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At least 919 records · Page 51Linked to original sources
PubMed2003

Crosstalk between voltage-independent Ca2+ channels and L-type Ca2+ channels in A7r5 vascular smooth muscle cells at elevated intracellular pH: evidence for functional coupling between L-type Ca2+ channels and a 2-APB-sensitive cation channel.

This study was designed to investigate the role of voltage-independent and voltage-dependent Ca2+ channels in the Ca2+ signaling associated with intracellular alkalinization in A7r5 vascular smooth muscle cells. Extracellular administration of ammonium chloride (20 mmol/L) resulted in elevation of intracellular pH and activation of a sustained Ca2+ entry that was inhibited by 2-amino-ethoxydiphenyl borate (2-APB, 200 micromol/L) but not by verapamil (10 micro;mol/L). Alkalosis-induced Ca2+ entry was mediated by a voltage-independent cation conductance that allowed permeation of Ca2+ (PCa/PNa approximately 6), and was associated with inhibition of L-type Ca2+ currents. Alkalosis-induced inhibition of L-type Ca2+ currents was dependent on the presence of extracellular Ca2+ and was prevented by expression of a dominant-negative mutant of calmodulin. In the absence of extracellular Ca2+, with Ba2+ or Na+ as charge carrier, intracellular alkalosis failed to inhibit but potentiated L-type Ca2+ channel currents. Inhibition of Ca2+ currents through voltage-independent cation channels by 2-APB prevented alkalosis-induced inhibition of L-type Ca2+ currents. Similarly, 2-APB prevented vasopressin-induced activation of nonselective cation channels and inhibition of L-type Ca2+ currents. We suggest the existence of a pH-controlled Ca2+ entry pathway that governs the activity of smooth muscle L-type Ca2+ channels due to control of Ca2+/calmodulin-dependent negative feedback regulation. This Ca2+ entry pathway exhibits striking similarity with the pathway activated by stimulation of phospholipase-C-coupled receptors, and may involve a similar type of cation channel. We demonstrate for the first time the tight functional coupling between these voltage-independent Ca2+ channels and classical voltage-gated L-type Ca2+ channels.

Ammonium Chloride↗
PubMed2001

Coordinated control of cell Ca(2+) loading and triggered release from the sarcoplasmic reticulum underlies the rapid inotropic response to increased L-type Ca(2+) current.

The aim of this study was to investigate how sarcoplasmic reticulum (SR) Ca(2+) content and systolic Ca(2+) are controlled when Ca(2+) entry into the cell is varied. Experiments were performed on voltage-clamped rat and ferret ventricular myocytes loaded with fluo-3 to measure intracellular Ca(2+) concentration ([Ca(2+)](i)). Increasing external Ca(2+) concentration ([Ca(2+)](o)) from 1 to 2 mmol/L increased the amplitude of the systolic Ca(2+) transient with no effect on SR Ca(2+) content. This constancy of SR content is shown to result because the larger Ca(2+) transient activates a larger Ca(2+) efflux from the cell that balances the increased influx. Decreasing [Ca(2+)](o) to 0.2 mmol/L decreased systolic Ca(2+) but produced a small increase of SR Ca(2+) content. This increase of SR Ca(2+) content is due to a decreased release of Ca(2+) from the SR resulting in decreased loss of Ca(2+) from the cell. An increase of [Ca(2+)](o) has two effects: (1) increasing the fraction of SR Ca(2+) content, which is released on depolarization and (2) increasing Ca(2+) entry into the cell. The results of this study show that the combination of these effects results in rapid changes in the amplitude of the systolic Ca(2+) transient. In support of this, the changes of amplitude of the transient occur more quickly following changes of [Ca(2+)](o) than following refilling of the SR after depletion with caffeine. We conclude that the coordinated control of increased Ca(2+) entry and greater fractional release of Ca(2+) is an important factor in regulating excitation-contraction coupling.

4-Aminopyridine↗
PubMed2001

A calcium-dependent feedback mechanism participates in shaping single NMDA miniature EPSCs.

NMDA receptors (NMDARs) are highly calcium-permeable and are negatively regulated by intracellular calcium during prolonged exposure to agonist. We have investigated whether calcium-mediated feedback occurs during transient exposure to glutamate during single synaptic events. Examination of miniature EPSCs (mEPSCs) indicated that the decay kinetics of the NMDAR component was markedly slowed by the intracellular perfusion of exogenous calcium buffers (BAPTA or Fluo-3). In contrast, the AMPA receptor component of the miniature EPSC was unaffected. Slow on-rate calcium buffers, such as EGTA, did not alter kinetics of the NMDAR component of the mEPSC. Addition of exogenous fast calcium buffers did not slow the decay kinetics of glutamate-evoked currents mediated by NR1/NR2A heteromers expressed in HEK 293 cells, suggesting that the effect we observed in neurons may be specific to processes associated with synaptically activated receptors. Trial-to-trial amplitude variability of miniature calcium transients mediated by NMDARs increased with the injection of exogenous calcium buffers, suggesting that the amplitude of synaptic calcium transients are maintained at a rather constant level by a calcium-mediated feedback mechanism.

