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Ketogenesis in the living rat followed by carbon-13 NMR spectroscopy (1984)

Cross, T. A. ; Pahl, C. ; Oberhaensli, R. ; [et al.]

s.l. : American Chemical Society

Biochemistry 23 (1984), S. 6398-6402

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ISSN: 1520-4995

Source: ACS Legacy Archives

Topics: Biology , Chemistry and Pharmacology

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1021/bi00321a018

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Ubergangsmetall-methylen-komplexe - IXL. Uber metallzentrierte umlagerungsreaktionen von diazoalkanen und die einfache synthese von alkylidenamido- sowie isocyanato-komplexen

Herrmann, W.A. ; Bell, L.K. ; Ziegler, M.L. ; [et al.]

Amsterdam : Elsevier

Journal of Organometallic Chemistry 247 (1983), S. 39-60

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ISSN: 0022-328X

Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Topics: Chemistry and Pharmacology

Type of Medium: Electronic Resource

URL: http://linkinghub.elsevier.com/retrieve/pii/S0022-328X(00)98829-6

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Effect of secretin and inhibitors of HCO3 −/H+ transport on the membrane voltage of rat pancreatic duct cells (1993)

Novak, I. ; Pahl, C.

Springer

Pflügers Archiv 425 (1993), S. 272-279

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ISSN: 1432-2013

Keywords: Pancreas ; Ducts ; Secretin ; Acetate ; NH4 +/NH3 ; EIPA ; DIDS ; Ethoxzolamide ; K+ conductance

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract The aim of the present study was to study the effect of secretin on the electrophysiological response of pancreatic ducts. Furthermore, we investigated the effects of lipid-soluble buffers and inhibitors of HCO3 −/H+ transport. Ducts obtained from fresh rat pancreas were perfused in vitro. Secretin depolarized the basolateral membrane voltage, V bl, by up to 35 mV (n=37); a halfmaximal response was obtained at 3×10−11 mol/l. In unstimulated ducts a decrease in the luminal Cl− concentration (120 to 37 mmol/l) had a marginal effect on V bl, but after maximal secretin stimulation it evoked a 14±2 mV depolarization (n=6), showing that a luminal Cl− conductance G Cl- was activated. The depolarizing effect of secretin on V bl was often preceded by about a 6 mV hyperpolarization, most likely due to an increase in the basolateral G K+. Perfusion of ducts with DIDS (4,4′ — diisothiocyanatostilbene — 2,2′ — disulphonic acid, 0.01 mmol/l) or addition of ethoxzolamide (0.1 mmol/l) to the bath medium diminished the effect of secretin. Acetate or pre-treatment of ducts with NH4 +/NH3 (10 mmol/l in the bath) depolarized the resting V bl of −65±2 mV by 16±4 mV (n=7) and 19±3 mV (n=10), respectively. The fractional resistance of the basolateral membrane (FR bl) doubled, and the depolarizing responses to changes in bath K+ concentrations (5 to 20 mmol/l) decreased from 22±1 to 11±2 mV. The Na+/H+ antiporter blocker EIPA (5-[N-ethyl-N-isopropyl]-amiloride, 0.1 mmol/l) also depolarized V bl by 10±1 mV, FRbl increased and the response to K+ concentration changes decreased (n=7). Effects of EIPA and ethoxzolamide on V bl were greater in ducts deprived of exogenous HCO3 −/CO2. Taken together, the present study shows that secretin increased the basolateral G K+ and the luminal G Cl-. The depolarizing effect of secretin was diminished following inhibition of HCO3 − transport (DIDS), or HCO3 −/H+ generation (ethoxzolamide). Manoeuvres that presumably led to lowered intracellular pH (NH4 +/NH3 removal, acetate, EIPA) decreased the basolateral G K+. The present data support our previously published model for pancreatic HCO3 − secretion, and indicate that the basolateral membrane possesses a pH-sensitive G K+.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00374178

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Effect of ATP, carbachol and other agonists on intracellular calcium activity and membrane voltage of pancreatic ducts (1994)

Hug, M. ; Pahl, C. ; Novak, I.

Springer

Pflügers Archiv 426 (1994), S. 412-418

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ISSN: 1432-2013

Keywords: Pancreatic ducts ; Fura-2 ; Intracellular Ca2+ ; Membrane voltage ; ATP ; Carbachol ; Neurotensin ; Bombesin

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract The pancreatic duct has been regarded as a typical cAMP-regulated epithelium, and our knowledge about its Ca2+ homeostasis is limited. Hence, we studied the regulation of intracellular calcium, [Ca2+]i, in perfused rat pancreatic ducts using the Ca2+-sensitive probe fura-2. In some experiments we also measured the basolateral membrane voltage, V bl, of individual cells. The resting basal [Ca2+]i was relatively high, corresponding to 263±28 nmol/l, and it decreased rapidly to 106±28 nmol/l after removal of Ca2+ from the bathing medium (n=31). Carbachol increased [Ca2+]i in a concentration-dependent manner. At 10 μmol/l the fura-2 fluorescence ratio increased by 0.49±0.06 (n=24), corresponding to an increase in [Ca2+]i by 111±15 nmol/l (n=17). ATP, added to the basolateral side at 0.1 mmol/l and 1 mmol/l, increased the fluorescence ratio by 0.67±0.06 and 1.01±14 (n=46; 12), corresponding to a [Ca2+]i increase of 136±22 nmol/l and 294±73 nmol/l respectively (n= 15; 10). Microelectrode measurements showed that ATP (0.1 mmol/l) hyperpolarized V bl from −62±3 mV to-70±3 mV, an effect which was in some cases only transient (n=7). This effect of ATP was different from that of carbachol, which depolarized Vbl. Applied together with secretin, ATP delayed the secretin-induced depolarization and prolonged the initial hyperpolarization of V bl (n=4). Several other putative agonists of pancreatic HCO 3 − secretion were also tested for their effects on [Ca2+]i. Bombesin (10 nmol/l) increased the fura-2 fluorescence ratio by 0.24±0.04 (n=8), neurotensin (10 nmol/l) by 0.25±0.04 (n=6), substance P (0.1 μmol/l) by 0.22±0.06 (n=6), and cholecystokinin (10 nmol/l) by 0.14±0.03 (n=7). Taken together, our studies show that Ca2+ homeostasis plays a role in pancreatic ducts. The most important finding is that carbachol and ATP markedly increase [Ca2+]i, but their different electrophysiological responses indicate that intracellular signalling pathways may differ.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00388304

