Search PubMed⌕ Search

Biomedical subjects

G Sachs

Publications and source records attributed to G Sachs.

At least 145 records · Page 8Linked to original sources
PubMed1993

Histamine secretion from rat enterochromaffinlike cells.

BACKGROUND: In vivo studies have suggested an important role for gastric enterochromaffinlike (ECL) cells in mediating acid secretion. Direct evidence for this function is lacking and requires a preparation of highly purified ECL cells. This work investigates the possible role and mechanism of histamine release from the ECL cell in the peripheral regulation of acid secretion, using purified ECL cells from rat fundic mucosa. METHODS: A combination of elutriation and density-gradient centrifugation was used to purify rat fundic ECL cells. Enrichment was determined by the presence of acidic vacuoles containing a V type adenosine triphosphatase, electron microscopy, immunostaining, and histamine content and release. RESULTS: ECL cells were enriched at least 65-fold with respect to the fundic epithelium. Gastrin (EC50 0.2 nmol/L) and cholecystokinin octapeptide (nonsulfated, EC50 0.04 nmol/L) stimulated histamine release in a time- and dose-dependent manner, suggesting a CCK-B receptor subtype, confirmed by the inhibition of gastrin/CCK stimulation with the CCK-B antagonist L365,260. Somatostatin also inhibited gastrin-mediated histamine release. Single cell imaging showed that gastrin elevated intracellular cytosolic calcium concentration biphasically. Carbachol and the C kinase activator 120-tetradecanoylphorbol-13-acetate also stimulated histamine release. Epinephrine (blocked by propranolol), forskolin, and dibutyryl-5'-cyclic adenosine monophosphate were also effective, implicating a beta-adrenergic pathway. The H3 agonist R-alpha-methyl-histamine inhibited, whereas the H3-antagonist thioperamide potentiated gastrin/CCK stimulated histamine release. CONCLUSIONS: These in vitro results support a central role for the ECL cell in the peripheral regulation of gastric acid secretion.

Animals↗
PubMed1993

Hormonal and blood glucose responsiveness as an indicator of specific emotional arousal in type 1 diabetics.

The aim of the present study was to examine, whether individual emotional arousal induced by a specific stress interview may effect growth hormone (GH), cortisol, catecholamine and blood glucose levels in diabetes patients. To test the validity of this hypothesis we subjected 18 Type 1 diabetics and 18 healthy controls to a life event interview which produces individual arousal. During this stress interview catecholamines and plasma cortisol levels showed no significant increase, whereas there was a significant increase of GH over time in both group (p < 0.04), with a trend in diabetics to have a more marked GH response than controls (p < 0.10). Blood glucose levels remained unaffected by the interview. Depressed diabetics showed significantly higher cortisol increases (p < 0.004) than non-depressed diabetics, whereas there was no difference among depressed and non-depressed controls. Depression was not associated with an increase of other hormones or blood glucose levels in both groups. The results of our study confirm specific pathways in which individual emotional arousal and depression may lead to chronic metabolic disturbances as a result of GH and cortisol hypersecretion.

Adaptation, Psychological↗
PubMed1993

The continuing development of gastric acid pump inhibitors.

The synthesis and action of H2-receptor antagonists changed the understanding of gastric acid secretion as well as changing medical therapy for peptic ulcer disease. It is now known that peripheral regulation of gastric acid secretion depends largely, but not entirely, on histamine release from the enterochromaffin-like cell. There is, therefore, no final common pathway for stimulation of the parietal cell. In contrast, all stimuli converge to activate the acid pump, the H+,K(+)-ATPase. Inhibition of this pump by clinically useful drugs was achieved by developing derivatives of timoprazole, pyridyl-2-methylsulfinyl benzimidazole. Two of these derivatives, omeprazole and lansoprazole, have shown superiority in acid control and therefore in therapy for peptic ulcer disease compared to the available H2-receptor antagonists.

Anti-Ulcer Agents↗
PubMed1993

Whole-cell currents in isolated resting Necturus gastric oxynticopeptic cells.

