independent activation of the small G-protein RhoA and of a downstream target, Rho-kinase. Isolated arteries from hypertensive animals have been shown to have an increased contractile sensitivity to various agonists and to exhibit evidence of remodeling. Recent data suggest that some of these vascular changes may be mediated by increased activity of RhoA/Rho-kinase, potentially introducing a novel therapeutic approach for the treatment of hypertension.

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Section: Increased Vasoconstrictor Sensitivity In Hypertensionmentioning

confidence: 84%

RhoA/Rho-kinase, vascular changes, and hypertension

Chitaley

Weber

Webb

2001

Current Science Inc

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“…Vascular smooth muscle cells (VSMC) were isolated from rat thoracic aortas according to the method described by Tostes et al (1997). Briefly, the thoracic aorta was rapidly removed, placed in 0.1 mM Ca 2+ Hank's solution at 22 -C, cleaned of fat and connective tissue.…”

Section: Measurement Of Cytosolic Ca 2+ Concentration In Aortic Smootmentioning

confidence: 99%

Vasorelaxant effect of the flavonoid galangin on isolated rat thoracic aorta

et al. 2006

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“…Under similar conditions, VSMCs isolated from the thoracic aorta of DOCA-salt rats exhibit an increase in [Ca 2+ ] i while no changes are observed in normotensive cells. Contractions and increases in [Ca 2+ ] i do not occur in the presence of the Ca 2+ channel antagonist, nifedipine (21). Other investigators have demonstrated that high concentrations of Ca 2+ induce contractions in aortic segments from spontaneously hypertensive rats (SHR) but do not alter tone in those from normotensive rats (3).…”

Section: Abnormalities Of Vascular Function Vs Ca 2+ Handlingmentioning

confidence: 99%

Calcium handling by vascular myocytes in hypertension

Tostes¹,

Wilde²,

Bendhack³

et al. 1997

Braz J Med Biol Res

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Calcium ions (Ca 2+ ) trigger the contraction of vascular myocytes and the level of free intracellular Ca 2+ within the myocyte is precisely regulated by sequestration and extrusion mechanisms. Extensive evidence indicates that a defect in the regulation of intracellular Ca 2+ plays a role in the augmented vascular reactivity characteristic of clinical and experimental hypertension. For example, arteries from spontaneously hypertensive rats (SHR) have an increased contractile sensitivity to extracellular Ca 2+ and intracellular Ca 2+ levels are elevated in aortic smooth muscle cells of SHR. We hypothesize that these changes are due to an increase in membrane Ca 2+ channel density and possibly function in vascular myocytes from hypertensive animals. Several observations using various experimental approaches support this hypothesis: 1) the contractile activity in response to depolarizing stimuli is increased in arteries from hypertensive animals demonstrating increased voltage-dependent Ca 2+ channel activity in hypertension; 2) Ca 2+ channel agonists such as Bay K 8644 produce contractions in isolated arterial segments from hypertensive rats and minimal contraction in those from normotensive rats; 3) intracellular Ca 2+ concentration is abnormally increased in vascular myocytes from hypertensive animals following treatment with Ca 2+ channel agonists and depolarizing interventions, and 4) using the voltage-clamp technique, the inward Ca 2+ current in arterial myocytes from hypertensive rats is nearly twice as large as that from myocytes of normotensive rats. We suggest that an alteration in Ca 2+ channel function and/or an increase in Ca 2+ channel density, resulting from increased channel synthesis or reduced turnover, underlies the increased vascular reactivity characteristic of hypertension.

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The effects of cyclopiazonic acid on intracellular Ca2+ in aortic smooth muscle cells from DOCA-hypertensive rats

Cited by 14 publications

References 34 publications

RhoA/Rho-kinase, vascular changes, and hypertension

RhoA/Rho-kinase, vascular changes, and hypertension

Vasorelaxant effect of the flavonoid galangin on isolated rat thoracic aorta

Calcium handling by vascular myocytes in hypertension

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