P oc.
Na i.
Acad.
Sci.
USA
Vol.
88,
pp.
2927-2930,
Ap il
1991
Neu obiology
Single
K+
channels
in
memb ane
pa ches
o
a e ial
chemo ecep o
cells
a e
modula ed
by
02
ension
(02
sensing/glomus
cells)
MARiA
D.
GANFORNINA
AND
Jose
L6PEZ-BARNEO
Depa amen o
de
Fisiologia
y
Bio isica,
Facul ad
de
Medicina,
Uni e sidad
de
Se illa,
A da.
Sanchez
Pizjudn,
4,
41009
Se ille,
Spain
Communica ed
by
R.
Llinas,
Decembe
26,
1990
ABSTRACT
Type
I
cells
o
he
ca o id
body
a e
known
o
pa icipa e
in
he
de ec ion
o
02
ension
in
a e ial
blood
bu
he
p ima y
chemo ansduc ion
mechanisms
a e
no
well
unde -
s ood.
He e
we
epo
he
exis ence
in
excised
memb ane
pa ches
o
ype
I
cells
o
a
single
K+
channel
ype
modula ed
by
changes
in
P02.
Open
p obabili y
o
he
O2-sensi i e
K+
channel
e e s-
ibly
dec eased
by
a
leas
50%
on
exposu e
o
hypoxia
bu
single-channel
conduc ance
(-20
pS)
was
unal e ed.
In
he
ange
be ween
70
and
150
mmHg
(1
mmHg
=
133
Pa)
he
dec ease
o
single-channel
open
p obabili y
was
p opo ional
o
he
Po2
measu ed
in
he
icini y
o
he
memb ane
pa ch.
The
inhibi ion
o
K+
channel
ac i i y
by
low
P02
was
independen
o
he
p esence
o
non-hyd olyzable
guanine
iphospha e
ana-
logues
a
he
in e nal
ace
o
he
memb ane.
The
esul s
indica e
ha
he
02
senso
o
ype
I
cells
is
in
he
plasma
memb ane
and
sugges
ha
en i onmen al
02
in e ac s
di ec ly
wi h
he
K+
channels.
Type
I,
o
glomus,
cells
o
he
ca o id
body
ha e
been
conside ed
o
decades
o
be
esponsible
o
he
de ec ion
o
oxygen
ension
(Po2)
in
he
a e ial
blood
bu
he
mechanisms
in ol ed
in
he
p ocess
o
chemo ansduc ion
ha e
emained
obscu e
(1,
2).
Howe e ,
i
has
been
ecen ly
disco e ed
ha
ype
I
cells
om
adul
abbi s
can
gene a e
ac ion
po en ials
and
ha
hey
ha e
a
ol age-dependen
K+
cu en
selec i ely
and
e e sibly
a enua ed
by
lowe ing
Po2
(3-8).
Inhibi ion
o
his
K+
cu en
unde
hypoxic
condi ions
could
p oduce
an
inc ease
in
he
i ing
equency
o
chemo ecep o
cells,
leading
o
Ca2'
in lux,
enhanced
ansmi e
elease,
and
ac i a ion
o
he
a e en
ibe s
o
he
sinus
ne e
(1,
2,
6).
The
p ima y
si e
o
02
de ec ion
is,
howe e ,
unknown.
Exposu e
o
cyanide
o
o
ex eme
hypoxia
(<40
mmHg;
1
mmHg
=
133
Pa)
induces
an
inc ease
o
[Ca2+]j
in
ype
I
cells,
possibly
due
o
Ca2'
elease
om
mi ochond ia,
and
a
subsequen
ac i a ion
o
a
Ca2+-dependen
K+
cu en
(9,
10).
The e o e
i
has
been
a gued
ha
he
modi ica ion
o
he
K+
cu en
by
lowe ing
Po2
migh
be
a
seconda y
phenomenon
a he
han
an
ini ial
s ep
in
he
p ocess
o
chemo ansduc ion.
Now
we
epo
he
iden i ica ion
o
a
single
K+
channel
ype
ha
ully
accoun s
o
he
p ope ies
o
he
mac oscopic
02-sensi i e
K+
cu en .
Fu he mo e,
we
show
ha
in
excised
memb ane
pa ches
he
ac i i y
o
hese
K+
channels
is
e e sibly
modula ed
by
P02.