Aniline Compounds↗
PubMed1989

Multiple effects of honokiol on catecholamine secretion from adrenal chromaffin cells.

The molecular mechanism of honokiol, extracted from the bark of Magnolia obovata, was studied using bovine adrenal chromaffin cells as a model system. Honokiol inhibits catecholamine secretion induced by carbachol and DMPP and that induced by exposure to high K+ and Ba2+ but to a lesser extent. The inhibitory effects of trifluoperazine and honokiol on carbachol-, high K(+)- and Ba2(+)- induced secretion were not additive. The results suggest that honokiol interferes with the interaction between the acetylcholine receptor and its agonists and that honokiol may also affect the steps in exocytosis after intracellular calcium has been raised, possibly at the site(s) where calmodulin acts.

Adrenal Medulla↗
PubMed1987

Antagonism of picumast and ketotifen against histamine, acetylcholine, LTC4, slow-reacting substance of anaphylaxis and barium chloride in the guinea pig ileum bioassay.

The antagonism of the antiallergic compounds picumast (PIC; Boehringer Mannheim) and ketotifen (K; Sandoz) against pro-allergic mediators like histamine (H), acetylcholine (ACh), SRS-A and LTC4 as well as against the unspecific spasmogen BaCl2 was compared in the bioassay of superfused guinea pig ileum. For the evaluation of an SRS-A antagonism crude SRS-A from antigen-stimulated guinea pig lung fragments in Krebs buffer was used with the addition of atropine and mepyramine. PIC (approximately 10(-6)-10(-5) mol/l) antagonized clearly all tested spasmogens in a concentration-dependent manner. Its predominant antagonism (IC30: 2-3 X 10(-6) mol/l) was against H, LTC4 and SRS-A, which are presumably important mediators of allergic reactions. ACh- or BaCl2-induced spasms were inhibited to the same extent with a 4 or 6 times higher concentration of PIC. K was approximately 20 times more potent as antagonist against H and approximately 8 times more potent against ACh, whereas the antagonism against LTC4- or BaCl2-induced spasms reached only 1/3 of that of PIC. An antagonism of PIC against SRS-A, LTC4 and H may contribute to its antiallergic activity in vivo. K showed little activity against LTC4 but could antagonize more selectively H- and ACh-mediated effects.

Acetylcholine↗
PubMed1997

Low density barium and bentonite mixture versus high density barium: a comparative study to optimize negative gastrointestinal contrast agents for MRI.

The purpose of this study was to compare the patient tolerance and efficacy, as magnetic resonance imaging negative oral contrast agents, of a mixture of clay compound bentonite and low density barium sulfate suspension with that of higher density barium sulfate. Twenty patients were randomized into two groups: 10 patients receiving a mixture of low concentration 60% w/v barium sulfate plus 2.5% w/v bentonite, and 10 patients receiving 220% w/v barium sulfate Liuqid-HD (E-Z-EM, Westbury, NY). Post-contrast Spin-echo (SE) T1- and T2-weighted images (WI) were obtained on a 1.0T magnet. Two independent readers scored the overall intraluminal signal intensity and delineation of the gastrointestinal tract and adjacent organs. Patient acceptance was evaluated via a short questionnaire, by recording spontaneous comments and documenting the quantity of contrast agent ingested. There was greater intraluminal bowel signal reduction and organ delineation with 220% w/v barium than with the barium-bentonite mixture on both SE T1WI (p = 0.03) and SE T2WI (p = 0.42). With both agents there was greater signal reduction on SE T2WI than SE T1WI. Higher scores for organ delineation for both contrast agents were seen with SE T1WI. With 220% w/v barium, there was significantly better delineation of the pancreatic body (p = 0.02) and pancreatic tail (p = 0.02) on T1WI compared with SE T2WI. With the barium-bentonite mixture, SE T1WI showed improved delineation of jejunum compared with SE T2WI (p = 0.03). There were no statistically significant differences between the volume of contrast ingested in the two groups. Abdominal cramps were recorded for one patient in each group. These results suggest that barium-bentonite mixture, although useful as a negative gastro-intestinal contrast agent, is not as effective as 220% w/v barium. Further studies with a larger patient population and concentration optimization studies are needed.

Abdomen↗
PubMedDate not supplied

[Comparative evaluation and analysis of the bradykinin-potentiating properties of D-penicillamine and other thiol and non-thiol kininase inhibitors].

In experiments with an isolated guinea-pig ileum D-penicillamine (3,3-dimethylcysteine) potentiated the spasmogenic effect of bradykinin and exerted no influence on the analogous effects of acetylcholine, histamine and barium chloride. These properties distinguish the drug from other thiol compounds -- unithiol and cysteine. The bradykinin-potentiating action of D-penicillamine excludes the effect on the cholinergic and histaminergic systems, while the bradykinin-potentiating effect of unithiol and cysteine is reversed by atropine and tavegil. 1, 10-Phenanthroline and 8-hydroxyquinoline do not possess the bradykinin-potentiating properties, and, when administered in high doses, reduce the spasmogenic effect of the polypeptide.

