PMID- 9625880
OWN - NLM
STAT- MEDLINE
DCOM- 19980901
LR  - 20190512
IS  - 0022-3751 (Print)
IS  - 1469-7793 (Electronic)
IS  - 0022-3751 (Linking)
VI  - 510 ( Pt 1)
IP  - Pt 1
DP  - 1998 Jul 1
TI  - Importance of basolateral K+ conductance in maintaining Cl- secretion in murine 
      nasal and colonic epithelia.
PG  - 237-47
AB  - 1. Epithelia lining the nasal passages and descending colon of wild-type and 
      cystic fibrosis (CF) mice were examined by the short-circuit current technique. 
      Additionally, intracellular Ca2+ ion determinations were made in nasal epithelial 
      cells. Forskolin produced anion secretory currents in wild-type and CF nasal 
      epithelia. It produced similar effects in wild-type colonic epithelia, but not in 
      colonic epithelia from CF mice. 2. After electrogenic Na+ transport was blocked 
      with amiloride and electrogenic Cl- secretion was stimulated with forskolin, the 
      ability of K+ channel blockers to inhibit the forskolin-induced Cl- current was 
      determined. The order of efficiency for nasal epithelium was: Ba2+ > clofilium 
      >>> TEA = azimilide >>> 
      trans-6-cyano-4-(N-ethylsulphonyl-N-methylamino)-3-hydroxy-2, 2-dimethyl-chromane 
      (293B) = charybdotoxin, whereas for the colonic epithelium the order was: Ba2+ = 
      293B >>> azimilide = TEA >>> clofilium = charybdotoxin. 3. 
      1-Ethyl-2-benzimdazolinone (1-EBIO) was able to generate large Cl--secretory 
      currents in colonic epithelia which were partially sensitive to charybdotoxin, 
      with the remaining current being inhibited by 293B. In nasal epithelia 1-EBIO 
      produced only a small transient effect on current. 4. Forskolin released 
      intracellular Ca2+ in nasal epithelial cells; this activity was attenuated when 
      more powerful Ca2+-releasing agents were applied first. 5. It is concluded that 
      an action on basolateral cAMP-sensitive K+ channels is an important determinant 
      of the maintained responses to forskolin in nasal and colonic epithelia, in 
      addition to the effects on the cystic fibrosis transmembrane conductance 
      regulator (CFTR) in the apical membrane. In CF nasal epithelia the activation of 
      calcium-activated chloride channels (CACs) substitutes for the effect on CFTR. On 
      the basis of the different orders of potency of the blocking agents and the 
      differential response to 1-EBIO it is concluded that the cAMP-sensitive K+ 
      channels are different in the airways and the gut.
FAU - MacVinish, L J
AU  - MacVinish LJ
AD  - Department of Pharmacology, University of Cambridge, Tennis Court Road, Cambridge 
      CB2 1QJ, UK.
FAU - Hickman, M E
AU  - Hickman ME
FAU - Mufti, D A
AU  - Mufti DA
FAU - Durrington, H J
AU  - Durrington HJ
FAU - Cuthbert, A W
AU  - Cuthbert AW
LA  - eng
GR  - Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Physiol
JT  - The Journal of physiology
JID - 0266262
RN  - 0 (Benzimidazoles)
RN  - 0 (Calcium Channel Agonists)
RN  - 0 (Chlorides)
RN  - 0 (Potassium Channel Blockers)
RN  - 1F7A44V6OU (Colforsin)
RN  - 7DZO8EB0Z3 (Amiloride)
RN  - M82W79SS4W (1-ethyl-2-benzimidazolinone)
RN  - RWP5GA015D (Potassium)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Amiloride/pharmacology
MH  - Animals
MH  - Benzimidazoles/pharmacology
MH  - Calcium/metabolism
MH  - Calcium Channel Agonists/pharmacology
MH  - Chlorides/*metabolism
MH  - Colforsin/pharmacology
MH  - Colon/drug effects/*metabolism
MH  - Cystic Fibrosis/*metabolism
MH  - Electric Conductivity
MH  - Intestinal Mucosa/drug effects/*metabolism
MH  - Intracellular Membranes/metabolism
MH  - Mice
MH  - Nasal Mucosa/drug effects/*metabolism
MH  - Osmolar Concentration
MH  - Potassium/*physiology
MH  - Potassium Channel Blockers
PMC - PMC2231036
EDAT- 1998/06/17 00:00
MHDA- 1998/06/17 00:01
PMCR- 1999/07/01
CRDT- 1998/06/17 00:00
PHST- 1998/06/17 00:00 [pubmed]
PHST- 1998/06/17 00:01 [medline]
PHST- 1998/06/17 00:00 [entrez]
PHST- 1999/07/01 00:00 [pmc-release]
AID - 10.1111/j.1469-7793.1998.237bz.x [doi]
PST - ppublish
SO  - J Physiol. 1998 Jul 1;510 ( Pt 1)(Pt 1):237-47. doi: 
      10.1111/j.1469-7793.1998.237bz.x.