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PubMed1996

Inhibition of regulated neuropeptide secretion from mouse pituitary cells by propofol.

Neuropeptides modulate neuronal responses to stimuli. Secretion of neuropeptides is a potential site for anesthetic action. This paper examines the hypothesis that propofol alters the secretion of beta-endorphin. Cultures of a mouse pituitary cell line (AtT-20) were exposed to propofol in vitro, then induced to secrete beta-endorphin. Secretion was measured by immunoassay. Propofol caused statistically significant inhibition of secretion. Secretion stimulated by phorbol ester was inhibited by propofol with a calculated 50% inhibitory concentration (IC50) value of 48 microM. The propofol IC50 values for secretion stimulated by other secretagogs were 47 microM (barium), 42 microM (Bay K 8644, a calcium channel agonist), and 28 microM (a cyclic adenosine monophosphate [cAMP] analog). AtT-20 cells recovered their ability to secrete beta-endorphin upon removal of the propofol, which demonstrated that they were not damaged permanently by propofol. The effect was relatively specific to neuropeptide secretion, as AtT-20 cells grew normally for 5 days in the presence of 10 or 80 microM propofol. The finding suggests that propofol inhibited a site in neuropeptide exocytosis common to the three studied pathways of secretion.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1997

ANG II modifies cardiomyocyte function via extracardiac and intracardiac neurons: in situ and in vitro studies.

To determine whether angiotensin II (ANG II) affects cardiac performance via neurons in intrathoracic cardiac ganglia, studies were performed on anesthetized dogs. To exclude possible vascular regulatory effects of ANG II, experiments were also performed using long-term cultures of adult guinea pig ventricular cardiomyocytes with or without intrathoracic neurons. 1) In in situ experiments in 10 anesthetized dogs, cardiac augmentation occurred when ANG II (10 microl or 0.1 ml; 10-100 microM) was administered into limited loci within acutely decentralized stellate or middle cervical ganglia that were neurally connected to, but not those disconnected from, the heart. In another 18 dogs, ANG II increased intrinsic cardiac neuronal activity when administered adjacent to such neurons or into their local arterial blood supply. Ventricular ionotropic effects elicited by ANG II were eliminated by timolol, whereas increases in intrinsic cardiac neuronal activity were not affected. Effects elicited by ANG II were eliminated by administration of a selective AT1 receptor antagonist (losartan) but not by a selective AT2 receptor antagonist (PD-123319). 2) In in vitro experiments, ANG II (100 nM) induced positive chronotropic effects on cultured adult guinea pig cardiomyocytes innervated with adult extrinsic or intrinsic cardiac neurons, but not those cultured without neurons. The frequency of calcium inward current (Ca(i)) transients (recorded by fura 2 fluorescence) increased in innervated cocultures but not in the noninnervated cardiomyocyte cultures; however, the amplitude of Ca(i) transients was not affected by ANG II in cultures or in freshly isolated adult guinea pig cardiomyocytes. ANG II-induced effects in cocultures were blocked by losartan but not PD-123319 or timolol. Thus 1) ANG II-sensitive neurons exist in intrathoracic extracardiac and intrinsic cardiac ganglia; 2) these neurons possess AT1 receptors; and 3) these neurons appear to act directly and indirectly via adrenergic neurons to enhance cardiomyocyte function.

Angiotensin II↗

PubMed1983

Comparison of isotropic calcium signals from intact frog muscle fibers injected with Arsenazo III or Antipyrylazo III.

Intact single skeletal muscle fibers were micro-injected with either of the metallochromic indicator dyes Arsenazo III or Antipyrylazo III, and dye-related Ca2+ signals from each were measured during a twitch. In comparison with the Arsenazo III Ca2+ signal, the signal from Antipyrylazo III had three favorable features: (a) it was temporally faster, (b) its spectral dependence agreed with a cuvette calibration, and (c) its kinetic behavior was consistent with a single Ca2+ -dye stoichiometry. It is therefore suggested that the Antipyrylazo III Ca2+ signal is a more accurate monitor of the time course of the underlying myoplasmic free Ca2+ transient and one that may be more reliably calibrated.

Animals↗

PubMed2007

Differential effects of AT1 receptor and Ca2+ channel blockade on atherosclerosis, inflammatory gene expression, and production of reactive oxygen species.