1. Necturus gastric mucosa secretes Cl- actively across the gastric glands which are composed almost entirely of acid- and enzyme-secreting oxynticopeptic cells. Single channel studies on Necturus oxynticopeptic cells have shown that the basolateral membrane possesses multiple K(+)-selective channels but no observable Cl- channels while the apical membrane has Cl- channels but no observable K+ channels. To relate these channel properties to the conductance of the whole cell we have investigated the macroscopic membrane currents with conventional whole-cell patch-clamp techniques. 2. When bathed in amphibian Ringer solution, gastric oxynticopeptic cells had a membrane resistance of 47.8 +/- 2.8 M omega and a membrane capacitance of 75.5 +/- 2.7 pF (n = 82). This gave a specific membrane resistance of 3260 +/- 160 omega cm2 (n = 82). Reversal potentials of the oxynticopeptic cells were -13.8 +/- 1.2 mV (n = 45) for an intracellular Cl- concentration ([Cl-]i) of 42 mM and were significantly more negative -24.4 +/- 3.1 mV (n = 31, P < 0.001) for [Cl-]i = 22 mM. 3. In the absence of ATP in the pipette solution, there was an 80% reduction of the whole-cell current with a typical half-time (t1/2) of 5 min. The run-down was not observed when the pipette solution contained 4 mM ATP. 4. A slow and voltage-independent inhibition of 80% of the whole-cell currents occurred after addition of NPPB (35 microM). Ba2+ (10 mM) produced a reversible inhibition of 20% of the total current. Together, 35 microM NPPB and 10 mM Ba2+ eliminated 95% of the whole-cell currents. These data suggest that in the resting oxynticopeptic cells Cl- carried the major fraction of the current while K+ ions carried only a small fraction. 5. Total replacement of Cl- in the pipette and bath solution by gluconate- increased the membrane resistance to 751 +/- 104 M omega (n = 53) and shifted the reversal potential to -38.1 +/- 2.8 mV (n = 53). 6. Increasing the bath K+ concentration from 6 to 91 mM activated a current which had a high selectivity for K+ over choline+, Li+, Na+, Rb+ and Cs+ and was independent of Cl-. The activation of this K+ current (IK*) by high external K+ was not seen with ATP-free pipette solution. 7. Ba2+ or Cs+ had a voltage-dependent blocking effect of this inward K+ current. Ouabain (1 mM) or SCH 28080 (200 microM), specific inhibitors of the Na+,K(+)-ATPase and H+,K(+)-ATPase, had no effect.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗
PubMed1993

Role of histamine2 receptor in increased expression of rat gastric H(+)-K(+)-ATPase alpha-subunit induced by omeprazole.

Omeprazole is a specific inhibitor in vivo of the functioning gastric acid pump, the H(+)-K(+)-adenosinetriphosphatase (ATPase), in the secretory canaliculus of the parietal cell. It has been shown previously that omeprazole in rats led to an increase in the mRNA for the alpha-subunit of the H(+)-K(+)-ATPase. Omeprazole causes a marked increase in circulating gastrin in this species, which in turn stimulates release of histamine from the enterochromaffin-like cell. The possible role of this pathway was investigated by the in vivo administration of famotidine, a potent H2 receptor antagonist. A single intraperitoneal dose of famotidine, 200 mg/kg, produced a transient hypergastrinemia peaking at 3 h and normalizing at 12 h, inhibition of secretion that lasted for 12 h, but no change in the level of the alpha-subunit mRNA or of beta-actin mRNA. In contrast, a single dose of omeprazole, 100 mg/kg, inhibited acid secretion and produced hypergastrinemia, peaking at 12 h, both effects lasting for the 24-h observation period. Omeprazole elevated the alpha-subunit mRNA transiently by more than threefold at 3 h, with normal levels being restored at 24 h. The administration of famotidine 1 h after omeprazole did not change the effects of omeprazole on acid secretion but elevated the gastrin levels further. There was now no elevation of the alpha-subunit mRNA for the first 6 h, but a small increase at 12 h and a further increase to approximately 2.5-fold at 24 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

[Soda lime--service life, consumption and costs in relation to fresh gas flow].

