Vasorelaxant mechanisms of the antidiabetic anagliptin in rabbit aorta: roles of Kv channels and SERCA pump.

Aims: The present study investigated the vasorelaxant mechanisms of an oral antidiabetic drug, anagliptin, using phenylephrine (Phe)-induced pre-contracted rabbit aortic rings.

Methods: Arterial tone measurement was performed in rabbit thoracic aortic rings.

Results: Anagliptin induced vasorelaxation in a dose-dependent manner.

Asenapine, an atypical antipsychotic, blocks voltage-gated potassium channels in rabbit coronary artery smooth muscle cells.

We investigated the effect of asenapine, a commonly used atypical antipsychotic, on voltage-dependent K (Kv) channels in rabbit coronary artery smooth muscle cells. Asenapine inhibited the Kv current in a concentration-dependent manner, with an half-inhibitory concentration (IC) value of 8.59 ± 2.

The antidiabetic drug teneligliptin induces vasodilation via activation of PKG, Kv channels, and SERCA pumps in aortic smooth muscle.

Diabetes mellitus (DM) is a metabolic disease closely related to cardiovascular disease. The dipeptidyl peptidase-4 inhibitor teneligliptin is used to treat DM and has recently been shown to have a cardiovascular protective effect against diseases such as hypertension and heart failure. The present study demonstrates the vasodilatory effect of teneligliptin using aortic rings pre-contracted with phenylephrine.

Antidiabetic omarigliptin dilates rabbit aorta by activating voltage-dependent K channels and the sarco/endoplasmic reticulum Ca -ATPase pump.

We investigated the vasodilatory effect of omarigliptin, an oral antidiabetic drug in the dipeptidyl peptidase-4 inhibitor class, and its related mechanisms using phenylephrine (Phe)-induced pre-contracted aortic rings. Omarigliptin dilated aortic rings pre-constricted with Phe in a dose-dependent manner. Pretreatment with the voltage-dependent K channel inhibitor 4-aminopyridine significantly attenuated the vasodilatory effect of omarigliptin, whereas pretreatment with the inwardly rectifying K channel inhibitor Ba , ATP-sensitive K channel inhibitor glibenclamide, and large-conductance Ca -activated K channel inhibitor paxilline did not alter its vasodilation.

Inhibition of voltage-dependent K channels by antimuscarinic drug fesoterodine in coronary arterial smooth muscle cells.

Fesoterodine, an antimuscarinic drug, is widely used to treat overactive bladder syndrome. However, there is little information about its effects on vascular K channels. In this study, voltage-dependent K (Kv) channel inhibition by fesoterodine was investigated using the patch-clamp technique in rabbit coronary artery.

Blockade of Voltage-Dependent K+ Channels by Benztropine, a Muscarinic Acetylcholine Receptor Inhibitor, in Coronary Arterial Smooth Muscle Cells.

We investigated the effect of the acetylcholine muscarinic receptor inhibitor benztropine on voltage-dependent K+ (Kv) channels in rabbit coronary arterial smooth muscle cells. Benztropine inhibited Kv currents in a concentration-dependent manner, with an apparent IC50 value of 6.11 ± 0.

Inhibitory effects of the atypical antipsychotic, clozapine, on voltage-dependent K channels in rabbit coronary arterial smooth muscle cells.

To investigate the adverse effects of clozapine on cardiovascular ion channels, we examined the inhibitory effect of clozapine on voltage-dependent K (Kv) channels in rabbit coronary arterial smooth muscle cells. Clozapine-induced inhibition of Kv channels occurred in a concentration-dependent manner with an half-inhibitory concentration value of 7.84 ± 4.

The inhibitory effects of pimozide, an antipsychotic drug, on voltage-gated K channels in rabbit coronary arterial smooth muscle cells.

Pimozide is an antipsychotic drug used to treat chronic psychosis, such as Tourette's syndrome. Despite its widespread clinical use, pimozide can cause unexpected adverse effects, including arrhythmias. However, the adverse effects of pimozide on vascular K channels have not yet been determined.

Downregulation of large-conductance Ca-activated K channels in human umbilical arterial smooth muscle cells in gestational diabetes mellitus.

Aims: We investigated the changes in large-conductance Ca-activated K (BK) channels from human umbilical arterial smooth muscle cells experiencing gestational diabetes mellitus (GDM).

Main Methods: Whole-cell patch-clamp technique, arterial tone measurement, RT-PCR, Quantitative real-time PCR, western blot were performed in human umbilical arterial smooth muscle cells.

Key Findings: Whole-cell BK current density was decreased in the GDM group compared with the normal group.

Mechanisms underlying the vasodilatory effects of canagliflozin in the rabbit thoracic aorta: Involvement of the SERCA pump and Kv channels.

Aims: Canagliflozin is an anti-diabetic agent and sodium glucose co-transporter-2 inhibitor. Despite numerous clinical trials demonstrating its beneficial effects on blood pressure, the cellular mechanisms underlying the effects of canagliflozin on vascular reactivity have yet to be clarified. We investigated the vasodilatory effect of canagliflozin on aortic rings isolated from rabbits.

