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PubMed1997

Effects of divalent cations and of a calcimimetic on adrenocorticotropic hormone release in pituitary tumor cells.

The calcium sensing receptor (CaSR), a member of the G-protein coupled receptor family, is expressed on a variety of cell types and responds to extracellular calcium. We have characterized pharmacological properties of (+/-)NPS 568, a calcimimetic, toward cloned rat brain extracellular Ca2+-sensing receptor (CaSR) expressed in Chinese hamster ovary (CHO) cells and constitutive mouse CaSR in AtT-20 cells. In the presence of 1.3 mM Ca2+, the calcimimetic displayed a potency in the micromolar range in augmenting the inositol phosphates (IP) response in both cell lines and behaved as a full agonist. (+/-)NPS 568 stimulated formation of arachidonic acid release in CHO(CaSR) with a similar potency. The IP dose response curves of (+/-)NPS 568 were shifted to the left in the presence of increasing Ca2+, indicating that the potency of the drug is dependent on extracellular Ca2+ in both cells. In AtT-20 cells, Ca2+ and Ba2+, two CaSR agonists, induced a potent stimulation of adrenocorticotropic hormone (ACTH) secretion. In the presence of 1.8 mM Ca2+, (+/-)NPS 568 led to a dose dependent secretion of ACTH with an EC50 of 0.3 microM and a maximal effect comparable to Ca2+. The similar potency of the calcimimetic on IP and ACTH responses and the sensitivity of these responses to extracellular Ca2+ indicate that the Ca2+-sensing receptor expressed in AtT-20 cells is implicated in ACTH release. These data further characterize the pharmacology of the Ca2+-sensing receptor and argue for a role for extracellular Ca2+ and CaSRs in controlling ACTH secretion, a hormone implicated in several types of stress.

Adrenocorticotropic Hormone↗
PubMed1977

Bladder muscle contractility. Comparative effects and mechanisms of action of atropine, propantheline, flavoxate, and imipramine.

The anticholinergic and antispasmodic activity of atropine, propantheline, imipramine, and flavoxate were judged by each drug's ability to inhibit bethanechol chloride and barium chloride-induced canine detrusor contractions. In this in vitro model, atropine and propantheline are pure anticholinergic agents. Imipramine significantly decreases both bethanechol and barium-induced contractions, while flavoxate only minimally inhibits the response to either stimulant.

Animals↗
PubMed1993

Identification of M-channels in outside-out patches excised from sympathetic ganglion cells.

We have identified the species of K+ channel that underlies the neuronal M-current in rat sympathetic ganglion cells. The channels were kinetically and pharmacologically defined using outside-out and cell-attached patches. They exhibited multiple conductance levels, predominantly 3-9 pS. Their slow gating in response to voltage change in outside-out patches was exhibited only in the presence of AIF-4 or GTP gamma S on the inner membrane surface and when the lower conductance states were dominant. In the absence of AIF-4 or GTP gamma S, the channels exhibited rapid activation and deactivation. We conclude that M-channel gating may be controlled by an associated GTP-binding protein.

Aluminum↗
PubMed2003

GEA3162 stimulates Ca2+ entry in neutrophils.