The utilisation time of carbon dioxide absorbers in anaesthesia textbooks is nearly identically specified to last about 5 hours. Therefore in most departments the soda lime of the absorbers is changed routinely on a daily schedule. As rebreathing volume increases considerably with fresh gas flow reduction, the question arises as to whether the soda lime should be changed at even shorter intervals--if low-flow anaesthesia is performed routinely--to to guarantee carbon dioxide absorption safely. In three anaesthesia machines with different technical properties the carbon dioxide absorbers were only changed when the inspiratory carbon dioxide concentration increased to 1 vol. %, indicating definite exhaustion of the soda lime. If a fresh gas flow of 4.4 l/min was used exclusively, utilisation times of 42.7 and 62.3 hours were measured using absorbers filled with 1 l of soda lime pellets, whereas a utilisation time of 98.7 hours was noted with a 1.5 l absorber, all values being surprisingly higher than the above-mentioned figure. If, however, minimal flow anaesthesia is performed routinely in clinical practice, the percentage of time in which the fresh gas flow can really be reduced to 0.5 l/min does not exceed 50 to 80%. Under these conditions the utilisation time of the absorbers decreases to between one half (1/2) and one quarter (1/4) of the utilisation time which can be gained if a flow of 4.4 l/min is used. Thus, the performance of minimal-flow anaesthesia increases the consumption of soda lime two- to fourfold.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1993

[Effectiveness of relaxation groups in patients with chronic respiratory tract diseases].

In the long-term treatment of patients with chronic respiratory diseases, patient education contributes significantly towards improving the effectiveness of conventional drugs in the treatment of asthma-specific complaints and anxiety, as well as playing a role in improved disease coping. The aim of this study was to verify whether relaxation training programs undertaken subsequent to patient education may have an additional effect with regard to both medical and psychological variables. Relaxation training encompasses the basic exercises of autogenics, as well as exercises of functional relaxation. 49 patients participated in the relaxation group (22 male, 27 female). The mean age was 50.5 +/- 16.5 years. The control group used was made up of 37 patients with chronic respiratory diseases (17 male, 20 female) who had received asthma education, but no further therapeutic intervention. Prior to and immediately after the relaxation training, the following investigations were undertaken: lung function, patient diary, Spielberger anxiety scale, Giessen list of complaints (modified and augmented) and Ziegler coping questionnaire. The linear rating scale model was used for measuring changes. The following significant changes were observed in the relaxation group as compared with the control group: decrease of trait fear, alleviation of asthma-specific complaints and asthma attacks, decrease in sleep disturbances and in morning coughing urge, reduction in the required quantities of controlled-dosage aerosol, and a modified attitude toward the disease in the sense of an improved subjective coping competence.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Psychological↗
PubMed1993

Postoperative complication rate of thoracotomy in patients with normal and abnormal pulmonary function.

Recent advances in perioperative monitoring, anesthesia, and postoperative care have resulted in a more generous attitude towards performing thoracic surgery in patients with reduced pulmonary function. In our hospital 100 patients admitted for thoracotomy with or without pulmonary resection were classified on the basis of their pulmonary function: group I (n = 33) normal, group II (n = 40) moderate reduction, group III (n = 27) marked reduction. The mean and standard deviation in groups I, II, and III were: FEV 1 in % VC: 78 +/- 6, 72 +/- 7, and 58 +/- 10; RV in % TLC: 24 +/- 7, 35 +/- 8, and 43 +/- 9; Resistance, kPal/1/sec: 0.2 versus 0.3 versus 0.5. After surgery there were three postoperative deaths from cardiovascular complications without respiratory failure; all 3 patients were in group II and younger than 70 years. Only one patient (classified as group III and 59 years old) died from a respiratory complication (respiratory insufficiency) after a palliative operation on a large adenocarcinoma. Our data demonstrate that markedly reduced preoperative lung function is not necessarily associated with high risk in thoracic surgery--even in elderly persons--provided intensive pre- and postoperative care is guaranteed.

Adolescent↗
PubMed1992

Determination of the sidedness of the C-terminal region of the gastric H,K-ATPase alpha subunit.

