Inhibitory effect of Pyr6 (an Orai channel blocker) on agonist‐induced contractions in rat uterus

2021 ◽  
Author(s):  
Ícaro Araújo de Sousa ◽  
Gabriel Medina Sobreira de Meneses ◽  
José Victor Miranda Cardoso ◽  
Pablo Queiroz Lopes ◽  
Joubert Aires de Sousa ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Inhibitory Effect ◽  
Rat Uterus

scholarly journals Effect of Potassium Channel Modulators on Morphine Withdrawal in Mice

2010 ◽  
Vol 4 ◽  
pp. SART.S6211 ◽  
Author(s):  
Vikas Seth ◽  
Mushtaq Ahmad ◽  
Prerna Upadhyaya ◽  
Monika Sharma ◽  
Vijay Moghe
Keyword(s):  
Potassium Channel ◽  
Withdrawal Syndrome ◽  
Channel Blocker ◽  
Inhibitory Effect ◽  
Morphine Withdrawal ◽  
The Other ◽  
Opioid Antagonist ◽  
Potassium Channel Openers ◽  
Potassium Channel Modulators ◽  
Withdrawal Signs

The present study was conducted to investigate the effect of potassium channel openers and blockers on morphine withdrawal syndrome. Mice were rendered dependent on morphine by subcutaneous injection of morphine; four hours later, withdrawal was induced by using an opioid antagonist, naloxone. Mice were observed for 30 minutes for the withdrawal signs ie, the characteristic jumping, hyperactivity, urination and diarrhea. ATP-dependent potassium (K+ATP) channel modulators were injected intraperitoneally (i.p.) 30 minutes before the naloxone. It was found that a K+ATP channel opener, minoxidil (12.5–50 mg/kg i.p.), suppressed the morphine withdrawal significantly. On the other hand, the K+ATP channel blocker glibenclamide (12.5–50 mg/kg i.p.) caused a significant facilitation of the withdrawal. Glibenclamide was also found to abolish the minoxidil's inhibitory effect on morphine withdrawal. The study concludes that K+ATP channels play an important role in the genesis of morphine withdrawal and K+ATP channel openers could be useful in the management of opioid withdrawal. As morphine opens K+ATP channels in neurons, the channel openers possibly act by mimicking the effects of morphine on neuronal K+ currents.

Blockade of chloride channels by DIDS stimulates renin release and inhibits contraction of afferent arterioles

1996 ◽  
Vol 270 (5) ◽  
pp. F718-F727 ◽  
Author(s):  
B. L. Jensen ◽  
O. Skott
Keyword(s):  
Angiotensin Ii ◽  
Chloride Channels ◽  
Channel Blocker ◽  
Inhibitory Effect ◽  
Renin Release ◽  
Disulfonic Acid ◽  
Basal Diameter ◽  
Chloride Channel Blocker ◽  
Afferent Arterioles ◽  
Dose Dependent

Calcium-activated chloride channels have been proposed to control renin release from juxtaglomerular cells and to be involved in the excitation-contraction coupling of the renal afferent arteriole. The hypothesis was tested on renin release from rat glomeruli and in microperfused rabbit afferent arterioles with the chloride channel blocker 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). Renin secretion was equally enhanced by omission of extracellular calcium and by addition of 0.5 mM DIDS. The inhibitory effect of calcium was blocked by DIDS. The stimulatory effects of low calcium [with or without ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid] and DIDS were not additive. In the absence of chloride, basal renin release was suppressed and the stimulatory effect of DIDS was abolished. The DIDS-induced enhancement of renin release was not dependent on bicarbonate. Norepinephrine (5 x 10(-7)-1 x 10(-6) M) and angiotensin II (1 x 10(-8)-10(-6) M) evoked reversible and dose-dependent contractions of microperfused rabbit afferent arterioles. DIDS (0.5 mM) did not affect the basal diameter of the arterioles but strongly inhibited the response to angiotensin II and attenuated the duration of the contractile response to norepinephrine. The results support the hypothesis that DIDS-sensitive calcium-activated chloride channels are involved in regulation of renin release and in the afferent arteriolar contraction after angiotensin II but do not play a pivotal role in the response to norepinephrine.

