Duloxetine inhibits voltage-dependent K channels in rabbit coronary arterial smooth muscle: Electrophysiological evidence and mechanistic insights.

Duloxetine, a serotonin-norepinephrine reuptake inhibitor, has been associated with increased blood pressure and other vascular side effects. However, the mechanisms underlying these effects remain poorly understood. Voltage-dependent K (Kv) channels are key regulators of membrane potential and vascular tone in arterial smooth muscle cells.

The Second-Generation Antipsychotic Perospirone Inhibits Voltage-Gated K Channels in Coronary Arterial Smooth Muscle Cells.

Perospirone is a second-generation antipsychotic classified as a serotonin-dopamine antagonist that is primarily used to treat schizophrenia and bipolar disorder. While its therapeutic effects have been attributed to D and 5-HT receptor antagonism and partial 5-HT agonism, its potential interactions with ion channels remain unexplored. In this study, we investigated the effects of perospirone on vascular voltage-gated K (Kv) channels in freshly isolated rabbit coronary arterial smooth muscle cells.

The sodium-glucose cotransporter 2 inhibitor tofogliflozin induces vasodilation of rabbit femoral artery by activating Kv channels, the SERCA pump, and the sGC/cGMP pathway.

Tofogliflozin is a sodium-glucose cotransporter 2 inhibitor widely used to treat type 2 diabetes mellitus, but it also exhibits cardio-protective effects. This study investigated the vasodilatory action of tofogliflozin using rabbit femoral artery rings pre-contracted with phenylephrine (1 μM). The results showed the concentration-dependent induction of vasodilation by tofogliflozin, a response that remained unchanged following endothelial removal, pretreatment with the nitric oxide synthase inhibitor L-NAME (100 μM), or the inhibition of low- and intermediate-conductance Ca-activated K channels using apamin (1 μM) in combination with TRAM-34 (1 μM).

The SGLT2 inhibitor remogliflozin induces vasodilation in the femoral artery of rabbits via activation of a Kv channel, the SERCA pump, and the cGMP signaling pathway.

This study explored the vasodilatory mechanisms of the sodium-glucose cotransporter-2 inhibitor remogliflozin using femoral arteries of rabbits. Remogliflozin dilated femoral arterial rings pre-contracted with phenylephrine in a concentration-dependent manner. Pretreatment with the Ca-sensitive K channel inhibitor (paxilline), the ATP-sensitive K channel inhibitor (glibenclamide), or the inwardly rectifying K channel inhibitor (Ba) did not alter the vasodilatory effect.

Blockade of Voltage-Gated K Channels in Rabbit Coronary Arterial Smooth Muscle Cells by the Antipsychotic Drug Zotepine.

Zotepine is a second-generation antipsychotic that demonstrates significant efficacy in antagonizing D and 5-HT receptors. Although clinical investigations have shown that administering zotepine is associated with an increased prevalence of hyperglycemia and a heightened risk of cardiovascular disease, the side effects of zotepine on voltage-gated K (Kv) channels have not been established. Zotepine suppressed the vascular Kv channels in rabbit coronary arterial smooth muscle cells in a concentration-dependent manner, with an IC of 5.

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.

Inhibition of voltage-gated potassium channel by aripiprazole in rabbit coronary arterial smooth muscle cells.

Aripiprazole, a third-generation antipsychotic, has been widely used to treat schizophrenia. In this study, we evaluated the effect of aripiprazole on voltage-gated potassium (Kv) channels in rabbit coronary arterial smooth muscle cells using the patch clamp technique. Aripiprazole reduced the Kv current in a concentration-dependent manner with a half-maximal inhibitory concentration of 0.

The antidiabetic drug ipragliflozin induces vasorelaxation of rabbit femoral artery by activating a Kv channel, the SERCA pump, and the PKA signaling pathway.

We explored the vasorelaxant effects of ipragliflozin, a sodium-glucose cotransporter-2 inhibitor, on rabbit femoral arterial rings. Ipragliflozin relaxed phenylephrine-induced pre-contracted rings in a dose-dependent manner. Pre-treatment with the ATP-sensitive K channel inhibitor glibenclamide (10 μM), the inwardly rectifying K channel inhibitor Ba (50 μM), or the Ca-sensitive K channel inhibitor paxilline (10 μM) did not influence the vasorelaxant effect.

Inhibition of voltage-dependent K channels in rabbit coronary arterial smooth muscle cells by the atypical antipsychotic agent sertindole.

The regulation of membrane potential and the contractility of vascular smooth muscle cells (VSMCs) by voltage-dependent K (Kv) potassium channels are well-established. In this study, native VSMCs from rabbit coronary arteries were used to investigate the inhibitory effect of sertindole, an atypical antipsychotic agent, on Kv channels. Sertindole induced dose-dependent inhibition of Kv channels, with an IC of 3.

Lurasidone blocks the voltage-gated potassium channels of coronary arterial smooth muscle cells.

Lurasidone is a second-generation antipsychotic drug used to treat schizophrenia, mania, and bipolar disorder. The drug is an antagonist of the 5-HT and D receptors. No effect of lurasidone on the voltage-gated K (Kv) channels has yet been identified.

Inhibition of voltage-dependent K currents of rabbit coronary arterial smooth muscle cells by the atypical antipsychotic paliperidone.

Paliperidone, an atypical antipsychotic, is widely used to treat schizophrenia. In this study, we explored whether paliperidone inhibited the voltage-dependent K (Kv) channels of rabbit coronary arterial smooth muscle cells. Paliperidone reduced Kv channel activity in a concentration-dependent manner with a half-maximal inhibitory concentration (IC ) of 16.