The anti-diabetic drug trelagliptin induces vasodilation via activation of Kv channels and SERCA pumps.

Aims: In this study, we investigated the vasodilatory effects of trelagliptin (a dipeptidyl peptidase-4 inhibitor) and its related mechanisms using rabbit aortic rings.

Main Methods: Arterial tone measurement was performed in rabbit thoracic aortic rings.

Key Findings: Trelagliptin induced vasodilation in a dose-dependent manner.

Atypical antipsychotic olanzapine inhibits voltage-dependent K channels in coronary arterial smooth muscle cells.

Background: Olanzapine, an FDA-approved atypical antipsychotic, is widely used to treat schizophrenia and bipolar disorder. In this study, the inhibitory effect of olanzapine on voltage-dependent K (Kv) channels in rabbit coronary arterial smooth muscle cells was investigated.

Methods: Electrophysiological recordings were performed in freshly isolated coronary arterial smooth muscle cells.

The anti-diabetic drug alogliptin induces vasorelaxation via activation of Kv channels and SERCA pumps.

In the present study, we investigated the vasorelaxant effects of alogliptin, an oral antidiabetic drug in the dipeptidyl peptidase-4 (DPP-4) inhibitor class, using phenylephrine (Phe)-induced pre-contracted aortic rings. Alogliptin induced vasorelaxation in a dose-dependent manner. Pre-treatment with the voltage-dependent K (Kv) channel inhibitor 4-aminopyridine (4-AP) significantly decreased the vasorelaxant effect of alogliptin, whereas pre-treatment with the inwardly rectifying K (Kir) channel inhibitor Ba, ATP-sensitive K (K) channel inhibitor glibenclamide, and large-conductance Ca-activated K (BK) channel inhibitor paxilline did not alter the effects of alogliptin.

The effects of tegaserod, a gastrokinetic agent, on voltage-gated K channels in rabbit coronary arterial smooth muscle cells.

Tegaserod, a gastroprokinetic agent, is used to treat irritable bowel syndrome. Despite its extensive clinical use, little is known about the effects of tegaserod on vascular ion channels, especially K channels. Therefore, we examined the effects of tegaserod on voltage-gated K (Kv) channels in rabbit coronary arterial smooth muscle cells using the whole-cell patch-clamp technique.

Suppression of voltage-gated K channels by darifenacin in coronary arterial smooth muscle cells.

Darifenacin, an anticholinergic agent, has been used to treat overactive bladder syndrome. Despite its extensive clinical use, there is little information about the effect of darifenacin on vascular ion channels, specifically K channels. This study aimed to investigate the effect of the anti-muscarinic drug darifenacin on voltage-gated K (Kv) channels, vascular contractility, and coronary blood flow in rabbit coronary arteries.

Inhibition by Imipramine of the Voltage-Dependent K+ Channel in Rabbit Coronary Arterial Smooth Muscle Cells.

Imipramine, a tricyclic antidepressant, is used in the treatment of depressive disorders. However, the effect of imipramine on vascular ion channels is unclear. Therefore, using a patch-clamp technique we examined the effect of imipramine on voltage-dependent K+ (Kv) channels in freshly isolated rabbit coronary arterial smooth muscle cells.

Empagliflozin dilates the rabbit aorta by activating PKG and voltage-dependent K channels.

We investigated the vasodilatory effects of empagliflozin (a sodium-glucose co-transporter 2 inhibitor) and the underlying mechanisms using rabbit aorta. Empagliflozin induced vasodilation in a concentration-dependent manner independently of the endothelium. Likewise, pretreatment with the nitric oxide synthase inhibitor L-NAME or the SKca inhibitor apamin together with the IKca inhibitor TRAM-34 did not impact the vasodilatory effects of empagliflozin.

The inhibitory effect of ziprasidone on voltage-dependent K channels in coronary arterial smooth muscle cells.

We investigated the effect of ziprasidone, a widely used treatment for schizophrenia, on voltage-dependent K (Kv) channels of coronary arterial smooth muscle cells using the patch-clamp technique. Ziprasidone dose-dependently inhibited Kv channels with an IC value of 0.39 ± 0.

The vasodilatory effect of gemigliptin via activation of voltage-dependent K channels and SERCA pumps in aortic smooth muscle.

This study investigated the vasodilatory effects and acting mechanism of gemigliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor. Tests were conducted in aortic rings pre-contracted with phenylephrine. Gemigliptin induced dose-dependent vasodilation of the aortic smooth muscle.

Inhibition of voltage-dependent K channels by iloperidone in coronary arterial smooth muscle cells.

Iloperidone, a second-generation atypical antipsychotic drug, is widely used in the treatment of schizophrenia. However, the side-effects of iloperidone on vascular K channels remain to be determined. Therefore, we explored the effect of iloperidone on voltage-dependent K (Kv) channels in rabbit coronary arterial smooth muscle cells using the whole-cell patch-clamp technique.