Rat Prl and TSH secretion are regulated differently by K(+)-channel blockers

1994 ◽  
Vol 266 (1) ◽  
pp. E39-E43 ◽  
Author(s):  
X. Wang ◽  
T. Inukai ◽  
M. A. Greer ◽  
S. E. Greer
Keyword(s):  
Channel Blocker ◽  
Cell Types ◽  
Inhibitory Effect ◽  
Thyroid Stimulating Hormone ◽  
K Channel ◽  
Channel Blockers ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
K Channels ◽  
Tsh Secretion

All four different K(+)-channel blockers [tetraethylammonium (TEA), a nonselective K(+)-channel blocker; tolbutamide, an ATP-sensitive K(+)-channel blocker; quinine and 4-aminopyridine, both primarily voltage-dependent K(+)-channel blockers] stimulated prolactin (Prl) secretion by acutely dispersed anterior pituitary cells but had no effect on thyroid-stimulating hormone (TSH) secretion. TEA stimulated Prl secretion in a dose-dependent manner between 1 microM and 20 mM, but even as high as 20 mM, TEA did not induce TSH secretion. Valinomycin (2 microM), a K+ ionophore, inhibited both basal and TEA-induced Prl secretion. TEA-stimulated Prl secretion was abolished by using a Ca(2+)-depleted medium or adding 10 microM dopamine. TEA did not reverse the inhibitory effect of dopamine on thyrotropin-releasing hormone-induced Prl secretion. Our data indicate that K+ channels may play a role in the secretion of adenohypophysial hormones that is idiosyncratic for each hormone. Differences in the role of K+ channels may reflect differences between the various pituitary cell types in plasma membrane ion channel composition, membrane potential, or the mechanism of exocytosis.

A ROLE FOR PROSTAGLANDINS IN DECIDUALIZATION OF THE RAT UTERUS

1981 ◽  
Vol 89 (1) ◽  
pp. 25-33 ◽  
Author(s):  
NICOLE SANANÈS ◽  
ETIENNE-EMILE BAULIEU ◽  
CLAUDE LE GOASCOGNE
Keyword(s):  
Arachidonic Acid ◽  
Dienoic Acid ◽  
Inhibitory Effect ◽  
Rat Uterus ◽  
Hormonal Stimulation ◽  
Immature Rats ◽  
Decidual Reaction ◽  
Dose Dependent ◽  
Related Compounds

The deciduogenic action of various kinds of prostaglandin (PG), i.e. PGE1, PGE2, PGF2α and PGI2, methylated prostaglandins (15-met-PGE1, 15-met-PGE2 and 15-met-PGF2α), PGF2α-13-dehydro analogues (13-DH-PGF2α, ent-15-epi-13-DH-PGF2α), endoperoxide analogues (15S)-hydroxy-9α,11α-(epoxymethano)-prosta-5Z,13E-dienoic acid (U 44069) and (15S)-hydroxy-11α,9α-(epoxymethano)-prosta-5Z,13E-dienoic acid (U 46619), and of the prostaglandin precursor, arachidonic acid, has been demonstrated after intraluminal instillation of these compounds into the uterus of immature rats sensitized with progesterone alone. Under this minimal hormonal stimulation, in which a trauma (a scratch) of the endometrium is required to induce the decidual response, all these compounds elicited the formation of deciduomata, substantiating the suggestion that the scratch-induced decidual reaction is mediated through release of prostaglandin. Confirmation was obtained through the effect of indomethacin and cortisol, both of which decreased the decidual response brought on by a scratch or by arachidonic acid, whereas the effect of PGF2α was decreased by indomethacin but not by cortisol. Histamine, thromboxane B2, and oleic, palmitic and homo-γ-linolenic acids were not deciduogenic. A dose-dependent inhibitory effect of indomethacin on deciduoma formation by instillation of oil into animals sensitized by progesterone plus oestradiol was also observed. The results support the proposal that the decidual reaction involves prostaglandins and we suggest that the deciduoma is a valuable model for studying the action of prostaglandin-related compounds.

Effects of Mg2+ on Ca2+ waves and Ca2+ transients of rat ventricular myocytes

1996 ◽  
Vol 270 (3) ◽  
pp. H907-H914 ◽  
Author(s):  
H. Terada ◽  
H. Hayashi ◽  
N. Noda ◽  
H. Satoh ◽  
H. Katoh ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Channel Blocker ◽  
Ventricular Myocytes ◽  
Inhibitory Effect ◽  
Antiarrhythmic Action ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Triggered Activity ◽  
Rat Ventricular Myocytes ◽  
High Concentrations