Angiotensin II receptor blockade has been shown to inhibit atherosclerosis in several different animal models. We sought to determine if this effect was the result of blood pressure reduction per se or a result of the anti-inflammatory effects of receptor blockade. ApoE-deficient mice were fed a high fat diet and treated with either an angiotensin II receptor antagonist, candesartan (0.5 mg/kg/day, s.c.) or a calcium channel blocker, amlodipine (7.5 mg/kg/day, mixed with food). Atherosclerotic lesion area, aortic inflammatory gene expression as well as aortic H2O2 and superoxide production were assayed. We found that candesartan but not amlodipine treatment dramatically attenuated the development of atherosclerosis despite a similar reduction in blood pressure. Similarly, candesartan treatment inhibited aortic expression of inflammatory genes and production of reactive oxygen species, effects not seen with amlodipine. These data demonstrate that angiotensin II receptor blockade inhibits atherosclerosis by reducing vascular oxidative stress and inflammatory gene production independent of blood pressure reduction.

Amlodipine↗

PubMed1992

Effects of semotiadil fumarate (SD-3211) on renal hemodynamics and function in dogs.

Studies were carried out to define the effect of semotiadil on renal hemodynamics, renal function and renin release in pentobarbital-anesthetized dogs. Intrarenal arterial infusion of semotiadil resulted in a significant increase in renal blood flow (RBF), glomerular filtration rate (GFR), urine flow, urinary excretion of electrolytes and renin release. Semotiadil did not affect the linear relationship between osmolar clearance and the free water reabsorption rate, and increased the urinary excretion of sodium and calcium to the same extent. These results suggest that the main tubular site of action of semotiadil is the proximal tubule. Intrarenal infusion of a potent non-peptide angiotensin II antagonist, DuP753 (15 micrograms/kg per min), resulted in an increase in RBF, GFR, urine flow and UNaV. In spite of the blockade of the intrarenal renin angiotensin system(RAS) with DuP753, semotiadil caused almost the same effects as it did in the absence of DuP753. These results suggest that the renal effects of semotiadil are independent of the intrarenal RAS.

Analysis of Variance↗

PubMed1988

Dissociation of the metabolic from the contractile response to muscarinic stimulation in the rabbit urinary bladder.

The calcium dependence of contraction and NADH fluorescence was investigated in rabbit bladder stimulated with bethanechol or KCl. The absence of calcium in the bathing solution induced a rightward shift in the dose response to bethanechol for both contraction and NADH fluorescence. The contractile response was shifted to a greater degree than the fluorescence response and the maximal response to bethanechol was reduced by 80% for contraction but only 20% for NADH fluorescence. This rightward shift was also induced by the benzothiazepine calcium antagonist diltiazem (200 microM) and again the contractile response was shifted significantly more than the fluorescence response. The combination of zero calcium and 200 microM diltiazem virtually abolished contractions but only inhibited the NADH fluorescence by 65% at maximally effective bethanechol concentrations. Unlike the effect of diltiazem on the response to bethanechol, diltiazem (200 microM) shifted both the contraction and fluorescence curves to the right equally in response to KCl stimulation. These results indicate that a metabolic response to muscarinic stimulation (decreased NADH) can occur in the absence of any observable contractile response. This metabolic response may be due to post receptor signal processing events. For KCl stimulation, the NADH response is probably secondary to and a result of the contractile response.

Animals↗

PubMed2006

Activation of P2Y1 receptor triggers two calcium signaling pathways in bone marrow erythroblasts.

In this study, we describe the presence of P2 receptor subtypes and Ca2+ signaling in erythroblasts. ATP and ADP produced a biphasic increase of intracellular Ca2+ concentration ([Ca2+]i), with an initial transient phase followed by a sustained phase. Reverse transcription polymerase chain reaction (RT-PCR) showed the expression of P2Y1, P2Y2 and P2Y12. The selective P2Y1 receptor antagonist 2'-deoxy-N6-methyl-adenosine-3',5'-diphosphate (MRS2179) and the G(i) protein inhibitor pertussis toxin blocked Ca2+ increase. The initial transient [Ca2+]i increase phase was sensitive to the 1,4,5-inositol trisphosphate (IP3) receptor blocker 2-aminoethoxy-diphenylborate (2-APB), while the sustained phase was sensitive to the protein kinase C (PKC) inhibitor 2-[1-(3-dimethylaminopropyl)-1H-indol-3-yl]-3-(1H-indol-3-yl)-maleimide (GF109203X) and calcium calmodulin kinase II (CaMKII) inhibitor 1-[N,O-bis(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenylpiperazine (KN-62). In addition, the PKC activator phorbol-12,13-dibutyrate (PDBu) produced increase of [Ca2+]i. Flow cytometry analysis showed the expression of Ca2+-dependent PKC alpha, betaI, gamma and phospho-CaMKII. These results suggest that the activation of the P2Y1 receptor triggers two different [Ca2+]i increase pathways, one IP3-dependent and the other kinase-dependent.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMedDate not supplied

Stability determination of solid lipid nanoparticles (SLN) in aqueous dispersion after addition of electrolyte.

