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PubMed1991

Effects of sodium bicarbonate and potassium chloride drinking water supplementation. 2. Meat and carcass characteristics of broilers grown under thermoneutral and cyclic heat-stress conditions.

Two broiler trials were conducted to investigate the effect on post-mortem carcass and meat quality of NaHCO3 and KCl drinking water supplementation under thermoneutral and cyclic heat-stress climatic conditions. Water chill carcass weight change, water- and oven-cooked breast filled yields, and breast meat tenderness were measured. In Trial 1, neither environmental regimen, nor water treatments, nor their interaction was a significant (P less than .05) source of variation for the parameters measured. In Trial 2, environmental regimen was a highly significant (P less than .01) source of variability for chilled carcass weight change; the cyclic heat-stressed broiler carcasses gained more weight than the thermoneutral (control) broiler carcasses during ice-water chilling. Oven-cooked fillet yield was significantly (P less than .05) affected by environmental regimen; fillets from cyclic heat-stressed broilers had lower yields than thermoneutral (control) broiler fillets. Drinking water treatments were a significant (P less than .05) source of variation for breast meat tenderness in Trial 2. Broilers given .5% NaHCO3 from 5 to 8 wk of age had higher shear resistance values than broilers given a combination of .5% NaHCO3 and .5% KCl or tap water-fed controls. Breast meat shear values were negatively correlated (P less than .05) with 8-wk broiler body weight and 5- to 8-wk gain.

Analysis of Variance↗
PubMed1991

Different potency of endothelium-derived relaxing factors against thromboxane, endothelin, and potassium chloride in intramyocardial porcine coronary arteries.

Endothelium-derived relaxing factors (EDRFs) and prostacyclin (PGI2) released from endothelial cells are potent vasodilators; endothelin-1 and thromboxane A2 may be their physiological antagonists. Interactions between these vasodilators and vasoconstrictors were studied in isolated intramyocardial porcine coronary arteries suspended in myographs for isometric tension recording. Endothelium-dependent relaxations to bradykinin and serotonin were reduced to a similar extent in arteries contracted with endothelin-1 and KCl as compared to those contracted with the thromboxane analog U 46619 (p less than 0.05; n = 5-6). In contrast, relaxations to the nitric oxide donor SIN-1 were comparable. PGI2 was most potent in arteries exposed to U 46619, while its effects were inhibited in the presence of endothelin-1 or acetylcholine and prevented by KCl (p less than 0.05-0.0001; n = 5). At high concentrations PGI2 evoked contractions in arteries contracted with endothelin-1, acetylcholine, or KCl, but not in those with U 46619, which were prevented by the thromboxane receptor antagonist SQ 30741 (p less than 0.05; n = 5), indicating that PGI2 is a partial agonist for the thromboxane receptor. Thus, in intramyocardial porcine coronary arteries, contractile agonists differently interact with the release and action of EDRFs and PGI2. Both are most effective against contractions induced by thromboxane. In contrast, endothelin-1 and particularly KCl reduce the potency of these endogenous vasodilator systems.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1977

Leukocyte migration inhibition in patients with Ewing's sarcoma by 3-M potassium chloride extracts of fresh and tissue-cultured Ewing's sarcomas.

Leukocyte migration inhibition (LMI) assays were performed to detect cell-mediated immune reactions against tumor-associated antigens (TAA) of Ewing's sarcoma. With the use of crude antigen preparations obtained by 3M KCl extractions of fresh Ewing's sarcoma or of tissue culture cells derived from a pleural effusion of a Ewing's sarcoma patient, assays were performed with leukocytes from these patients, patients with other cancers, and normal donors. The results demonstrated approximately 60% or greater positive LMI reactivity in Ewing's sarcoma patients, as compared to less than 10% reactivity of normal donors, with the use of extracts of either fresh or tissue-cultured Ewing's sarcoma cells. A lower proportion of positive reactivity was observed in patients with breast and lung cancer. Further specificity tests indicated that a smaller proportion of patients with Ewing's sarcoma had LMI reactivity with KCl extracts of tissue-cultured cells derived from breast cancer of fresh lung cancer cells than did patients with the homologous disease. The results indicate that many patients with Ewing's sarcoma have cell-mediated immunity toward TAA on Ewing's sarcomas. Inasmuch as all the LMI assay were performed with allogeneic extracts, the data also suggested that different Ewing's sarcomas possess common antigens and that some breast and lung cancers may share some TAA with Ewing's sarcoma.

