Wall stretch and thromboxane A₂ activate NO synthase (eNOS) in pulmonary arterial smooth muscle cells via H₂O₂ and Akt-dependent phosphorylation.

Pulmonary arteries (PAs) have high compliance, buffering the wide ranges of blood flow. Here, we addressed a hypothesis that PA smooth muscle cells (PASMCs) express nitric oxide synthases (NOS) that might be activated by mechanical stress and vasoactive agonists. In the myograph study of endothelium-denuded rat PAs, NOS inhibition (L-NAME) induced strong contraction (96 % of 80 mM KCl-induced contraction (80K)) in the presence of 5 nM U46619 (thromboxane A2 (TXA2) analogue) with relatively high basal stretch (2.

Modulation of L-type Ca²⁺ channel activity by neuronal nitric oxide synthase and myofilament Ca²⁺ sensitivity in cardiac myocytes from hypertensive rat.

Neuronal nitric oxide synthase (nNOS) is important in cardiac protection in diseased heart. Recently, we have reported that nNOS is associated with myofilament Ca(2+) desensitization in cardiac myocytes from hypertensive rats. So far, the effect of myofilament Ca(2+) desensitization or nNOS on L-type Ca(2+) channel activity (I(Ca)) in cardiac myocyte is unclear.

Low K⁺ current in arterial myocytes with impaired K⁺-vasodilation and its recovery by exercise in hypertensive rats.

K(+) channels determine the plasma membrane potential of vascular myocytes, influencing arterial tone. In many types of arteries, a moderate increase in [K(+)]e induces vasorelaxation by augmenting the inwardly rectifying K(+) channel current (I Kir). K(+)-vasodilation matches regional tissue activity and O2 supply.

Myofilament Ca2+ desensitization mediates positive lusitropic effect of neuronal nitric oxide synthase in left ventricular myocytes from murine hypertensive heart.

Neuronal nitric oxide synthase (NOS1 or nNOS) exerts negative inotropic and positive lusitropic effects through Ca(2+) handling processes in cardiac myocytes from healthy hearts. However, underlying mechanisms of NOS1 in diseased hearts remain unclear. The present study aims to investigate this question in angiotensin II (Ang II)-induced hypertensive rat hearts (HP).

Exercise training increases inwardly rectifying K(+) current and augments K(+)-mediated vasodilatation in deep femoral artery of rats.

Aims: A moderate increase in extracellular [K(+)] ([K(+)](e)) induces relaxation of small arteries by activating inwardly rectifying K(+) current (I(Kir)). The K(+)-induced vasodilatation is an important mechanism for exercise-induced hyperaemia in skeletal muscle. We investigated whether I(Kir) and K(+)-induced vasodilatation are enhanced in deep femoral arteries (DFAs) from exercise-trained rats (ET rats; treadmill running for 20 min at 20 m/min, 3 days/week for 2 weeks).

Inhibition of Ca2+-release-activated Ca2+ channel (CRAC) and K+ channels by curcumin in Jurkat-T cells.

The increase in cytoplasmic Ca(2+) concentration (Δ[Ca(2+)](c)) mediated by the Ca(2+)-release-activated Ca(2+) channel (CRAC) is a critical signal for the activation of lymphocytes. Also, the voltage-gated K(+) channel (K(v)) and intermediate-conductance Ca(2+)-activated K(+) channel (IKCa1/SK4) have drawn attention as pharmacological targets for regulating immune responses. Since polyphenolic agents have various immunomodulatory effects, here we compared the effects of curcumin, rosmarinic acid, resveratrol, and epigallocatechin gallate on the ionic currents through CRAC (I(CRAC)), K(v) (I(Kv)), SK4 (I(SK4)) and on the Δ[Ca(2+)](c) of Jurkat-T cells using the patch clamp technique and fura-2 spectrofluorimetry.

Inhibition of Ca-Release-Activated Ca Channel (CRAC) and K Channels by Curcumin in Jurkat-T Cells.

The increase in cytoplasmic Ca concentration (Δ[Ca]) mediated by the Ca-release-activated Ca channel (CRAC) is a critical signal for the activation of lymphocytes. Also, the voltage-gated K channel (K) and intermediate-conductance Ca-activated K channel (IKCa1/SK4) have drawn attention as pharmacological targets for regulating immune responses. Since polyphenolic agents have various immunomodulatory effects, here we compared the effects of curcumin, rosmarinic acid, resveratrol, and epigallocatechin gallate on the ionic currents through CRAC (I), K (I), SK4 (I) and on the Δ[Ca] of Jurkat-T cells using the patch clamp technique and fura-2 spectrofluorimetry.