The KCa3.1 Channel Blocker TRAM-34 and Minocycline Prevent Fructose-Induced Hypertension in Rats.

Background: High fructose consumption increases blood pressure through microglia-related neuroinflammation in rats. Since intermediate-conductance calcium-activated potassium channels (KCa3.1) potentiates microglial reactivity, we examined whether the pretreatment with the KCa3.

Trimethylamine-N-oxide (TMAO) Selectively Disrupts Endothelium-Dependent Hyperpolarization-Type Relaxations in a Time-Dependent Manner in Rat Superior Mesenteric Artery.

The vascular action of trimethylamine-N-oxide (TMAO)-the gut microbiota-derived metabolite-in contributing cardiovascular disease is a controversial topic. A recent study has shown that acute exposure of TMAO at moderate concentrations inhibits endothelium-dependent hyperpolarization (EDH)-type relaxations selectively in rat isolated femoral arteries, but not in mesenteric arteries. Here we determined the efficacy of higher TMAO concentrations with longer exposure times on vascular reactivity in rat isolated superior mesenteric arteries.

β-adrenergic Receptor Blocker ICI 118,551 Selectively Increases Intermediate-Conductance Calcium-Activated Potassium Channel (IK )-Mediated Relaxations in Rat Main Mesenteric Artery.

Endothelial IK and/or SK channels play an important role in the control of vascular tone by participating in endothelium-dependent relaxation. Whether β-AR antagonists, mainly used in hypertension, affect endothelial K channel function is unknown. In this study, we examined the effect of the β2-AR antagonist and inverse agonist ICI 118,551 on the IK /SK channel activity by assessing functional relaxation responses to several agonists that stimulate these channels.

Electrical field stimulation (EFS)-induced relaxations turn into contractions upon removal of extracellular calcium in rat mesenteric artery.

In the present study, we aimed to examine the effect of blockade of L-type Ca(2+) channels (LTCC) and in addition the removal of extracellular Ca(2+), on EFS-induced relaxations in rings of rat mesenteric artery. EFS applied to the tissues precontracted with phenylephrine caused relaxations which were markedly inhibited by nifedipine (10(-7)M) and tetraethylammonium (TEA) (1mM). Addition of LTCC opener BAY K 8644 (10(-7)M) failed to enhance the relaxations.

Does endothelium-derived hyperpolarizing factor play a role in endothelium-dependent component of electrical field stimulation-induced vasorelaxation of rat mesenteric arterial rings?

Electrical field stimulation (EFS)-induced, nonadrenergic, noncholinergic vasodilation was investigated in rat mesenteric arterial rings. Tetrodotoxin (10(-6) M), capsaicin (10(-5) M), or L-NAME (10(-4) M) failed to change the EFS-induced relaxations, whereas they were increased with indomethacin (10(-5) M). Removal of the endothelium caused approximately 20% reduction in the maximum response, whereas precontraction with 40 mM KCI abolished the relaxations at all frequencies.

Torsion/detorsion of the testis does not modify responses to nitric oxide in rat isolated penile bulb.

Ischaemia-reperfusion damage induced by torsion/detorsion of the testicles may be a causative factor leading to erectile dysfunction through oxidative stress-dependent changes in the responses of the penile bulb, an erectile tissue of the penis. We aimed at investigating the effects of unilateral testicular torsion/detorsion (2 or 24 hr) treatment on relaxations induced by electrical field stimulation and sodium nitroprusside in rat isolated penile bulb. Male Sprague-Dawley rats used in the study were divided into two groups.

Inhibition of acetylcholine-induced EDHF response by elevated glucose in rat mesenteric artery.

The effects of high glucose on endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxations of isolated rat mesenteric artery and the possible involvement of reactive oxygen species in these responses were investigated. After precontraction with phenylephrine (3 x 10(-8)-10(-7) M), acetylcholine (10(-8)-3 x 10(-6) M) and A 23187 (10(-8)-3 x 10(-6) M), a calcium ionophore, induced concentration-dependent relaxations in the presence of N(W)-nitro-l-arginine methyl ester (L-NAME) (10(-4) M) and indomethacin (10(-5) M). These relaxations were abolished in the presence of charybdotoxin (2 x 10(-7) M) plus apamin (10(-7) M) and were assumed to be mediated by EDHF.