Cellular mechanisms of adrenaline-induced hyperpolarization in renal epitheloid MDCK cells

Pfeilschifter, Josef; Paulmichl, Markus; Wöll, Ewald; Paulmichl, R; Läng, Florian

doi:10.1042/bj2740243

Cited by 14 publications

(9 citation statements)

References 46 publications

(30 reference statements)

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“…Phorbol esters similarly blunt the effect of bradykinin and epinephrine on IP3 formation and release of intracellular calcium (Aboolian et al, 1989;Lang et al, 1991;Pfeilschifter et al, 1991;Portilla et al, 1988a;Slivka and Insel, 1988). Thus, phorbol esters appear to generally inhibit phospholipase C. Since pretreatment with TPA blunts the ATP-induced rise of intracellular calcium both in the presence and absence of extracellular calcium, it interferes obviously with both release of intracellular calcium and entry of calcium across the cell membrane.…”

Section: Results Formation Of Inositol Phosphatesmentioning

confidence: 85%

“…In MDCK-cells-as in other cells (Boeynaems et al, 1988;Dubyak, 1986;Okajima et al, 1988;Tsuda et al, 1988)-the stimulation of phospholipase C involves obviously pertussis toxin sensitive G-proteins and can presumably be prevented by stimulation of protein kinase C with phorbolesters. Bradykinin, similar to ATP, activates phospholipase C in MDCK cells by a pertussis toxin sensitive mechanism (Portilla et al, 1988b;Lang et al, 1991), whereas epinephrine stimulated increase of IP3 formation is apparently not sensitive to pertussis toxin (Terman et al, 1987;Pfeilschifter et al, 1991). Obviously, phospholipase C is activated by both pertussis toxin insensitive and pertussis toxin sensitive G-proteins in MDCK cells.…”

Section: Results Formation Of Inositol Phosphatesmentioning

confidence: 95%

“…INC. enhance intracellular calcium activity both, in the presence and absence of extracellular calcium . Other hormones, able to increase intracellular calcium activity in MDCK cells include bradykinin (Lang et al, 1991;Pidikiti et al, 1985;Portilla et al, 1988a) and epinephrine (Breuer et al, 1988;Pfeilschifter et al, 1991). Both, bradykinin (Lang et al, 1991;Lopez-Burillo et al, 1988;Portilla and Morrison, 1986;Portilla et al, 1988a,b;Slivka and Insel, 1988) and epinephrine (Pfeilschifter et al, 1991); Slivka and Insel, 1987;Terman et al, 1987) have been shown to stimulate the cellular formation of inositoltrisphosphate, which mediates cellular release of calcium (Berridge, 1987).…”

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confidence: 92%

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Cellular mechanisms of ATP‐induced hyperpolarization in renal epitheloid MDCK‐cells

Paulmichl

Pfeilschifter

Wöll

et al. 1991

Journal Cellular Physiology

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Previous studies have shown that ATP enhances intracellular calcium concentration and activates potassium channels in Madin Darby canine kidney (MDCK)-cells, thus leading to hyperpolarization of the cell membrane. The present study has been performed to elucidate the intracellular mechanisms involved. To this end, the effects of ATP on the potential difference across the cell membrane (PD), on formation of inositol phosphates, and on intracellular calcium concentration (Cai) have been analyzed in cells without or with pretreatment with pertussis toxin or 12-O-tetradecanoyl phorbol 13-acetate diester (TPA). In untreated cells, ATP leads to a sustained hyperpolarization and an increase of inositol 1,4,5-trisphosphate (IP3), inositol 1,3,4,5-tetrakisphosphate (IP4), and Cai. In the absence of extracellular calcium, the effect of ATP on PD and Cai is only transient. In cells pretreated with pertussis toxin, the effect of ATP on inositol trisphosphate is almost abolished, but ATP still leads to an increase of PD and Cai, which is sustained in the presence, and transient in the absence, of extracellular calcium. In cells pretreated with TPA, the effect of ATP on inositol trisphosphate is reduced and the effect on Cai blunted; but ATP still leads to a hyperpolarization of the cell membrane, which is sustained in the presence, and transient in the absence, of extracellular calcium. The observations indicate that ATP activates phospholipase C by a phorbol ester and pertussis toxin sensitive mechanism. In addition, ATP enhances Cai by pertussis toxin insensitive mechanisms allowing recruitment of calcium from both, extracellular fluid and intracellular stores. Calcium then activates the potassium channels and thus leads to the hyperpolarization of the cell membrane.

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Section: Results Formation Of Inositol Phosphatesmentioning

confidence: 85%

Section: Results Formation Of Inositol Phosphatesmentioning

confidence: 95%

mentioning

confidence: 92%

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Cellular mechanisms of ATP‐induced hyperpolarization in renal epitheloid MDCK‐cells

Paulmichl

Pfeilschifter

Wöll

et al. 1991

Journal Cellular Physiology

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“…However, in MDCK cells, pretreatment with TPA did not prevent the swellinginduced initial transient hyperpolarization of PD. Activa tion of protein kinase C by pretreatment with TPA has been shown to suppress agonist-induced formation of ino sitol phosphates due to down-regulation of phospholipase C [7][8][9], In addition, G proteins have been suggested to be involved in both RVD [32. 33] and regulatory volume increase [10].…”