The contribution of mono-, di- and trivalent ions to the destabilization of solid lipid nanoparticle (SLN) dispersions was investigated, i.e. particle growth and subsequent formation of semi-solid gels. Sodium, calcium and aluminium chloride were added in varying concentrations to a Compritol formulation which had proved to be highly sensitive towards destabilizing effects. Dispersions containing up to 10(-3) M sodium chloride remained stable for 14 days. The same concentrations of calcium or aluminium induced slight and rapid particle growth, respectively. Generally, a pronounced destabilizing effect was observed with increasing electrolyte concentration and increasing valence. Higher concentrations of electrolyte (10(-2), 10(-1) M) induced gelation of the systems. The extent of solidification was highly dependent on the crystallinity of the lipid phase. The recrystalization indices of the gels were distinctly higher compared to the liquid systems. Additionally, unstable modifications, being present in liquid dispersions, were transformed into stable ones with increasing solidification. The mechanisms of the destabilizing effect of the electrolytes are reduced electrostatic repulsion and transformation of the lipid Compritol to the beta' modification promoting gel formation.

Aluminum Chloride↗

PubMed1994

Hypertrophic growth of cultured neonatal rat heart cells mediated by type 1 angiotensin II receptor.

Primary cultures of neonatal cardiac myocytes were used to determine the identity of second messengers that are involved in angiotensin II (ANG II) receptor-mediated effects on cardiac hypertrophy and the type of ANG II receptor that is involved in ANG II-induced cell growth. Treatment of myocytes with ANG II significantly increased the protein-to-DNA and the RNA-to-DNA ratios. ANG II accelerated rates of protein synthesis by 24.9%. Intracellular free calcium was transiently increased after ANG II exposure. The activity of protein kinase C in particulate fractions was transiently increased after exposure to ANG II but returned to control level. The activity of protein kinase C in the cytosol was significantly decreased at all times after exposure to ANG II. After ANG II treatment, the content of c-Fos mRNA was increased. The stimulatory effects of ANG II on these parameters were inhibited by the type 1 angiotensin II receptor (AT1) antagonist, losartan. These studies demonstrate that ANG II-induced hypertrophic growth is, at least in part, mediated through AT1 receptors.

Angiotensin II↗

PubMedDate not supplied

[Modulatory effects of polyamines and GABA on rat ileal motility in vitro].

AIM: The aim of our work was to determine the effects of polyamines and GABA on rat ileum motility in vitro. METHODS: Longitudinal strips dissected from control ileum or ileum without myenteric plexus after benzalkonium chloride (BAC) treatment were placed in organ bath chambers. RESULTS: Spermine significantly inhibited spontaneous activity and nerve stimulation-induced response. Inhibition of spontaneous activity was not altered by BAC treatment or tetrodotoxin but was antagonized by BAY K 8644, a L-type calcium channel agonist. Spermine inhibitory effect on nerve-stimulation induced response disappeared after BAC treatment. GABA enhanced the response induced by nerve stimulation but did not antagonize spermine effects; its action was inhibited in presence of atropine and was mimicked by baclofen, a GABAB agonist. CONCLUSION: Polyamines and GABA can modulate rat ileum motility in vitro. GABA acted via neural GABAB receptors. We demonstrate for the first time that spermine exerts a dual action through different mechanisms on both smooth muscle cells and probably intramural neurons.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1995

Swelling-induced chloride currents in neuroblastoma cells are calcium dependent.

The effects of osmotic stress on chloride (CI-) currents in the human neuroblastoma cell line CHP-100 were evaluated. Following exposure to hypoosmotic solution, an increase in whole-cell CI- current was observed. This current was blocked by the CI- channel blocker 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB). In cells loaded with the CI- permeability marker 125I, exposure to hypoosmotic solution increased 125I efflux by 197 +/- 14% (n = 41, p < 0.05) over controls. This increase was sensitive to NPPB. Hypoosmotic stress also increased cytosolic calcium levels (Ca2+) in fura-2-loaded cells. Pretreatment with EGTA inhibited the increase in cytosolic Ca2+, 125I efflux, and whole-cell CI- current produced by hypoosmotic solution. Antagonists of N-, L-, and T-type Ca2+ channels did not alter stimulation in 125I efflux or cytosolic Ca2+ levels during osmotic stress. However, omega-conotoxin MVIIC, a P-type Ca2+ channel blocker, inhibited hypoosmotically activated whole-cell CI- currents and increases in cytosolic Ca2+. It is concluded that a Ca(2+)-dependent change in CI- permeability is activated in CHP-100 cells in response to osmotic stress.