It has been shown that the occurrence of the transient inward current, which is responsible for triggered activity, was often associated with propagating regions of increased intracellular Ca2+ concentration ([Ca2+]i), i.e., the “Ca2+ wave.” To investigate the mechanism of antiarrhythmic action of Mg2+, we have studied effects of high concentrations of Mg2+ on Ca2+ waves in isolated rat ventricular myocytes. [Ca2+]i was estimated using the Ca(2+)-indicating probe indo 1. Ca2+ waves in myocytes, stimulated at 0.2 Hz, were induced by perfusion of isoproterenol (10(-7) M). High Mg2+ concentration suppressed Ca2+ waves in a concentration-dependent manner (36% at 4 mM, 70% at 8 mM, and 82% at 12 mM). The Ca2+ channel blocker verapamil also suppressed Ca2+ waves in a similar way. In contrast with marked depression of Ca2+ transients by verapamil, Ca2+ transients were not affected by high Mg2+ concentration (8 mM). High Mg2+ concentration also reduced frequencies of Ca2+ waves in the absence of electrical stimulation, whereas verapamil failed to reduce frequencies of Ca2+ waves. Reduction in frequency of Ca2+ waves by high Mg2+ concentration was associated with slowing of propagation velocity of Ca2+ waves. To examine whether suppressive effects of high Mg2+ concentration on Ca2+ waves were related to an increase in intracellular Mg2+ concentration ([Mg2+]i), the effect of high-Mg2+ solution on [Mg2+]i was examined in myocytes loaded with mag-fura 2. An increase in extracellular Mg2+ concentration from 1 to 12 mM increased [Mg2+]i from 1.06 +/- 0.16 to 1.87 +/- 0.22 mM (P < 0.01) in 30 min. To examine the effect of high Mg2+ concentration on amount of releasable Ca2+ in the sarcoplasmic reticulum, the effect of high Mg2+ concentration on the Ca2+ transient induced by a rapid application of caffeine was examined. High-Mg2+ solution increased the peak of the caffeine-induced Ca2+ transient. These results suggest that the inhibitory effect of Mg2+ on Ca2+ waves was not due to inhibition of the sarcolemmal Ca2+ channel but could be due to a decreased propensity for the sarcoplasmic reticulum to divest itself of excess Ca2+.

scholarly journals Inhibitory Effect of Lomerizine, a Diphenylpiperazine Ca2+-Channel Blocker, on Ba2+ Current through Voltage-Gated Ca2+ Channels in PC12 Cells

1997 ◽  
Vol 75 (2) ◽  
pp. 209-213
Author(s):  
Watano Tomokazu ◽  
Hara Hideaki ◽  
Sukamoto Takayuki
Keyword(s):  
Pc12 Cells ◽  
Channel Blocker ◽  
Inhibitory Effect ◽  
Voltage Gated ◽  
Ca2 Channels

scholarly journals Hydrogen peroxide and superoxide anion modulate pregnant human myometrial contractility

Reproduction ◽  
2005 ◽  
Vol 130 (4) ◽  
pp. 539-544 ◽  
Author(s):  
Averil Y Warren ◽  
Balwir Matharoo-Ball ◽  
Robert W Shaw ◽  
Raheela N Khan
Keyword(s):  
Hydrogen Peroxide ◽  
Channel Blocker ◽  
Inhibitory Effect ◽  
Isometric Tension ◽  
Human Myometrium ◽  
Response Curves ◽  
Tetraethylammonium Chloride ◽  
Myometrial Contractility ◽  
Macromolecular Damage ◽  
Maximal Reduction

Reactive oxygen species (ROS) have the propensity to cause macromolecular damage with consequent modification of cellular function. We investigated the effects of two particular oxidants, superoxide (O2−) anions and hydrogen peroxide (H2O2), on oxytocin-induced myometrial contractility using biopsies from women undergoing Caesarean section at term gestation. Isometric tension recordings were performed and concentration–response curves derived after addition of test agents. A maximal reduction in myometrial contractility to 27.2 ± 4.5% of control was observed followed application of H2O2. The enzyme scavenger catalase (CAT) reduced the inhibitory effect of H2O2but had little effect at 10-fold lower concentrations. Addition of dialysed xanthine oxidase ± hypoxanthine significantly inhibited contractility to 23.8.0 ± 4.2% compared with control. Pre-incubation with superoxide dismutase and CAT diminished this effect. The non-specific potassium channel blocker, tetraethylammonium chloride (1 mM), had no effect on myometrial contractility. We conclude that human myometrium is susceptible to the effects of ROS, which may be produced by reperfusion–ischaemic episodes during labour. Our findings could, in part, explain the weak or prolonged depression of contractions characteristic of myometrial dysfunction culminating in difficult labours.

Phytochemical analysis and inhibitory effect of Pyrenacantha staudtii leaf extract on isolated rat uterus

2006 ◽  
Vol 2 (2) ◽  
Author(s):  
Abiodun Falodun ◽  
Cyril O Usifoh ◽  
Zuleikha AM Nworgu
Keyword(s):  
Leaf Extract ◽  
Inhibitory Effect ◽  
Phytochemical Analysis ◽  
Rat Uterus ◽  
Isolated Rat

scholarly journals Inhibitory Effect of Lomerizine, a Diphenylpiperazine Ca2+-Channel Blocker, on Ba2+ Current through Voltage-Gated Ca2+ Channels in PC12 Cells.

1997 ◽  
Vol 75 (2) ◽  
pp. 209-213 ◽  
Author(s):  
Tomokazu Watano ◽  
Hideaki Hara ◽  
Takayuki Sukamoto
Keyword(s):  
Pc12 Cells ◽  
Channel Blocker ◽  
Inhibitory Effect ◽  
Voltage Gated ◽  
Ca2 Channels
Sign in / Sign up

Export Citation Format

Share Document