Antigens, Neoplasm↗
PubMed1991

Effects of sodium bicarbonate and potassium chloride drinking water supplementation. 1. Performance and exterior carcass quality of broilers grown under thermoneutral or cyclic heat-stress conditions.

Two broiler trials were conducted using two environmentally controlled chambers. From 4 to 8 wk of age in Trial 1, and from 5 to 8 wk of age in Trial 2, male broilers were grown under either constant environmental conditions [25 C, 50% relative humidity (RH)], or a daily cyclic heat stress period (4 h of 35 to 38 C, 40% RH). One of four water solutions was provided to each of 16 pens per chamber: 1) 5% NaHCO3: 2) .5% KCl; 3) .5% KCl and NaHCO3, or 4) an unsupplemented control of tap water. Seven-wk body weight, 8-wk weight, weight gain, water consumption, infected feather follicle score, prekill and carcass without giblets weight were all significantly (P less than .05) affected by environmental treatment in both trials. In Trial 1, a significant effect due to water treatment was detected for infected feather follicle score, with control broilers significantly less afflicted than broilers on the other three water treatments. In Trial 2, a significant (P less than .05) temperature treatment effect was detected for abdominal fat pad weight, where differences in fat pad weight were found among water treatments under constant conditions but not under cyclic environmental conditions. These differences in fat pad weight, when expressed as a percentage of carcass weight, were at a probability of .0814. Overall, no appreciable improvements were detected in the broiler production parameters measured under either environmental regimen for the water treatments tested.

Animals↗
PubMed1995

Potassium chloride improves the thermotolerance of chickens exposed to acute heat stress.

Experiments were designed to test the hypothesis that chicks that drank an electrolyte solution containing K prior to and during an acute exposure to heat would have greater thermotolerance than chicks that consumed only water. In three experiments, 5- or 7-wk-old male chickens drank distilled water (control), or .3, .6, or .9% KCl solutions (Experiments 1 and 2), and .6 or .9% KCl or .8% KHCO3 solutions (Experiment 3) for 48 h before acute heat stress (HS) and during HS. Body temperature (Tb), blood pH, partial pressure of blood carbon dioxide (pCO2), ionized Ca (Ca2+), plasma Na, K, Cl, total Ca, inorganic P (Pi), and osmolality (Osm), and water consumption were determined. Water intake increased with the concentration of KCl. Before HS, .6% KCl increased plasma K and Ca2+, whereas .9% KCl resulted in a marked increase in K, Ca2+, Na, Cl, and Osm and a decrease in pH. During HS, .6% KCl-birds had lower hyperthermic Tb and pH values and higher Ca2+ and K concentrations than controls. Plasma Na and Osm of .6% KCl birds decreased whereas those of the control birds remained unchanged. Providing K as KHCO3 aggravated respiratory alkalosis and failed to influence either Tb or plasma electrolytes, suggesting that the beneficial effect of .6% KCl may in part be attributed to the accompanying Cl. Hyperthermic Tb and Ca2+ values were highly correlated. The results showed that .6% KCl solution reduced HS-related responses and indicated a relationship among supplemental KCl, blood Ca2+, and Tb.

Acid-Base Equilibrium↗
PubMed1975

Effects of potassium chloride and smooth muscle relaxants on tension and cyclic nucleotide levels in rat myometrium.

Ten minutes after KCl-depolarization of rat myometrial strips, at which time the muscles were in a state of sustained contracture, tissue levels of adenosine 3',5'-cyclic monophosphate (cyclic AMP) were increased by approximately 40% over relaxed controls, and levels of guanosine 3',5'-cyclic monophosphate (cyclic GMP) were decreased by 40%. At this point both nitroglycerin (4 X 10(-4) M) and papaverine (2 X 10(-5) M) were capable of relaxing the depolarized muscles without significantly increasing cyclic AMP levels. Isoproterenol, in concentrations from 5 X 10(-9) M to 10(-6) M, relaxed the depolarized muscles and significantly increased tissue levels of cyclic AMP. However, the magnitudes of the cyclic AMP increases seen after the lower concentrations of isoproterenol were small relative to the increases observed during KCl-contracture alone. For example, the 40% elevation of cyclic AMP seen 10 min after KCl-depolarization did not cause the muscles to relax, whereas 5 X 10(-9) M isoproterenol caused relaxation with an increase in cyclic AMP levels of only 16% over depolarized controls. It was concluded that changes in total tissue levels of cyclic AMP were not responsible for the uterine relaxation caused by nitroglycerin, papaverine or isoproterenol in these experiments. Cyclic GMP levels in the depolarized muscles were not significantly changed by isoproterenol or papaverine but were increased approximately 80% by nitroglycerin. The above results are not consistent with the previously suggested roles for cyclic GMP and cyclic AMP as mediators of smooth muscle contraction and relaxation, respectively.

