Modulation of agonist‐induced calcium mobilisation in bovine aortic endothelial cells by phorbol myristate acetate and cyclic AMP but not cyclic GMP

Buchan, Kevin W.; Martin, William J.

doi:10.1111/j.1476-5381.1991.tb12436.x

Cited by 35 publications

(11 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…41 Nevertheless, a potentiating effect on agonist-induced [Ca 2ϩ ] i mobilization was reported in bovine aortic endothelial cells, but only when the cAMP-elevating agents were added during the plateau phase of thrombin-, bradykinin-, or ATP-induced [Ca 2ϩ ] i responses. 42 Contrary to our results, it has been reported that cAMP-elevating agents increase bradykinin-induced NO formation by enhancing the agonist-induced rise in [Ca 2ϩ ] i in pig aortic endothelial cells, 43 probably by facilitating the activation of Ca 2ϩ -sensitive K ϩ channels and thereby promoting membrane hyperpolarization. 44 The different cardiovascular effects provoked by EGb 761 in vivo may be explained in part by these sorts of differences for the cross-talk between cAMP and [Ca 2ϩ ] i at different regions of the vascular tree.…”

Section: Discussioncontrasting

confidence: 84%

Inhibition of Type 4 Phosphodiesterase by Rolipram and Ginkgo biloba Extract (EGb 761) Decreases Agonist-Induced Rises in Internal Calcium in Human Endothelial Cells

Campos‐Toimil

Lugnier

Droy-Lefaix

et al. 2000

ATVB

View full text Add to dashboard Cite

The effects of Gingko biloba extract EGb 761 on 5 isolated, vascular, cyclic nucleotide phosphodiesterase (PDE) isoforms were evaluated. EGb 761 preferentially inhibited PDE4 (IC(50)=25.1 mg/L), the isoform that is mainly present in endothelial cells, in a competitive manner (K:(i)=12.5 mg/L). Because changes in cyclic nucleotide levels may affect intracellular calcium ([Ca(2+)](i)) levels in endothelial cells, we examined the effects of EGb 761 on both resting [Ca(2+)](i) levels and agonist-induced rises in [Ca(2+)](i) in single human umbilical vein endothelial cells (HUVECs) in culture. The effects of EGb 761 were compared with those of rolipram, a selective PDE4 inhibitor that increases cellular cAMP levels, and the cAMP analogue dibutyryl cAMP (db-cAMP). EGb 761 (20 and 100 mg/L), rolipram (50 micromol/L), and db-cAMP (100 micromol/L) significantly inhibited histamine-, ATP-, and thrombin-induced [Ca(2+)](i) increases in HUVECs without modifying resting [Ca(2+)](i) levels. Similar results were obtained by using a Ca(2+)-free bath solution. EGb 761 (100 mg/L), but not rolipram (50 micromol/L) or db-cAMP (100 micromol/L), also inhibited Ca(2+) influx into cells having thapsigargin-depleted internal Ca(2+) stores and bathed in a Ca(2+)-free external solution. Our results are consistent with an inhibition of PDE activity that causes a reduction of agonist-induced increases in [Ca(2+)](i) in HUVECs, mainly by inhibition of Ca(2+) mobilization from internal stores. It thus may be that the cardiovascular effects of EGb 761 involve inhibition of PDE4 activity and subsequent modification of Ca(2+) signaling in endothelial cells.

show abstract

Section: Discussioncontrasting

confidence: 84%

Inhibition of Type 4 Phosphodiesterase by Rolipram and Ginkgo biloba Extract (EGb 761) Decreases Agonist-Induced Rises in Internal Calcium in Human Endothelial Cells

Campos‐Toimil

Lugnier

Droy-Lefaix

et al. 2000

ATVB

View full text Add to dashboard Cite

show abstract

“…Certain authors (e.g. Buchan & Martin, 1991) do not agree with the latter statement. Our observation that the exogenous NO donor produced a substantial reduction in pressure with no significant change in [Ca¥]é adds strength to our argument that NO has a vasodilator action which is independent of any effect on vascular wall [Ca¥]é.…”