Section: Discussionmentioning

confidence: 99%

Calcium Entry Stimulated by Swelling of Madin-Darby Canine Kidney Cells

Wöll¹,

Ritter²,

Haller

et al. 1996

Nephron

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Cell swelling in Madin-Darby canine kidney (MDCK) cells by reduction of extracellular osmolarity (omission of 70 and 150 mmol/l mannitol, respectively) leads to the activation of anion channels and Ca²⁺ sensitive K⁺ channels. The K⁺ channel activation leads to an initial transient hyperpolarization of the cell membrane potential (PD) followed by a sustained depolarization due to activation of anion channels. The present study elucidates the role of intracellular calcium (Ca²⁺_i) in regulatory cell volume decrease (RVD) of MDCK cells. While reduction of extracellular osmolarity by omitting 70 mmol/l mannitol did not lead to a detectable change in Ca²⁺_i, severe cell swelling by omitting 150 mmol/l mannitol led to a transient rise in Ca²⁺_i. PD changes, on the other hand, were not different under either condition. In addition, the response of PD to cell swelling was not altered by treatment of the cells with 12-O-tetrade-canoylphorbol-13-acetate diester, pertussis toxin or cholera toxin. In the nominal absence of extracellular Ca²⁺, reduction of extracellular osmolarity did not lead to an increase in Ca²⁺_i and no initial transient hyperpolarization was observed, whereas addition of 10 μmol/l ATP still led to a significant hyperpolarization. Omission of extracellular Ca²⁺ was followed by a strong decrease in cell membrane resistance (Rm) due to activation of a depolarizing cation conductance. Subsequent readdition of Ca²⁺ caused a marked increase in Ca²⁺_i due to Ca²⁺ influx. This Ca²⁺ entry was further stimulated by cell swelling. RVD was significantly blunted in the absence of extracellular Ca²⁺. The results suggest that cell swelling stimulates a Ca²⁺-permeable pathway in the cell membrane favoring Ca²⁺ entry into the cell with subsequent activation of Ca²⁺-sensitive K⁺ channels.

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“…Activation of adrenoceptors on epithelial cells triggers cascades of biochemical reactions leading to increased concentrations of intracellular second messengers like adenosine 3':5'-cyclic monophosphate (cyclic AMP) (Wong & Huang, 1990) and/or Ca2" (Pfeilschifter et al, 1991). These messengers act on different components of the secretory pathway to stimulate chloride secretion (for review see Donowitz & Welsh, 1986).…”

Section: Introductionmentioning

confidence: 99%

Characterization of adrenoceptors involved in the electrogenic chloride secretion by cultured rat epididymal epithelium

Leung

Yip

Wong

1992

British J Pharmacology

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1 Short-circuit current (SCC) technique was used to study the adrenoceptors involved in the electrogenic chloride secretion by cultured cauda epididymal epithelium of rats. Stimulation of the epithelium with noradrenaline (primarily PI-adrenoceptor selective agonist), salbutamol (132-adrenoceptor selective agonist) and adrenaline (non-selective P-adrenoceptor agonist) led to a rise in SCC. At a low chart-speed (2 mm min-'), the response profile to these agonists consisted of a peak followed by a sustained response considerably higher than the basal SCC. 2 The EC50s (doses of agonist producing 50% maximum response) of noradrenaline, salbutamol and adrenaline were 300, 115 and 10 nM respectively. Pretreating the tissues with 1 gM atenolol (PI-selective antagonist) and 10 AM butoxamine (132-selective antagonist) shifted the dose-response curves of noradrenaline (shifted EC50 = 4000 nM) and salbutamol (shifted EC50 = 1050 nM) to the right. Atenolol (1 LM) and butoxamine (10 LM) shifted the dose-response curve of adrenaline to the right with new EC50s of 30 nM and 115 nM, respectively. 3 The rapidly rising phase of the SCC response to noradrenaline and adrenaline observed at low chart-speed consisted of a brief and transient retraction followed by a rebound increase in SCC. At a high chart-speed (1 mm s-'), the retraction and rebound phenomenon manifested as a fast initial spike which could be blocked by phentolamine (non-specific x-adrenoceptor antagonist) in a dose-dependent fashion. Similar initial spikes were observed when the tissues were stimulated with phenylephrine (al-selective agonist) but not with isoprenaline (non-selective P-agonist) or forskolin (activator of adenylate cyclase). The response of the initial spike triggered by noradrenaline was dose-dependent and the EC50 was 2000 nM. 4 The present study showed that the electrogenic chloride secretion by rat epididymis could be stimulated by (xi-, 13I-and P2-adrenoceptor agonists. The al-mediated response had a faster onset and more transient action than the 3-counterpart. It is postulated that epididymal chloride secretion might be regulated by neural (noradrenaline-mediated) and humoral (adrenaline-mediated) controls and that the stimulus-secretion coupling mechanisms might involve both Ca2+ (al-mediated response) and adenosine 3':5'-cyclic monophosphate (P-mediated response) as intracellular second messengers.

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Cellular mechanisms of adrenaline-induced hyperpolarization in renal epitheloid MDCK cells

Cited by 14 publications

References 46 publications

Cellular mechanisms of ATP‐induced hyperpolarization in renal epitheloid MDCK‐cells

Cellular mechanisms of ATP‐induced hyperpolarization in renal epitheloid MDCK‐cells

Calcium Entry Stimulated by Swelling of Madin-Darby Canine Kidney Cells

Characterization of adrenoceptors involved in the electrogenic chloride secretion by cultured rat epididymal epithelium

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