Animals↗
PubMed1977

The oral apparatus of Tetrahymena pyriformis, strain WH-6. IV. Observations on the organization of microtubules and filaments in the isolated oral apparatus and the differential effect of potassium chloride on the stability of oral apparatus microtubules.

This report is an ultrastructural analysis of the organization of the isolated oral apparatus of Tetrahymena pyriformis, strain WH-6, syngen 1. Attention has been focused on the organization of microtubules and filaments in oral apparatus membranelles. Oral apparatus membranellar basal bodies were characterized with respect to structural differentiations at the distal and proximal ends. The distal region of membranellar basal bodies contains the basal plate, accessory microtubules and filaments. The proximal end contains a dense material from which emanate accessory microtubules and filaments. There are at least two possibly three different arrangements of accessory structures at the proximal end of membranellar basal bodies. All membranellar basal bodies appear to have a dense material at the proximal end from which filaments emanate. Some of these basal bodies have accessory microtubules and filaments emanating from this dense material. A possible third arrangement is represented by basal bodies which have lateral projections, from the proximal end, of accessory microtubules and filaments which constitute cross or peripheral connectives. There are at least three examples of direct associations between oral apparatus microtubules and filaments: (1) filaments which form links between basal body triplet microtubules, (2) filaments which link the material of the basal plate to internal basal body microtubules, (3) filaments which link together microtubule bundles from membranellar connectives. KCl extraction of the isolated oral apparatus resulted in the selective solubilization of oral apparatus basal bodies, remnants of ciliary axonemes and fused basal plates. Based on their response to KCl extraction two distinct sets of morphologically similar micro tubules can be identified: (a) microtubules which constitute the internal structure of basal bodies and ciliary axonemes, (b) microtubules which constitute the fiber connectives between basal bodies.

Animals↗
PubMed1970

Effect of potassium chloride on the uptake and storage of phosphate by Saccharomyces mellis.

The inorganic and polyphosphate pools of Saccharomyces mellis, grown in a medium containing excess phosphate, remain associated with the cells when the cells are suspended in a saline medium. If the cells are incubated in a medium containing 2 m KCl, the cells are altered in some manner which permits most of the orthophosphate and approximately one-third of the polyphosphate to be subsequently eluted by osmotic shock. At lower salt concentrations, beta-mercaptoethanol enhances this salt effect but is inactive by itself in this respect. At equivalent ionic strengths, the sodium salt of ethylenediaminetetraacetic acid behaves exactly like KCl or any other monovalent ionic compound in altering the cell to susceptibility to osmotic shock. No special effect of this anion at either high or low concentration could be detected. Resting cells are refractory to being altered in this manner by salts if an energy source, such as glucose, is included in the reaction mixture. Cells which are depleted of phosphate reserves will immediately incorporate phosphate when suspended in a medium containing inorganic phosphate and an energy source. These cells exhibit the phenomenon of "überkompensation." In resting cells, the inclusion of KCl in the reaction mixture prevents the conversion of orthophosphate into polyphosphate and, also, gradually decreases the ability of the organism even to assimilate orthophosphate. This effect is reversible, however, since the cells will incorporate phosphate in a normal manner if the cells are transferred to a non-salinized medium, or if a nitrogen source is included in the salinized reaction mixture so that the cells are now in a medium adequate for growth.

Acid Phosphatase↗
PubMed1993

Induction of cortical spreading depression with potassium chloride upregulates levels of messenger RNA for glial fibrillary acidic protein in cortex and hippocampus: inhibition by MK-801.