Acetylcholine↗
PubMed2001

Lack of degradation of sevoflurane by a new carbon dioxide absorbent in humans.

BACKGROUND: Potent inhaled anesthetics degrade in the presence of the strong bases (sodium hydroxide or potassium hydroxide) in carbon dioxide (CO2) absorbents. A new absorbent, Amsorb (Armstrong Medical Ltd., Coleraine, Northern Ireland), does not employ these strong bases. This study compared the scavenging efficacy and compound A production of two commercially available absorbents (soda lime and barium hydroxide lime) with Amsorb in humans undergoing general anesthesia. METHODS: Four healthy volunteers were anesthetized on different days with desflurane, sevoflurane, enflurane, and isoflurane. End-tidal carbon dioxide (ETCO2) and anesthetic concentrations were measured with infrared spectroscopy; blood pressure and arterial blood gases were obtained from a radial artery catheter. Each anesthetic exposure lasted 3 h, during which the three fresh (normally hydrated) CO2 absorbents were used for a period of 1 h each. Anesthesia was administered with a fresh gas flow rate of 2 l/min of air:oxygen (50:50). Tidal volume was 10 ml/kg; respiratory rate was 8 breaths/min. Arterial blood gases were obtained at baseline and after each hour. Inspired concentrations of compound A were measured after 15, 30, and 60 min of anesthetic administration for each CO2 absorbent. RESULTS: Arterial blood gases and ETCO2 were not different among three CO2 absorbents. During sevoflurane, compound A formed with barium hydroxide lime and soda lime, but not with Amsorb. CONCLUSIONS: This new CO2 absorbent effectively scavenged CO2 and was not associated with compound A production.

Absorption↗
PubMed1998

[Compound A: toxicology and clinical relevance].

Sevoflurane, like all currently used volatile anaesthetics, is degraded by carbon dioxide absorbents. The most significant degradant is a haloalkene known trivially as "compound A". Compound A is nephrotoxic in rats and, at higher doses, in nonhuman primates, causing proximal tubular necrosis. There has been much interest in the potential for compound A toxicity in humans. Inhaled compound A concentrations are greatest at low flow rates, high sevoflurance concentrations, warmer absorbent, barium hydroxide vs soda lime, and drier absorbent. Typical inspired compound A concentrations during low-flow and closed-circuit sevoflurane anaesthesia in humans are 8-24 and 20-32 ppm with soda lime and barium hydroxide lime, respectively. Renal effects of compound A production during sevoflurane anesthesia have been examined in surgical patients and volunteers, using standard (creatinine clearance, serum BUN and creatinine) and experimental (urine excretion of protein, glucose, NAG, GST, AAP) markers of renal function. Investigations to date in surgical patients show similar renal effects of low-flow sevoflurane, low-flow isoflurane or high-flow sevoflurane. There have been no case reports of compound A-associated renal injuryin humans. In volunteers, one study found changes in experimental but not conventional renal markers, while other investigations show no significant changes in either standard or experimental markers. The mechanism of compound A nephrotoxicity in rats appears to involve metabolism to glutathione and cysteine conjugates, and their subsequent renal uptake and metabolism by pathways that are different in rats and humans.

Anesthetics, Inhalation↗
PubMedDate not supplied

Propranolol analogs containing natural monoterpene structures: synthesis and pharmacological properties.

A few derivatives of natural, bicyclic monoterpenes, which are propranolol analogs, were synthetized. Those compounds were studied pharmacologically in order to determine their toxicity, antiarrhythmic activity in selected experimental models of arrhythmia, the local anesthetic effect and influence on the cardiovascular system. The tested compounds showed a less potent or similar toxicity towards reference drugs, were devoid of an antiarrhythmic activity in the model of barium arrhythmia, yet some of them (compounds 9 and 12) increased the arrhythmogenic dose of strophanthin. All the compounds studied had a local anesthetic effect stronger than lidocaine in infiltration anesthesia, and compound 8--also in surface anesthesia.

Anesthetics, Local↗
PubMed1992

Age related alterations in the response of the pial arterioles to adenosine in the rat.

To evaluate the effects of aging on vasoreactivity of pial arterioles to adenosine and barium chloride, an hydraulically intact cranial window preparation was developed in the rat. The microvasculature of anesthetized 3- and 24-month-old Fischer-344 rats was studied during superfusion with artificial cerebrospinal fluid with and without test agents and results determined by videomicroscopy techniques. In both cohorts, the response of pial arterioles to adenosine was both dose and vessel size dependent: arteriolar dilation increased with increasing concentrations of adenosine and at any given concentration the percent increase in diameter was greater in the smaller vessels. During adenosine superfusion the absolute changes and percent increase in vessel caliber were greater in the young rats. Arteriolar vasoconstriction due to barium chloride was vessel size dependent but there were no significant differences in response between young and aged rats. The results indicated an attenuated cerebrovascular response in aged rats to adenosine, but not to barium chloride. This may be due to a difference in the mode of action in these two compounds. Venules did not respond to adenosine at any concentration.

Adenosine↗