It cannot be predicted from hydropathy analysis whether the C-terminal end of the alpha subunit of the gastric H,K-ATPase is cytoplasmic or extracytoplasmic. The sideness of the C-terminal amino acids was determined by taking advantage of the two C-terminal tyrosines in the primary sequence of the enzyme. Intact, cytoplasmic side out vesicles derived from hog gastric mucosa or detergent solubilized vesicles were iodinated by the lactoperoxidase method and then the C-terminal amino acids hydrolyzed by carboxypeptidase Y. The alpha and beta subunits were separated by SDS gel electrophoresis. The level of iodination of the alpha subunit following solubilization was about three fold greater than when intact vesicles were iodinated, and the beta subunit was iodinated only when solubilized enzyme was used. Carboxypeptidase Y removed 28 +/- 4% of the radioactivity from the alpha subunit iodinated in intact vesicles. These data are consistent with a cytoplasmic location of the C-terminal amino acids of the alpha subunit and with a mostly extracytoplasmic location of the amino acids of the beta subunit.

Animals↗
PubMed1992

Topology and sites in the H,K-ATPase.

Understanding the membrane topology of the EP-type pumps has been approached largely by analysis of hydrophobicity plots, which are confusing in the COOH-terminal third of the proteins. Each pair of predicted membrane-spanning segments with the extracytoplasmic loop contains at least one cysteine, allowing fluorescent labeling of these regions of the enzymes by cysteine reagents once the cytoplasmic domain has been removed. The membrane segment arrangement of the H,K and sr Ca ATPases was investigated by tryptic cleavage of intact cytoplasmic face-out vesicles. This was followed by fluorescein or coumarin maleimide labeling of the SDS solubilized residual membrane fragments, tricine gradient gel separation, and sequencing. The presence of four membrane-spanning pairs was demonstrated for the alpha subunit of the H,K-ATPase, with no membrane retention of H9 and H10, although H9 has four cysteines based on cDNA sequencing. A similar observation was made for the Ca pump, except that fluorescein-labeled H9 was detected in the membrane with a molecular weight of 4 kD, showing that cleavage had occurred at lys958 predicted to be extracytoplasmic in a 10 membrane segment model. It seems likely that for both these enzymes the membrane domain contains only 8 alpha helical spanning segments. Cleavage at ala236 in the beta subunit was found only in leaky, not in ion-tight vesicles, arguing for a single membrane segment in this subunit. In the H,K-ATPase additional evidence for the presence and arrangement of the first, third, and fourth pair of segments was obtained by labeling the intact enzyme with extracytoplasmic inhibitory reagents. The K competitive reagent, an imidazopyridine, MeDAZIP+, labeled the first pair of membrane segments. The acid-activated SH reagent class, the pyridinyl methyl sulfinyl benzimidazoles, labeled cysteines 813 and 822 in the M5/M6 region as well as cysteine 892 in the extracytoplasmic loop between M7 and M8. No labeling of the beta subunit was found, indicating the presence of three disulfide bonds in the extracytoplasmic domain of this subunit. Both sets of extracytoplasmic reagents are predicted to bind close to the fatty acid/phospholipid head group interface. Inhibition by these reagents shows that conformational changes are transmitted between cytoplasmic and extracytoplasmic domains.

Amino Acid Sequence↗
PubMed1992

Location of the cytoplasmic epitope for a K(+)-competitive antibody of the (H+,K+)-ATPase.

The monoclonal antibody (mAb) 95-111 binds the alpha subunit of (H+,K+)-ATPase and inhibits the K(+)-ATPase activity. To map the epitope, all of the partial sequences of the alpha subunit were expressed in Escherichia coli HB101 using rabbit alpha subunit cDNA restriction fragments ligated into PuEx vector. Bacterial recombinant lysates were separated by sodium dodecyl sulfate-gel electrophoresis, and the epitope was detected by Western blotting. The antibody site was mapped between Cys529 and Glu561. This is close to the Lys517 that binds fluorescein isothiocyanate (FITC) and is considered to be between M4 and M5 close to the ATP binding domain. However, the mAb inhibition of ATPase is not ATP-competitive but is K(+)-competitive with a KI of 2 x 10(-9) M. The mAb also inhibits K+ quench of FITC fluorescence competitively with a KI of 8 x 10(-9) M. The K+ activation of ATPase activity and quench of FITC fluorescence are dependent on K+ binding to an E2 form of the enzyme from the extracytoplasmic surface. The mAb epitope is cytoplasmic since the K(+)-ATPase activity of ion-tight gastric vesicles is inhibited. The 125I-mAb 95-111 binds to a single class of sites with an apparent KD of 2.3 +/- 0.8 x 10(-9) M and K+ does not displace bound mAb. Hence, antibody binding to a cytoplasmic Cys529-Glu561 epitope allosterically competes with K(+)-dependent reactions at extracytoplasmic sites.