We showed that 5-amino-3-(3,4-dichlorophenyl)1,2,3,4-oxatriazolium (GEA3162), a lipophilic nitric oxide (NO)-releasing agent, induced Ca(2+) entry into rat neutrophils in a concentration-dependent manner, whereas the guanylyl cyclase inhibitors, 6-anilino-5,8-quinolinequinone (LY83583) and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), had no effect on GEA3162-induced response. The GEA3162-induced Ca(2+) entry was not observed in a Ca(2+)-free medium. GEA3162 did not potentiate but reduced the store-emptying activated Ca(2+) entry caused by cyclopiazonic acid. Stimulation of cells with GEA3162 in the absence of extracellular Ca(2+) followed by addition of cations showed that only Ca(2+) but not Ba(2+) and Sr(2+) entry occurs. Store-operated Ca(2+) entry was sensitive to La(3+) and Ni(2+) inhibition, whereas the GEA3162-induced Ca(2+) entry was sensitive to La(3+) but resistant to Ni(2+). cis-N-(2-Phenylcyclopentyl)azacyclotridec-1-en-2-amine (MDL-12,330A) and calyculin A diminished the Ca(2+) entry activated by cyclopiazonic acid as well as by GEA3162. In contrast, 2-aminoethyldiphenyl borate (2-APB) diminished cyclopiazonic acid-but enhanced GEA3162-induced [Ca(2+)](i) change. Genistein effectively attenuated the cyclopiazonic acid-but slightly inhibited GEA3162-induced [Ca(2+)](i) change. Application of neomycin and high extracellular Ca(2+) concentration did not induce [Ca(2+)](i) rise. These data suggest that GEA3162 induced Ca(2+) entry and regulated Ca(2+) signal, through direct protein thiol oxidation. The action of GEA3162 demonstrates characteristics that distinguish it from the store-operated mechanism in neutrophils and therefore is likely to represent an entirely distinct pathway. Extracellular Ca(2+)-sensing receptor is not existing in neutrophils.

Adenylyl Cyclase Inhibitors↗
PubMed2003

Activation of vanilloid receptor type I in the endoplasmic reticulum fails to activate store-operated Ca2+ entry.

To evaluate interaction of vanilloid receptor type 1 (TRPV1) with endogenous Ca(2+) signalling mechanisms, TRPV1 was expressed in Spodoptera frugiperda (Sf 9) insect cells using recombinant baculovirus. Stimulation of TRPV1-expressing cells, but not control Sf 9 cells, with resiniferatoxin (RTX), capsaicin or anandamide, produced an increase in cytosolic free Ca(2+) concentration ([Ca(2+)](i)), with EC(50) values of 166 pM, 24.5 nM and 3.89 microM respectively. In the absence of extracellular Ca(2+), both capsaicin and RTX caused an increase in [Ca(2+)](i) with EC(50) values of approx. 10 microM and 10 nM respectively. This TRPV1-induced release of Ca(2+) from intracellular stores was not blocked by U73122, suggesting that phospholipase C was not involved. Substantial overlap was found between the thapsigargin- and RTX-sensitive internal Ca(2+) pools, and confocal imaging showed that intracellular TRPV1 immunofluorescence co-localized with the endoplasmic reticulum targeting motif KDEL. To determine if TRPV1-induced mobilization of intracellular Ca(2+) activates endogenous store-operated Ca(2+) entry, the effect of 2-aminoethoxydiphenyl borate (2-APB) on Ba(2+) influx was examined. 2-APB blocked thapsigargin-induced Ba(2+) influx, but not RTX-induced Ba(2+) entry. In the combined presence of thapsigargin and a store-releasing concentration of RTX, the 2-APB-sensitive component was essentially identical with the thapsigargin-induced component. Similar results were obtained in HEK-293 cells stably expressing TRPV1. These results suggest that TRPV1 forms agonist-sensitive channels in the endoplasmic reticulum, which when activated, release Ca(2+) from internal stores, but fail to activate endogenous store-operated Ca(2+) entry. Selective activation of intracellular TRPV1, without concomitant involvement of plasmalemmal Ca(2+) influx mechanisms, could play an important role in Ca(2+) signalling within specific subcellular microdomains.

Animals↗
PubMed2001

Characteristics of a store-operated calcium-permeable channel: sarcoendoplasmic reticulum calcium pump function controls channel gating.