Barium Compounds↗

PubMed2006

Simultaneous uptake of ammonium and phosphate ions by compounds prepared from paper sludge ash.

Al-containing CaO-SiO(2)-H(2)O phases were prepared by hydrothermal treatment of mixtures of paper sludge ash (PSA) with various silica and calcia sources and their properties were determined with particular reference to the simultaneous uptake of ammonium and phosphate ions, which are implicated in the eutrophication of lakes and ponds. After examination of various silica and calcia sources, Ca(OH)(2) and SiO(2) sol were selected as the most appropriate starting materials. Dry milling was found to be superior to wet milling in avoiding contamination from the milling media during mixing. Nine samples with three different Ca/Si ratios and Al(2)O(3) contents were prepared with various mass ratios of Ca(OH)(2), PSA and SiO(2). The chemical compositions of the hydrothermal products of these mixtures moved towards the tieline of CaSiO(3)-PSA, with respect to the starting compositions. The major phase formed in all samples was poorly crystalline C-S-H(I), with hydroxysodalite also formed in the Al-containing mixtures. All the products showed a capacity for the simultaneous uptake of ammonium and phosphate ions. The saturated sorption capacities calculated from the Langmuir equation ranged from 0.9 to 2.4mmol/g for the ammonium ion and from 3.3 to 5.2mmol/g for the phosphate ion. Since the sorption capacities for both ions increased with increasing Ca contents of the product, substitution of Ca(2+) for NH(4)(+) and the formation of calcium phosphate phases such as apatite and brushite by precipitation are thought to be the main sorption mechanisms.

Adsorption↗

PubMed2003

Increase in IP3 and intracellular Ca2+ induced by phosphate depletion in LLC-PK 1 cells.

The mechanisms by which Pi depletion rapidly regulates gene expression and cellular function have not been clarified. Here, we found a rapid increase in intracellular ionized calcium [Ca(2+)](i) by phosphate depletion in LLC-PK(1) cells using confocal microscopy with the green-fluorescence protein based calcium indicator "yellow cameleon 2.1." The increase of [Ca(2+)](i) was observed in the presence or absence of extracellular Ca(2+). At the same time, an approximately twofold increase in intracellular inositol 1,4,5-triphosphate (IP(3)) occurred in response to the acute Pi depletion in the medium. Furthermore, 2-aminoethoxydiphenyl borate completely blocked the [Ca(2+)](i) increase induced by Pi depletion. These results suggest that Pi depletion causes IP(3)-mediated release of Ca(2+) from intracellular Ca(2+) pools and rapidly increases [Ca(2+)](i) in LLC-PK(1) cells.

Animals↗

PubMed1995

Association of drug therapy with survival in cardiac arrest: limited role of advanced cardiac life support drugs.

OBJECTIVE: To generate hypotheses regarding the association of standard Advanced Cardiac Life Support (ACLS) drugs with human cardiac arrest survival. METHODS: This observational cohort study was conducted over a two-year period in the wards, intensive care units, and EDs of two tertiary care hospitals. Included werc adult patients who suffered cardiac arrest either inside or outside the hospital and who required epinephrine according to standard ACLS guidelines. Six standard ACLS drugs (given while CPR was in progress) were assessed for association with survival from resuscitation to one hour and to hospital discharge by univariate and multivariate logistic regression analyses. RESULTS: In the 529 patients studied, initial cardiac rhythm had no impact on the association between drug administration and survival. The time of drug administration (quartile of ACLS period) was associated with resuscitation for atropine (p < 0.05) and lidocaine (p < 0.01). The odds ratios (95% CIs) for successful resuscitation, after multivariate adjustment for potential confounders, were: a respiratory initiating cause, 3.7 (2.1 -6.4); each 5-minute increase in CPR-ACLS interval, 0.5 (0.4-0.7); each 5-minute duration of ACLS. 0.9 (()1.8- 1.0; atropine, 1.2 (1.0-1.3); bretylium. (0.4 (0.1-1.1); calcium 0.8 (0.2-2.4); lidocaine, 0.9 (0.7-1.1); procainamide. 21.0 (5.2-84.0) d sodium bicarbonate 1.2 (1.0-1.6). All other potential confounding variables entered into the model were not significantly associated with resuscitation. CONCLUSION: Initiating cause of arrest, time to ACLS, and duration of ACLS were important correlates of survival. Other than procainaimide, standard ACLS drugs had relatively little association with survival, but timing of administration may be an important factor. Further research using definitive large randomized controlled trials is warranted to assess the role of drug therapy in improving cardiac arrest survival.

