PMID- 9683726
OWN - NLM
STAT- MEDLINE
DCOM- 20110617
LR  - 20181201
IS  - 1432-2013 (Electronic)
IS  - 0031-6768 (Linking)
VI  - 436
IP  - 4
DP  - 1998 Jul
TI  - Does stimulation of NaCl secretion in in vitro perfused rectal gland tubules of 
      Squalus acanthias increase membrane capacitance?
PG  - 538-44
AB  - NaCl secretion in rectal gland tubules (RGT) of Squalus acanthias requires the 
      activation of Cl- channels in the luminal membrane. The RGT and its mechanism of 
      activation are an early evolutionary paradigm of exocrine secretion. The 
      respective Cl- channels probably resemble the shark equivalent of the cystic 
      fibrosis transmembrane conductance regulator (CFTR). Activation of these Cl- 
      channels occurs via cAMP. It has been hypothesized that the activation of CFTR 
      occurs via exocytosis or inhibited endocytosis. To examine this question directly 
      by electrical measurements we have performed whole-cell patch-clamp analyses of 
      in vitro perfused RGT. NaCl secretion was stimulated by a solution (Stim) 
      containing forskolin (10 micromol/l), dibutyryl-cAMP (0.5 mmol/l) and adenosine (0.5 
      mmol/l). This led to the expected strong depolarization and an increase in 
      membrane conductance (G m). The membrane capacitance (C m) was measured by a 
      newly devised two-frequency synchronous detector method. It was increased by Stim 
      significantly from 5.00+/-0.22 to 5.17+/-0.21 pF (n=50). The increase in C m 
      correlated with the increase in G m with a slope of 51 fF/nS. Next the effect of 
      furosemide (500 micromol/l) was examined in previously stimulated RGT. Furosemide was 
      supposed to inhibit coupled Na+2Cl-K+ uptake and to reduce cell volume but not 
      membrane trafficking of Cl- channels. Furosemide reduced G m slightly (due to the 
      fall in cytosolic Cl- concentration) and C m to the same extent by which Stim had 
      increased it. Both changes were statistically significant, and the slope of DeltaC 
      m/DeltaG m was similar to that caused by Stim. Inhibitors of microtubules or actin 
      (colchicine, phalloidin and cytochalasin D added at 10 micromol/l to the pipette 
      solution and dialysed for >10 min) did not alter cell voltage, G m or C m, nor 
      did these inhibitors abolish the stimulatory effect of cAMP. These data suggest 
      that the small C m changes observed with Stim reflect a minor cell volume 
      increase and an "unfolding" of the plasma membrane. The present data do not 
      support the exocytosis/endocytosis hypothesis of cAMP-mediated activation of Cl- 
      channels in these cells.
FAU - Greger, R
AU  - Greger R
AD  - Physiologisches Institut, Albert-Ludwigs-Universitat, Hermann-Herder-Strasse 7, 
      D-79104 Freiburg, Germany.
FAU - Thiele, I
AU  - Thiele I
FAU - Warth, R
AU  - Warth R
FAU - Bleich, M
AU  - Bleich M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Pflugers Arch
JT  - Pflugers Archiv : European journal of physiology
JID - 0154720
RN  - 0 (Chlorides)
RN  - 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator)
RN  - 1F7A44V6OU (Colforsin)
RN  - 451W47IQ8X (Sodium Chloride)
RN  - 63X7MBT2LQ (Bucladesine)
RN  - K72T3FS567 (Adenosine)
SB  - IM
MH  - Adenosine/pharmacology
MH  - Animals
MH  - Bucladesine/pharmacology
MH  - Chlorides/metabolism
MH  - Colforsin/pharmacology
MH  - Cystic Fibrosis Transmembrane Conductance Regulator/metabolism
MH  - *Electric Capacitance
MH  - Membrane Potentials/*physiology
MH  - Patch-Clamp Techniques
MH  - Salt Gland/anatomy & histology/drug effects/*metabolism
MH  - Sodium Chloride/*metabolism
MH  - Squalus acanthias/*anatomy & histology/*metabolism
EDAT- 1998/07/31 00:00
MHDA- 2011/06/18 06:00
CRDT- 1998/07/31 00:00
PHST- 1998/07/31 00:00 [pubmed]
PHST- 2011/06/18 06:00 [medline]
PHST- 1998/07/31 00:00 [entrez]
AID - 10.1007/s004240050669 [pii]
AID - 10.1007/s004240050669 [doi]
PST - ppublish
SO  - Pflugers Arch. 1998 Jul;436(4):538-44. doi: 10.1007/s004240050669.