Adenosine Triphosphate↗
PubMed1992

cDNA cloning and membrane topology of the rabbit gastric H+/K(+)-ATPase alpha-subunit.

We have cloned and sequenced a cDNA for the rabbit gastric proton-potassium pump (H+/K(+)-ATPase) alpha-subunit. The deduced peptide contains 1035 amino acids (Mr 114,201) and shows 97% sequence identity with the respective rat and hog proteins. A monoclonal antibody 146-14 has been shown previously to react with the extracytoplasmic side of the catalytic H+/K(+)-ATPase subunit and here we show that the epitope is in the region between amino acids 855 and 902 (the numbering of the H+/K(+)-ATPase catalytic subunit throughout the paper refers to the rabbit sequence). The localization of this epitope in conjunction with previously observed trypsin cleavage sites in the C-terminal one third of the enzyme and the hydrophobicity plot of the deduced peptide sequence are evidence for a structural model for the alpha-subunit of the H+/K(+)-ATPase which contains at least ten membrane spanning segments, similar to that deduced for the Ca(2+)-ATPase of sarcoplasmic reticulum.

Adenosine Triphosphatases↗
PubMed1992

Spatial and temporal patterns of intracellular calcium in colonic smooth muscle.

Intracellular calcium [Ca2+]i measurements in cell suspension of gastrointestinal myocytes have suggested a single [Ca2+]i transient followed by a steady-state increase as the characteristic [Ca2+]i response of these cells. In the present study, we used digital video imaging techniques in freshly dispersed myocytes from the rabbit colon, to characterize the spatiotemporal pattern of the [Ca2+]i signal in single cells. The distribution of [Ca2+]i in resting and stimulated cells was nonhomogeneous, with gradients of high [Ca2+]i present in the subplasmalemmal space and in one cell pole. [Ca2+]i gradients within these regions were not constant but showed temporal changes in the form of [Ca2+]i oscillations and spatial changes in the form of [Ca2+]i waves. [Ca2+]i oscillations in unstimulated cells (n = 60) were independent of extracellular [Ca2+] and had a mean frequency of 12.6 +/- 1.1 oscillations per min. The baseline [Ca2+]i was 171 +/- 13 nM and the mean oscillation amplitude was 194 +/- 12 nM. Generation of [Ca2+]i waves was also independent of influx of extracellular Ca2+. [Ca2+]i waves originated in one cell pole and were visualized as propagation mostly along the subplasmalemmal space or occasionally throughout the cytoplasm. The mean velocity was 23 +/- 3 microns per sec (n = 6). Increases of [Ca2+]i induced by different agonists were encoded into changes of baseline [Ca2+]i and the amplitude of oscillations, but not into their frequency. The observed spatiotemporal pattern of [Ca2+]i regulation may be the underlying mechanism for slow wave generation and propagation in this tissue. These findings are consistent with a [Ca2+]i regulation whereby cell regulators modulate the spatiotemporal pattern of intracellularly generated [Ca2+]i oscillations.

Animals↗
PubMed1992

Structural aspects of the gastric H,K-ATPase.

The gastric H,K-ATPase is an alpha, beta heterodimer. The large catalytic subunit is composed, in the case of the hog enzyme, of 1033 amino acids, whereas the beta subunit is composed of about 291 amino acids and is heavily glycosylated. The membrane topology of the alpha subunit is difficult to predict using hydropathy analysis. Tryptic hydrolysis of intact, inside out vesicles followed by cysteine labelling with fluorescein-5-maleimide provided experimental evidence for an 8 membrane spanning model for the alpha subunit, between residues 104 and 162 (M1/M2), 291 and 358 (M3/M4), 776 and 835 (M5/M6), and 853 and 946 (M7/M8). No evidence was found for a pair of segments (M9/M10) towards the C terminal end of the molecule, contrary to predictions for the Na,K- and Ca-ATPases. Iodination of intact vesicles followed by carboxypeptidase Y cleavage of the C terminal tyrosines showed that the C terminal end of the alpha subunit was cytoplasmic. The epitope for antibody 146 was extracytoplasmic and located between residues 871 to 874 between M7/M8. The binding site of the K competitive imidazo-pyridine, SCH28080, was to the extracytoplasmic loop between M1 and M2, whereas the binding of the covalent SH reagent generated from acid activation of omeprazole in acid transporting vesicles was to 2 cysteines at positions 813 (or 822) and 892 predicted to be in the extracytoplasmic loops connecting M5/M6 and M7/M8, respectively. The beta subunit was only hydrolysed in broken vesicles. A fragment beginning at position 236 was liberated under these conditions only in the presence of reducing agents, showing that cysteine 210 and 263 were disulfide linked.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1992