The present study evaluates the time course and spatial extent of changes in GFAP mRNA expression following the induction of spreading depression. Spreading depression was elicited by applying filterpaper pledgets soaked in KCl (3 M) to exposed parietal cortex for ten minutes. Animals were killed 1.5, 3, 6, 12, 24, 48, 96 and 192 h post-KCl application, and the forebrains were prepared for quantitative in situ hybridization. The KCl treatment led to a many-fold increase in GFAP mRNA content in the ipsilateral hippocampus and neocortex and, to a lesser extent, in the contralateral hippocampus, but did not affect GFAP mRNA levels in the contralateral cortex or in the thalamus. The time course of increased expression of GFAP mRNA in the hippocampus differed markedly from that of the cortex. In the hippocampus, GFAP mRNA levels rose rapidly to a maximum at 24 h post-exposure, then fell rapidly. In the cortex, levels rose more slowly and did not reach a maximum until 4 days post-exposure. Analysis of GFAP mRNA levels by dot blot hybridization using samples from a separate set of animals killed at one and 4 days following the KCl exposure confirmed both the upregulation in GFAP mRNA levels and the regional time course differences. Intraperitoneal injection of MK-801, a non-competitive NMDA antagonist which prevents spreading depression, blocked the upregulation of GFAP mRNA in both the hippocampus and the cortex, as demonstrated by both in situ and dot blot hybridization. The results suggest that the physiological changes accompanying spreading depression have a powerful influence on glial cell gene expression.

Animals↗
PubMed1988

Norepinephrine and adenosine triphosphate release in different ratio from guinea pig vas deferens by high potassium chloride, ouabain and monensin.

Release of norepinephrine (NE) and ATP from the guinea pig vas deferens evoked by ouabain in combination with monensin or by high KCl was measured by a high-pressure liquid chromatography-ECD and luciferin-luciferase assay, respectively. Ouabain (10-100 microM) induced a concentration-dependent liberation of NE, which was enhanced by 10 microM monensin, a Na+-ionophore. The marked NE release elicited by the combined administration of both the drugs was unaffected by Ca++-removal but was reduced by lowering Na+ from the medium. This NE release in the Ca++-free medium was diminished markedly after treatment with 6-hydroxydopamine or reserpine and in low-temperature (25 degrees C) medium. This release was also decreased by ruthenium red (10-30 microM), an uptake inhibitor of Ca++ to mitochondria, and carbonyl cyanide-m-chlorophenyl hydrazone (10 microM), a metabolic inhibitor. On the other hand, 100 mM KCl caused a moderate, extracellular Ca++-dependent release of NE. ATP-outflow from the tissue evoked by 100 microM ouabain plus 10 microM monensin was almost unaltered by Ca++-removal but was inhibited by 6-hydroxydopamine or prazosin (0.3 microM), whereas release induced by high KCl was reduced by 6-hydroxydopamine and Ca++-free medium but was unaffected by prazosin. ATP/NE ratios at respective maximum effluxes evoked by 100 mM KCl and ouabain plus monensin were 6.59 and 0.22, respectively. These findings suggest that there may be more than one site of corelease for NE and ATP. Ouabain plus monensin seems to produce an extracellular Ca++-independent neuronal release of NE and ATP from the cytoplasmic and vesicular storage sites which predominantly release NE.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1984

Differential extraction of tumor-specific transplantation antigen and embryonic antigen from simian virus 40- and adenovirus 7-induced sarcoma cells of hamsters with 1-butanol and 3 M potassium chloride.

Simian virus 40 (SV40)-induced sarcomas and adenovirus 7-induced sarcomas (Adv-7) exhibit both specific tumor-specific transplantation antigens (TSTA) and cross-protective embryonic antigens at the cell surface in the LAK:LVG(SYR) strain of Syrian golden hamsters. Specific SV40 TSTA could be released from the surfaces of living hamster sarcoma cells in a 2.5% crude 1-butanol extract (CBE) and served as immunogen to protect syngeneic recipients against subsequent homologous but not heterologous tumor cell challenge. The CBE-extracted SV40-induced TSTA (tumor-specific) was observed to be free of detectable, cross-protective embryonic antigens (EA) by tumor transplantation assays. The induction of cytotoxic lymphocyte-mediated immunity with the CBE-released TSTA was dependent on the administration of a single sensitizing injection of 12-20 micrograms antigen protein. Higher concentrations (50-1,000 micrograms) of the CBE tumor cell extract, given in a single injection, enhanced tumor growth as did two injections of 12.5 micrograms CBE-extracted SV40-induced TSTA at 1-week intervals. A cross-protective antigen(s), not detected in the CBE tumor extracts, was retained in the intact, 1-butanol-extracted SV40 and Adv-7-induced tumor cell lines after completion of the CBE extraction procedure and in similarly extracted 10-day hamster fetal cells. Some alterations in the normal immunogenicity of EA extracted with CBE followed by KCI from SV40-induced sarcoma cells could be detected in the transplantation assays and lymphocyte transformation assays, whereas EA extracted from CBE-KCI-treated Adv-7 cells or 10-day hamster fetal cells retained normal immunogenicity in vivo and in vitro. These procedures provide a means for successful separation of immunogenic SV40- and Adv-7-induced TSTA from detectable, biologically active, cross-protective EA from the surfaces of these sarcoma cells.