We examined the single channel properties and regulation of store-operated calcium channels (SOCC). In human submandibular gland cells, carbachol (CCh) induced flickery channel activity while thapsigargin (Tg) induced burst-like activity, with relatively lower open probability (NP(o)) and longer mean open time. Tg- and CCh-activated channels were permeable to Na(+) and Ba(2+), but not to NMDG, in the absence of Ca(2+). The channels exhibited similar Ca(2+), Na(+), and Ba(2+) conductances and were inhibited by 2-aminoethoxydiphenylborate, xestospongin C, Gd(3+), and La(3+). CCh stimulated flickery activity changed to burst-like activity by (i) addition of Tg, (ii) using Na(+) instead of Ca(2+), (iii) using Ca(2+)-free bath solution, or (iv) buffering [Ca(2+)](i) with BAPTA-AM. Buffering [Ca(2+)](i) induced a 2-fold increase in NP(o) of Tg-stimulated SOCC. Reducing free [Ca(2+)] in the endoplasmic reticulum with the divalent cation chelator, N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN), induced burst-like channel activity similar to that seen with CCh + Tg. Thus, SOCC is activated by stimulation of muscarinic receptors, inhibition of the sarcoendoplasmic Ca(2+) pump, and lowering [Ca(2+)] in the internal store. Importantly, SOCC activity depends on [Ca(2+)](i) and the free [Ca(2+)] in the internal store. These novel findings reveal that SERCA plays a major role in the gating of SOCC by (i) refilling the internal Ca(2+) store(s) and (ii) decreasing the [Ca(2+)](i)-dependent inhibition.

Barium↗
PubMed1992

Gastroesophageal reflux: diagnosis and management.

The pathologic potential of chronic esophagitis cannot be overemphasized. Persistent reflux causing cycles of mucosal damage followed by healing may eventually lead to end-stage disease, with development of peptic stricture. The most effective drugs available are those that inhibit acid production. Drugs that will enhance lower esophageal function are still in the future.

Alginates↗
PubMed2004

Spreading dilatation in rat mesenteric arteries associated with calcium-independent endothelial cell hyperpolarization.

Both ACh and levcromakalim evoke smooth muscle cell hyperpolarization and associated relaxation in rat mesenteric resistance arteries. We investigated if they could evoke conducted vasodilatation along isolated arteries, whether this reflected spreading hyperpolarization and the possible mechanism involved. Focal micropipette application of either ACh, to stimulate endothelial cell muscarinic receptors, or levcromakalim, to activate smooth muscle K(ATP) channels, each evoked a local dilatation (88 +/- 14%, n= 6 and 92 +/- 6% reversal of phenylephrine-induced tone, n= 11, respectively) that rapidly spread upstream (at 1.5 mm 46 +/- 19%, n= 6 and 57 +/- 13%, n= 9) to dilate the entire isolated artery. The local dilatation to ACh was associated with a rise in endothelial cell [Ca(2+)](i) (F/F(t = 0)= 1.22 +/- 0.33, n= 14) which did not spread beyond 0.5 mm (F/F(t = 0)= 1.01 +/- 0.01, n= 14), while the local dilatation to levcromakalim was not associated with any change in endothelial cell [Ca(2+)](i). In contrast, ACh and levcromakalim both stimulated local (12.7 +/- 1.2 mV, n= 10 and 13.5 +/- 4.7 mV, n= 10) and spreading (at 2 mm: 3.0 +/- 1.1 mV, n= 5 and 4.1 +/- 0.7 mV, n= 5) smooth muscle hyperpolarization. The spread of hyperpolarization could be prevented by cutting the artery, so was not due to a diffusible agent. Both the spreading dilatation and hyperpolarization were endothelium dependent. The injection of propidium iodide into either endothelial or smooth muscle cells revealed extensive dye coupling between the endothelial cells, but limited coupling between the smooth muscle cells. Some evidence for heterocellular spread of dye was also evident. Together, these data show that vasodilatation can spread over significant distances in mesenteric resistance arteries, and suggest this reflects an effective coupling between the endothelial cells to facilitate [Ca(2+)](i)-independent spread of hyperpolarization.

Acetylcholine↗
PubMed1987

Temporal changes in mechanical properties of rat jejunal smooth muscle after myenteric plexus ablation.