The muscarinic receptor gene expressed in rabbit parietal cells is the m3 subtype.

To investigate the nature of the muscarinic receptors present on parietal cell membranes, binding studies and polymerase chain reaction (PCR) amplification of parietal cell messenger (m) RNA were undertaken. Displacement of N-[3H]methylscopolamine by various muscarinic antagonists showed displacement with a single affinity. The apparent dissociation constant values were as follows: atropine (nonselective), 1.95 +/- 0.28 nmol/L; pirenzepine (M1), 169 +/- 24 nmol/L; AF-DX 116 (M2), 1542 +/- 33 nmol/L; and hexahydrosiladifenidol (M3), 29 +/- 3.4 nmol/L. These data confirmed the existence of only an M3 receptor linked to acid secretion as defined pharmacologically. PCR amplification of parietal cell mRNA with primers designed for detection of all known muscarinic receptor subtypes showed that only m3 fragments were produced from parietal cell mRNA, whereas m1 and m2 products could be detected in brain or cardiac mRNA. The m3 nature of the PCR product was confirmed by Southern blotting with 32P-labeled human m3 complementary DNA. Hence the two carbachol affinities and the separable cellular responses following muscarinic activation are caused by separate coupling pathways of the M3 receptor.

Animals↗
PubMed1992

Characterization of large-conductance chloride channels in rabbit colonic smooth muscle.

1. A large-conductance Cl- channel was characterized in cell-free membrane patches from the rabbit longitudinal colonic smooth muscle using the patch clamp technique. In addition, the regulation of these channels by neurokinin-1 (NK-1) receptor agonists and G proteins was studied. 2. No spontaneous channel activity was observed in cell-attached patches at the cell resting potential, or in excised patches at pipette potentials (Vp) between -20 and 20 mV. In excised patches, channel activity could be induced in thirty-six out of ninety-six patches by holding the patch at Vp values more negative than -60 mV or more positive than 60 mV. Once induced, the channel showed a bell-shaped voltage activation curve in high symmetric [Cl-], with maximal open probability between 20 and -5 mV. Varying cytosolic calcium concentration ([Ca2+]) between 5 x 10(-8) M and 1.0 mM had no effect on the voltage activation of the channel. 3. In inside-out and outside-out patches, when pipette and bath solutions contained equal [Cl-] (130 mM), the anion channel showed a linear current-voltage (I-V) relationship between -60 and 60 mV with a slope conductance of 309 +/- 20 pS (n = 13). Reversal potential measurements indicated that the channel was selective for Cl- over Na+ and K+ (PCl/PNa = 6:1). 4. Channel openings from the closed state to the full open state as well as transitions through smaller conductance states were observed. The smallest detectable substate had a conductance of 15.6 pS. Based on the similarities in selectivity and linearity of the I-V curve of the smaller conductances with the full open state, and kinetic analysis of channel activity, it is concluded that the large conductance channel is composed of multiple substates which can either open and close independently, or simultaneously via a main gate. 5. The stilbene derivative diiso-thiocyanato-stilbene-disulphonic acid (DIDS) and the diphenylamine-2-carboxylate analogue 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB) caused a dose-dependent, reversible flicker block of the small conductance and significantly reduced the macroscopic current flow through the channel. 6. In quiescent outside-out patches, when the pipette contained a 140 mM-CsCl solution with 10(-6) M-CaCl2, 1.2 mM-MgCl2 and 1 mM-GTP, and the bath contained Ringer solution, addition of the NK-1 receptor antagonists substance P methylester resulted in activation of the full conductance state and of smaller substates.(ABSTRACT TRUNCATED AT 400 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