1-Butanol↗
PubMed2006

Interstitial cystitis versus detrusor overactivity: a comparative, randomized, controlled study of cystometry using saline and 0.3 M potassium chloride.

PURPOSE: We compared cystometric findings in interstitial cystitis and detrusor overactivity using 0.3 M KCl and 0.9% normal saline. MATERIALS AND METHODS: Female patients with established diagnoses of IC (7 patients according to NIDDK criteria) and urodynamically proven DO (10 patients) underwent consecutive cystometrograms using 0.9% normal saline and 0.3 M KCl, the order of which was randomized for each patient. Individual CMGs were performed by separate investigators, and patients and investigators were blinded to the order in which the solutions were used and to the results of the other CMG. The results were analyzed on a comparative basis using a 2-tailed t test for comparison of the means and a Kolmogorov-Smirnov z test was used for group comparison. A ROC curve was used to plot sensitivity to the false-positive rate. RESULTS: Irrespective of the diagnosis or the type of infusion used, the volume at FDV was slightly lower with the first CMG compared to the second (mean 76.1 vs 94.2 ml) but did not reach statistical significance (p = 0.20). However, Cmax was similar for first and second CMGs (mean 214 vs 213.2 ml, p = 0.98). Although lower with KCl, there was no significant difference in FDVs obtained with either solution (mean 78.2 vs 92.2 ml for KCl and NS, respectively, p = 0.33). However, KCl produced a significant reduction in Cmax across the whole group (mean 244.5 vs 182.7 ml, p = 0.008). This was most marked in the DO group in which there was a 23% reduction in Cmax with KCl compared to NS, while the IC group showed only a 15% reduction in mean Cmax. The ROC curve, comparing Cmax values for NS with KCl cutoff values of 15% and 30%, resulted in poor positive predictive values (51% and 66%, respectively) for comparative cystometry in distinguishing IC from DO. CONCLUSIONS: The 0.3 M KCl reduces Cmax in IC and DO, the effect being more pronounced in DO. Urothelial hyperpermeability is not specific to IC. Comparative cystometry using NS and 0.3 M KCl does not help to differentiate IC from DO.

Adult↗
PubMed1975

Characterization of an inhibitor causing potassium chloride sensitivity of an RNA polymerase from T4 phage-infected Escherichia coli.

The nature of the inhibition by salt (KCl) of DNA-dependent RNA polymerase from T4 phage-infected Escherichia coli (T4 enzyme) was studied using holoenzyme preparations, core enzyme and sigma fractions obtained by phosphocellulose column chromatography, and sigma fractions further purified by gradient centrifugation in the presence and absence of 6 M urea. We showed with holoenzyme preparations that salt inhibits the formation of rifampicin-resistant preinitiation complexes. The inhibition was considerably reduced when a nonionic detergent (particularly of the Triton series) was included in the reaction mixtures. With T4 core enzyme and T4 sigma fractions together with the same fractions from uninfected cells (host enzyme fractions) and different DNA templates, we showed that the T4 sigma fraction plays a role in the salt-sensitive activity with T4 DNA. The salt sensitivity of the T4 sigma fraction was antagonized by Triton; it was not a function of sigma fractions isolated from phage cultures infected in the presence of chloramphenicol. As reported previously (Stevens, A. (1973), Biochem. Biophys. Res. Commun. 54, 488), the T4 sigma fraction inhibited the activity of host sigma when they were present together in reaction mixtures, particularly in the presence of salt. T4 sigma further purified by centrifugation in glycerol gradients had the same properties as the cruder fraction, and the T4-specific polypeptide of mol wt 10000 (Stevens, A. (1972), Proc. Natl. Acad. Sci. U.S.A. 69, 603) was found in the same fractions. If the glycerol gradients contained 6 M urea, the mol wt 10000 polypeptide was separated from the salt-stimulated sigma. Fractions containing the small polypeptide could be added back to produce the salt-inhibitory effects. The inhibitory activity of both the crude sigma fraction and the fractions containing the small polypeptide was inactivated at 65 degrees C. The results suggest that the mol wt 10000 protein is a salt-promoted inhibitor, but the small amounts of it which are present in purified fractions of the T4 enzyme have not yet allowed its isolation in large enough quantities to permit a detailed study of its properties.

