Nifedipine-Induced Vascular Endothelial Growth Factor Secretion from Coronary Smooth Muscle Cells Promotes Endothelial Tube Formation via the Kinase Insert Domain-Containing Receptor/Fetal Liver Kinase-1/NO Pathway

Miura, Shin‐ichiro; Fujino, Masahiro; Matsuo, Yoshino; Tanigawa, Hiroyuki; Saku, Keijiro

doi:10.1291/hypres.28.147

Cited by 58 publications

(44 citation statements)

References 29 publications

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“…However, it should be borne in mind that the non-dihydropyridine calcium channel blockers verapamil and diltiazem are CYP3A4 inhibitors, and nifedipine (another dihydropyridine calcium channel blocker) has been shown to induce VEGF secretion [22]. We have recently described a potential pharmacokinetic interaction between felodipine and sorafenib [23].…”

Section: Discussionmentioning

confidence: 99%

Treatment of bevacizumab-induced hypertension by amlodipine

et al. 2010

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Section: Discussionmentioning

confidence: 99%

Treatment of bevacizumab-induced hypertension by amlodipine

et al. 2010

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“…PlGF, acting synergistically with vascular endothelial growth factor (VEGF), may be necessary for the maintenance of endothelial cell health during pregnancy (17)(18)(19)(20)(21). The sFlt-1 is an anti-angiogenic protein that antagonizes VEGF and PlGF (21).…”

Section: Introductionmentioning

confidence: 99%

“…The level of PlGF and sFlt-1 changes according to the gestational age; for this reason, we must obtain reference values specific to each gestational age in order to determine whether a given PlGF or sFlt-1 value is normal for a particular gestational age (22,23). However, almost all the previous studies have used only fixed values for PlGF and sFlt-1 instead of employing gestational age-specific reference values (8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21). Recently, we constructed reference values for serum PlGF and SFlt-1 based on a longitudinal analysis of 148 cohorts of pregnant women at various gestational stages (22).…”

Section: Introductionmentioning

confidence: 99%

Alterations in Placental Growth Factor Levels before and after the Onset of Preeclampsia Are More Pronounced in Women with Early Onset Severe Preeclampsia

et al. 2007

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It has been established that the serum placental growth factor (PlGF) decreases and the soluble fms-like tyrosine kinase-1 (sFlt-1) increases in women with preeclampsia. However, there have been no studies on the relation between preeclampsia onset time and the changes in PlGF and sFlt-1. Furthermore, the PlGF and sFlt-1 levels have not been evaluated using their reference values specific to each gestational age. In this study we reevaluated the serum PlGF and sFlt-1 levels before and after the clinical manifestation of early and late onset severe preeclampsia using the new reference values developed in our recent longitudinal study. Blood specimens were obtained immediately after the clinical manifestation of severe preeclampsia in 34 referred women, and both before and after the clinical manifestation in 8 women receiving a routine checkup at our institute. Both women with early and those with late preeclampsia showed decreased PlGF and increased sFlt-1 levels compared to normotensive controls at 28 and 37 weeks (n =68). However, those with early onset preeclampsia had a higher incidence of low PlGF (<5th percentile on the reference values) and high sFlt-1 ( ≥ 95th percentile) than those with late onset (low PlGF: 93% vs. 55%; high sFlt-1: 100% vs. 60%). log10PlGF (r =0.574, p <0.001) and log10(sFlt-1/PlGF) (r =-0.556, p <0.001) were correlated with the week of onset of preeclampsia. Before the onset of preeclampsia, the incidence rate of low PlGF in the women with early onset preeclampsia was 100% (5/5), whereas that in the women with late onset preeclampsia was 0% (0/2) (p =0.048). Therefore, alterations in the PlGF levels both before and after the onset of preeclampsia may be more pronounced in women with early onset than those with late onset severe

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“…However, recent studies have suggested that several Ca 2+ channel blockers, including benidipine, also possess vasoprotective effects that are independent of the blood pressure-lowering actions (24). Although the mechanisms underlying the direct protective effects of Ca 2+ channel blockers on endothelial cells are not fully understood, such vasoprotective effects as the amelioration of endothelial dysfunction (25,26), induction of angiogenesis (27), and decrease in the proliferation of vascular smooth muscle cells (28), oxidative stress and inflammation (29,30), may be at least partly responsible for the beneficial effects against cardiovascular diseases.…”

Section: Discussionmentioning

confidence: 99%