Adult↗

PubMed1997

[Interaction of soda lime and halogenated anesthetics].

The increased use of soda lime for low flow anaesthesia leads to some problems related to the interaction with halogenated agents. These agents may be absorbed by soda lime or degradated according to their water content. Halothane and enflurane, in contact with soda lime, produce some metabolites, but their concentration is low when compared to their own lethal concentration. Sevoflurane degradates to four compounds. Compound A may reach a value between 13.3-42.1 ppm in the inspired fraction: these values are 50-100 times lower than the toxic concentrations. Isoflurane and desflurane are degradable at very low extent. Some case reports of unexpected high carboxyhemoglobin levels during anaesthesia indicate the possibility of CO production from soda lime and baralyme when halogenated agents are used. This reaction occurs only with anaesthetics containing CHF2-moiety (isoflurane, enflurane and desflurane) and when some specific factors make soda lime or baralyme completely dry. Low flow anaesthesia preserves the moisture content of the soda lime and protects from carbon monoxide production, by increasing water content in the circle.

Absorption↗

PubMed1991

Calcium-permeable ion channels in cerebellar neurons from mdx mice.

Recordings of single-channel activity were made from cell-attached patches on cerebellar granule cells from normal and mdx mice. Recordings from mdx granule cells show the activity of ion channels that are open for seconds at negative holding potentials near rest. These channels are permeable to divalent cations and have a conductance of 8-10 pS with either Ca2+ or Ba2+ as the charge carrier in the patch electrode. Under similar recording conditions, channel activity is virtually absent from normal mouse granule cells. The absence of dystrophin in neurons, as well as in skeletal muscle, is associated with an increase in the activity of Ca(2+)- permeable ion channels. Increased channel activity may be an early event leading to pathophysiological accumulation of intracellular Ca2+ in Duchenne muscular dystrophy.

Animals↗

PubMed2004

The effects of monobromobimane on calcium and phenylarsineoxide-induced mitochondrial swelling and cytochrome C release in isolated brain mitochondria.

A possible involvement of inhibitory effects of monobromobimane (MBM), a thiol reagent, on the swelling and the release of cytochrome c in the isolated brain mitochondria was examined. MBM dose-dependently inhibited the calcium and phenylarsineoxide-induced mitochondrial swelling and cytochrome c release. Significant relationships between mitochondrial swelling and cytochrome c release were detected. Furthermore, effects of in vivo treatment with MBM on neuronal cell damage after transient (15 min) global ischemia in rats were examined. Infusion of MBM (1 or 3 microg/animal) to cerebral ventricles attenuated an increased number of TUNEL-positive cells and neuronal cell death in the hippocampal CA1 region at 72 h of reperfusion. These results suggest that MBM may have an ability to inhibit mitochondria-associated apoptotic pathways through attenuation of the mitochondrial swelling and the release of cytochrome c.

Animals↗

PubMed2005

Effects of 2-APB on store-operated Ca2+ channel currents of hepatocytes after hepatic ischemia/reperfusion injury in rats.

The effects of hepatic ischemia/reperfusion (1/R) injuries on hepatocellular viability and store-operated calcium current (Isoc) in isolated rat hepatocytes and the effects of 2-APB on store-operated calcium current (Isoc) in isolated rat hepatocytes after hepatic ischemia/reperfusion injuries were studied. Hepatic ischemia and reperfusion injury model was established and whole cell patch-clamp techniques were used to investigate the effects of 2-APB on Isoc. The results showed that ischemia/reperfusion injuries could significantly reduce hepatocellular viability and further increase Isoc in hepatocytes and 2-APB (20, 40, 60, 80, 100 micromol/L,) produced a concentration-dependent decrease of Isoc with IC50 value of 64. 63 +/- 10.56 micromol/L, (n = 8). It was concluded that ischemia/reperfusion injuries could reduce hepatocellular viability, probably through increased Isoc in hepatocytes and 2-APB had a protective effect on ischemia/reperfusion-induced liver injury, probably though inhibiting Isoc.

Animals↗