Coliphages↗
PubMed1987

Mechanism of norepinephrine release elicited by renal nerve stimulation, veratridine and potassium chloride in the isolated rat kidney.

We have investigated the mechanism by which renal nerve stimulation (RNS), veratridine (Vt) and KCl promote release of norepinephrine in the isolated rat kidney perfused with Tyrode's solution and prelabeled with [3H]norepinephrine by examining the overflow of tritium elicited by these stimuli during 1) extracellular Ca++ depletion, 2) alterations in extracellular Na+ concentration and 3) administration of tetrodotoxin, amiloride, LiCl and calcium channel blockers. RNS (1-4 Hz), Vt (15-90 nmol) and KCl (150-500 mumol) produced renal vasoconstriction and enhanced the tritium overflow in a frequency- and concentration-dependent manner, respectively. Omission of Ca++ (1.8 mM) from the perfusion fluid abolished the renal vasoconstriction and the increase in tritium overflow elicited by RNA and KCl and substantially reduced that caused by Vt. Lowering the Na+ concentration in the perfusion medium (from 150 to 25 mM) reduced the overflow of tritium and the renal vasoconstriction caused by RNS (2 Hz) or Vt (45 nmol); the increase in tritium overflow in response to these stimuli was positively correlated with extracellular Na+ (25-150 mM). In contrast, KCl-induced tritium overflow was negatively correlated with extracellular Na+ concentration. Tetrodotoxin (0.3 microM) abolished the effect of RNS and Vt, but not that of KCl, to increase overflow of tritium and to produce renal vasoconstriction. Administration of amiloride (180 microM) enhanced the overflow of tritium but attenuated the associated renal vasoconstriction produced by RNS, Vt and KCl. Replacement of NaCl (75 mM) with equimolar concentration of LiCl enhanced the overflow of tritium elicited by RNS, Vt and KCl; the associated renal vasoconstriction remained unaltered. Administration of Ca++ channel blocker, flunarizine (2 microM), but not diltiazem (6 microM) or nifedipine (1.4 microM), inhibited RNS-, Vt- and KCl-induced overflow of tritium; nifedipine enhanced whereas diltiazem failed to alter tritium overflow elicited by these stimuli. The renal vasoconstriction produced by RNS, Vt and KCl was inhibited by diltiazem and nifedipine, as well as by flunarizine. These data suggest that RNS, Vt and KCl enhance release of the adrenergic transmitter by promoting influx of Ca++ into the nerve terminal, not by Na+-Ca++ exchange transport process, but rather through specific Ca++ channels that are distinct from those located in the vascular smooth muscle.

Amiloride↗
PubMed1984

Effects of acetylcholine and caerulein on 86Rb+ efflux in the mouse pancreas. Evidence for a sodium-potassium-chloride cotransport system.

The effects of acetylcholine and the cholecystokinin-like peptide, caerulein on the fractional efflux of 86Rb+ from preloaded isolated segments of mouse pancreas were studied. Both secretagogues evoked a marked transient increase in 86Rb+ efflux. The removal of Ca2+ from the superfusing medium and addition of 10(-4) M EGTA, markedly reduced, but did not abolish the responses to either acetylcholine or caerulein. Furosemide (10(-5)-10(-3) M) or piretanide (10(-4) M) reduced the basal efflux and inhibited the secretagogue-elicited responses. Stimulus-induced 86Rb+ outflow was abolished when the Cl- component of the superfusing solution was replaced by either NO3-, SO42- or I- but not in case of replacement by Br-. When Na+ was replaced with either Li+ or choline+ both acetylcholine and caerulein failed to elicit any detectable increase in 86Rb+ outflow. However, when Tris+ was substituted for Na+, acetylcholine caused a moderate increase in 86Rb+ efflux which was abolished by either furosemide (10(-4) M) or chloride depletion (nitrate substitution). The removal of extracellular K+ or pretreatment with 10(-3) M ouabain had little effect on secretagogue-evoked 86Rb+ efflux. These results indicate the presence of a diuretic-sensitive Na+-K+-Cl- cotransport system in the mouse pancreatic acinar cell membrane.

Acetylcholine↗