Publications by authors named "Wattana B Watanapa"

Postural orthostatic tachycardia syndrome (POTS) is a heterogeneous autonomic disorder. All patients have exaggerated tachycardia upon standing, but the pathophysiology may be diverse. We present a young adult Thai male with a chief complaint of palpitations while in an upright posture since childhood.

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Introduction: Inward rectifier K (Kir) channel, a major factor determining endothelial membrane potential, regulates Ca influx and vasodilator release, which is impaired in preeclamptic blood vessels. Previously, human umbilical vein endothelial cell (HUVEC) Kir currents were shown to decrease after incubating in preeclamptic plasma. We aimed to demonstrate whether sFlt-1, which is high in preeclamptic blood, could inhibit Kir channel function and expression.

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Objective: To study hesperetin-induced vasorelaxation after depolarizing contraction in human umbilical veins (HUVs) to elucidate the role of L-type Ca channel (LTCC) and related signaling pathway.

Methods: Isometric tension recording was performed in HUV rings pre-contracted with K. Hesperetin relaxing mechanism was investigated using a LTCC opener (BayK8644) and blockers of cyclic nucleotides and phosphodiesterases (PDEs).

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Objective: To investigate the effect of ferulic acid, a natural compound, on pancreatic beta cell viability, Ca channels, and insulin secretion.

Methods: We studied the effects of ferulic acid on rat insulinoma cell line viability using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide viability assay. The whole-cell patch-clamp technique and enzyme-linked immunosorbent assay were also used to examine the action of ferulic acid on Ca channels and insulin secretion, respectively.

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Aims: Ethanol is known to induce NO release and coronary vasorelaxation. Evidence suggests that K channels, especially a Ca-activated K channel (K), may regulate endothelial NO production. We aimed to investigate the ethanol effect on K currents in human coronary artery endothelial cells (HCAECs), identify the K channel type/subtype and signaling pathway involved, and demonstrate the relevance to ethanol-induced NO release.

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Human kidney stone disease (KSD) causes significant morbidity and public health burden worldwide. The etiology of KSD is heterogeneous, ranging from monogenic defects to complex interaction between genetic and environmental factors. However, the genetic defects causing KSD in the majority of affected families are still unknown.

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Testosterone has endothelium-dependent vasodilatory effects on the coronary artery, with some reports suggesting endothelial ion channel involvement. This study employed the whole-cell patch clamp technique to investigate the effect of testosterone on ion channels in human coronary artery endothelial cells (HCAECs) and the mechanisms involved. We found that 0.

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Aims: Ginsenosides, active components in ginseng, have been shown to increase nitric oxide (NO) production in aortic endothelial cells. This effect was reversed by tetraethylammonium (TEA) inhibition of endothelial Ca(2+)-activated K(+) (KCa) channels. The objectives of this study, therefore, were to test 1) whether vasorelaxing ginsenoside Re could affect KCa current, an important regulator of NO production, in human coronary artery endothelial cells (HCAECs); and 2) whether small-conductance KCa (SKCa) channel was the channel subtype involved.

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Background: Lupus nephritis is an important leading cause of chronic kidney disease (CKD) among the young population in Thailand. Systemic lupus erythematosus (SLE) is often characterized by the presence of sympathetic hyperactivity, which results in a perishing outcome. Some physiological studies reveal that meditation may reduce this autonomic dysfunction.

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Endothelial cell (EC) dysfunction in preeclampsia (PE) may be mediated by humoral factors secreted by placenta, thereby affecting the EC vasoactive compound production. Possible targets of these factors include potassium channels, which are important in EC membrane potential control, calcium influx, and vasoactive compound release. Alterations in potassium channel function may thus contribute to the pathogenesis of PE.

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