We determined length-stress properties and active tension development of rat jejunal longitudinal and circular muscle at various times after myenteric neuron ablation. Myenteric neurons were destroyed by serosal application of benzalkonium chloride. Active tension generation in response to both carbachol and barium was depressed in both muscle layers up to 7 days after treatment, at which times the responses were normal. At 15 days, circular muscle responses were still comparable to control, but longitudinal muscle responses were significantly increased. Length-stress parameters of circular muscle were minimally affected, while those of longitudinal muscle were significantly altered 15 and 30 days after treatment. These alterations include changes in resting stress and increased active stress generation at both times. Our results suggest that 1) normal myenteric innervation is necessary for normal contractile activity in rat jejunal smooth muscle and 2) changes in cellular or tissue morphology or alterations in intracellular calcium homeostasis, as seen in other tissue, may occur after myenteric plexus ablation.

Animals↗
PubMed1975

Ca++ and pancreatic amylase release.

The effects of Ca'++ on release of amylase by mouse pancreas in vitri was studied. The cholinergic agonist bethanechol was depressed about 50% in O Ca'++ medium. When pancreatic fragments were superfused with O Ca'++ medium, bethanechol still produced a normal stimulation of amylase release after half of the total tissue Ca'++ was washed out. This Ca'++ loss included both extracellular and some intracellularCa'++. Uptake and equilibration of '45Ca'++ into pancreatic fragments was multiphasic, with total equilibration with stable Ca'++ still not reached after 3 h. Addition of bethanechol had no effect on the rate of '45Ca uptake and equilibration. '45Ca'++ efflux was not influenced by superfision in O Ca'++ medium, while thestimulation of '45Ca'++ efflux by bethanechol was enhanced. It is concluded that extracellular Ca'++ and/or Ca'++ influx is not of major importance in triggering pancreatic enzyme release, but that extracellular Ca'++ may regulate the release process thus accounting for the parallel changes in unstimulated and stimulated amylase release.

Amylases↗
PubMed2000

Competition between internal AlF(4)(-) and receptor-mediated stimulation of dorsal raphe neuron G-proteins coupled to calcium current inhibition.

Intracellular aluminum fluoride (AlF(4)(-)), placed in a patch pipette, activated a G-protein, resulting in a "tonic" inhibition of the Ca(2+) current of isolated serotonergic neurons of the rat dorsal raphe nucleus. Serotonin (5-HT) also inhibits the Ca(2+) current of these cells. After external bath application and quick removal of 5-HT to an AlF(4)(-) containing cell, there was a reversal or transient disinhibition (TD) of the inhibitory effect of AlF(4)(-) on Ca(2+) current. A short predepolarization of the membrane potential to +70 mV, a condition that is known to reverse G-protein-mediated inhibition, reversed the inhibitory effect of AlF(4)(-) on Ca(2+) current and brought the Ca(2+) current to the same level as that seen at the peak of the TD current. With AlF(4)(-) in the pipette, the TD phenomenon could be eliminated by lowering pipette MgATP, or by totally chelating pipette Al(3+). In the presence of AlF(4)(-), but with either lowered MgATP or extreme efforts to eliminate pipette Al(3+), the rate of recovery from 5-HT on wash was slowed, a condition opposite to that where a TD occurred. The putative complex of AlF(4)(-)-bound G-protein (Galpha.GDP. AlF(4)(-)) appeared to free G-betagamma-subunits, mimicking the effect on Ca(2+) channels of the G.GTP complex. The ON-rate of the inhibition of Ca(2+) current, after a depolarizing pulse, by betagamma-subunits released by AlF(4)(-) in the pipette was significantly slower than that of the agonist-activated G-protein. The OFF-rate of the AlF(4)(-)-mediated inhibition in response to a depolarizing pulse, a measure of the affinity of the free G-betagamma-subunit for the Ca(2+) channel, was slightly slower than that of the agonist stimulated G-protein. In summary, AlF(4)(-) modified the OFF-rate kinetics of G-protein activation by agonists, but had little effect on the kinetics of the interaction of the betagamma-subunit with Ca(2+) channels. Agonist application temporarily reversed the effects of AlF(4)(-), making it a complementary tool to GTP-gamma-S for the study of G-protein interactions.

Adenosine Triphosphate↗