Section: Does the Adventitia Act As A Barrier?mentioning

confidence: 70%

Nitric oxide lowers the calcium sensitivity of tension in the rat tail artery

Tran

Spitzbarth

Robert

et al. 1998

The Journal of Physiology

View full text Add to dashboard Cite

Controversy exists as to whether a fall in the intracellular Ca2+ concentration ([Ca2+]i) is a requisite element of the vasodilatory response to nitric oxide (NO). We studied the effect of NO on the coupling between [Ca2+]i and vasoconstriction in arterial segments loaded with the [Ca2+]i‐sensitive, intracellular dye fura‐2. As data interpretation is equivocal when fura‐2 is loaded into both endothelial and smooth muscle cells, we compared results from in vitro experiments on segments of the rat tail artery in which fura‐2 and noradrenaline were applied on the luminal or adventitial side, and endothelium was removed ‘physically’ (rubbing or air) or ‘functionally’ (Nω‐nitro‐l‐arginine methyl ester). The use of air perfusion to remove endothelium is of considerable benefit since it allows paired observations in a single tissue. Fura‐2 loaded into endothelial cells but endothelial ‘contamination’ of the smooth muscle cell [Ca2+]i signal was minimal. Endogenous NO decreased vasoconstrictor responses to noradrenaline but had no effect on [Ca2+]i. Nitroglycerine decreased vasoconstrictor responses in a concentration‐dependent fashion but had no effect on [Ca2+]i. In conclusion, NO causes vasodilatation via a mechanism which is downstream of [Ca2+]i mobilization.

show abstract

“…Transient intercellular gap formation and apoptosis both increase permeability that contributes to pulmonary edema, decreasing the efficiency of gas exchange. The mutually opposing actions of intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) and intracellular cAMP concentrations ([cAMP] i ) control barrier function and are the focus of active investigations (2,5,14,20,(35)(36)(37). However, signaling events that trigger endothelial cell apoptosis are still poorly understood.…”

mentioning

confidence: 99%

Cyclic GMP-specific phosphodiesterase 5 regulates growth and apoptosis in pulmonary endothelial cells

Zhu

Strada

Stevens

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

Sustained increases in intracellular cGMP concentrations ([cGMP]i) inhibit cell growth and induce apoptosis. We now report that a cGMP-specific phosphodiesterase, PDE5, plays a dominant role in regulating [cGMP]i transitions that inhibit cell growth and control susceptibility to apoptosis in pulmonary endothelium. Atrial natriuretic peptide (ANP) activates guanylyl cyclase A/B and induces a rapid [cGMP]i rise 2-5 min after its application, in both pulmonary arterial endothelial cells (PAECs) and pulmonary microvascular endothelial cells (PMVECs). However, increased [cGMP]i in PAECs is transient and decays within 10 min due to cytosolic PDE5 hydrolytic activity. Increased [cGMP]i in PMVECs is sustained for >3 h due to the absence of PDE5. Indeed, at any ANP concentration, the sustained (30 min) [cGMP]i rise is greater in PMVECs than in PAECs, unless PAECs are also treated with the PDE5 inhibitor zaprinast. Using RT-PCR, Western blot analysis, immunoprecipitation, and DEAE chromatography, we resolved the expression and activity of PDE 5A1/A2 only in PAECs. Similarly, PDE5 expression was restricted to extra-alveolar endothelium in vivo. ANP induced growth inhibition and apoptosis in PMVECs, but similar effects were not seen in PAECs unless ANP treatment was combined with zaprinast. ANP blocked the VEGF-induced proliferation and migration in PMVECs. Collectively, these data suggest that PDE5-regulated [cGMP]i controls endothelial cell growth and apoptosis, representing a mechanism of heterogeneity between two endothelial phenotypes.

show abstract

Modulation of agonist‐induced calcium mobilisation in bovine aortic endothelial cells by phorbol myristate acetate and cyclic AMP but not cyclic GMP

Cited by 35 publications

References 32 publications

Inhibition of Type 4 Phosphodiesterase by Rolipram and Ginkgo biloba Extract (EGb 761) Decreases Agonist-Induced Rises in Internal Calcium in Human Endothelial Cells

Inhibition of Type 4 Phosphodiesterase by Rolipram and Ginkgo biloba Extract (EGb 761) Decreases Agonist-Induced Rises in Internal Calcium in Human Endothelial Cells

Nitric oxide lowers the calcium sensitivity of tension in the rat tail artery

Cyclic GMP-specific phosphodiesterase 5 regulates growth and apoptosis in pulmonary endothelial cells

Contact Info

Product

Resources

About