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Effect of vasoactive intestinal peptide, carbachol and other agonists on the membrane voltage of pancreatic duct cells (1993)

Pahl, C. ; Novak, I.

Springer

Pflügers Archiv 424 (1993), S. 315-320

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ISSN: 1432-2013

Keywords: Pancreas ; Ducts ; Cell membrane voltage ; Vasoactive intestinal peptide ; Carbachol ; Cholecystokinin ; Bombesin ; Neurotensin ; Substance P

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract The regulation of pancreatic exocrine secretion involves hormonal, neural and neurohormonal components. Many agonists are known to be effective in pancreatic acinar cells, but less is known about the ducts. Therefore, we wanted to investigate the influence of various agonists on isolated perfused pancreatic ducts and, as a physiological response, we measured the basolateral membrane voltage of the duct cells (V bl) with microelectrodes. Pancreatic ducts were dissected from pancreas of normal rats and bathed in a HCO3 −-containing solution. Under control conditions, the average V bl was between -50 and -70 mV. Vasoactive intestinal peptide (VIP) and carbachol (CCH) reversibly depolarized V bl when applied to the bath. VIP (9×10−9 mol/l) depolarized V bl from -72±3 mV to -53±3 mV (n=20) and CCH (10−5 mol/l) from -62±3 to -35±4mV (n=10). Furthermore, a decrease of the Cl− concentration in the lumen led to an increase of VIP-induced depolarization of V bl, suggesting that a luminal Cl− conductance was increased. Cholecystokinin (CCK, 10−10-10−7 mol/l) and bombesin (10−8, 10−5 mol/l), which stimulate pancreatic exocrine secretion in acini or whole glands, showed no significant effect on V bl of the duct cells tested in our preparation (n=7, 6). Neurotensin (10−8 mol/l) had a marked depolarizing effect in two out of ten cases; V bl depolarized from about -65 mV to-29 mV and the effect was reversible. Substance P (2×10−7 mol/l), alone or in combination with secretin, had no effect on V bl of the tested duct cells (n=11). We propose that the basolateral membrane of pancreatic duct cells possesses receptors for VIP, acetylcholine and neurotensin. CCK, bombesin and substance P had no detectable effects on V bl of the duct cells tested, which could be due to the lack of corresponding receptors on these cells, or due to the absence of electrophysiologically detectable effects, in spite of receptor presence.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00384358

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Calcium influx pathways in rat pancreatic ducts (1996)

Hug, M. J. ; Pahl, C. ; Novak, I.

Springer

Pflügers Archiv 432 (1996), S. 278-285

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ISSN: 1432-2013

Keywords: Key words Pancreatic ducts ; Intracellular Ca2+ ; Ca2+ influx ; Flufenamate ; Lanthanum ; pH ; ATP ; Carbachol

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract A number of agonists increase intracellular Ca2+ activity, [Ca2+]i, in pancreatic ducts, but the influx/efflux pathways and intracellular Ca2+ stores in this epithelium are unknown. The aim of the present study was to characterise the Ca2+ influx pathways, especially their pH sensitivity, in native pancreatic ducts stimulated by ATP and carbachol, CCH. Under control conditions both agonists led to similar changes in [Ca2+]i. However, these Ca2+ transients, consisting of peak and plateau phases, showed different sensitivities to various experimental manoeuvres. In extracellular Ca2+-free solutions, the ATP-induced [Ca2+]i peak decreased by 25%, but the CCH-induced peak was unaffected; both plateaus were inhibited by 90%. Flufenamate inhibited the ATP-induced peak by 35%, but not the CCH-evoked peak; the plateaus were inhibited by 75–80%. La3+ inhibited the ATP-induced plateau fully, but that induced by CCH by 55%. In resting ducts, an increase in extracellular pH, pHe, by means of HEPES and HCO3 −/CO2 buffers, increased [Ca2+]i; a decrease in pHe had the opposite effect. In stimulated ducts the pH-evoked effects on Ca2+ influx were more pronounced and depended on the agonist used. At pHe 6.5 both ATP- and CCH-evoked plateaus were inhibited by about 50%. At pH 8.0 the ATP-stimulated plateau was inhibited by 27%, but that stimulated by CCH was increased by 72%. Taken together, we show that CCH stimulates Ca2+ release followed by Ca2+ influx that is moderately sensitive to flufenamate, La3+, depolarisation, it is inhibited by low pH, but stimulated by high pH. ATP stimulates Ca2+ release and probably an early Ca2+ influx, which is more markedly sensitive to flufenamate and La3+, and is both inhibited by low and high pH. Thus our study indicates that there are at least two separate Ca2+ influx pathways in pancreatic ducts cells.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/s004240050134

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