Ou
esul s
suppo
he
iew
ha
he
K+
channels
a e
di ec ly
egula ed
by
02
and
s ongly
sugges
ha
he
02
senso
o
chemo ecep o
cells
is
in,
o
associa ed
wi h,
he
plasma
memb ane.
This
ype
o
Ke
channel
egula ion
ound
in
he
ca o id
body
may
ha e
an
e en
b oade
unc ional
in e es
because
i
could
also
be
in ol ed
in
physiological
esponses
o
hypoxia
in
o he
issues.
METHODS
Expe imen s
we e
pe o med
on
enzyma ically
dispe sed
ype
I
cells
isola ed
om
abbi
ca o id
bodies.
The
me hods
ollowed
in
cell
dissocia ion
and
cul u e
we e
he
same
as
p e iously
desc ibed
(3,
4).
Cells
we e
pla ed
on
agmen s
o
glass
co e slips
ea ed
wi h
poly(L-lysine).
Du ing
he
expe -
imen
a
co e slip
was
ans e ed
o
a
small
chambe
o
0.2
ml
wi h
con inuous
low o
solu ion
ha
could
be
comple ely
eplaced
in
10-15
s.
Solu ions
we e
equilib a ed
wi h
ei he
ai ,
N2,
o
a
mix u e
o
bo h,
in
o de
o
ob ain
he
desi ed
02
ension.
Po2
in
he
chambe
was
di ec ly
moni o ed
wi h
a
pola ized
100-
,m- hick
pla inum
wi e
(11)
placed
in
he
icin-
i y
o
he
pa ch
elec ode.
We
used
5-
o
8-M l
pa ch
pipe es
ab ica ed
om
bo osilica e
glass.
In
mos
expe imen s
cells
we e
i s
subjec ed
o
whole-cell
ol age
clamp
and
he ea e
he
ou side-ou
excised
memb ane
pa ch
con igu a ion
was
ob ained
by
pulling
he
elec ode
away
om
he
cell
(12).
Howe e ,
in
a
ew
expe imen s
he
e ec
o
hypoxia
on
K+
channels
included
in
inside-ou
excised
pa ches
was
also
es ed.
Composi ion
o
solu ions
and
o he
expe imen al
a -
iables
a e
gi en
in
he
igu e
legends.
RESULTS
The
majo
p ope ies
o
he
02-sensi i e
single
K+
channels
a e
summa ized
in
Fig.
1.
A
mac oscopic
K+
cu en
e-
co ded
in
whole-cell
mode
du ing
a
ol age
s ep
o
+20
mV
is
shown
in
Fig.
lA.
The
cu en
ace,
shown
o
compa i-
son,
illus a es
he
ypical
ime
cou se
o
he
02- egula ed
K+
cu en
o
ype
I
cells,
wi h
inac i a ion
du ing
a
main ained
depola iza ion
(6).
A e
excision
o
a
memb ane
pa ch
(Fig.
1B)
he
same
pulse
p o ocol
p oduced
he
appea ance
o
single-channel
e en s
wi h
a
uni a y
ampli ude
o
1.8
±
0.2
pA
(mean
±
SD,
n
=
14).
The
h ee
K+
channels
ac i a ed
on
depola iza ion
open
p e e en ially
a
he
beginning
o
he
pulse
and
p og essi ely
en e ed
an
inac i a ed
s a e.
Channel
inac i a ion
is
clea ly
e iden
in
Fig.
1C,
whe e
i
is
shown
he
a e age
o
23
consecu i e
single-channel
cu en
sweeps
wi h
a
ime
cou se
almos
iden ical
o
he
whole-cell
cu en .
Single-channel
ac i i y
was
blocked
by
5
mM
e ae hylam-
monium
(Fig.
1D),
which
also
abolishes
he
whole-cell
cu -
en
(4).
Single
K+
channels
simila
o
hose
o
Fig.
1B
we e
ound
in
e e y
expe imen
and
hei
es ima ed
densi y
is
=600
pe
cell.
Uni a y
cu en s
eco ded
om
a
pa ch
wi h
a
mos
one
open
K+
channel
a e
shown
in
Fig.
1E,
which
also
illus a es
he
inc ease
in
single-channel
cu en
ampli ude
wi h
memb ane
depola iza ion,
in
pa allel
wi h
he
inc ease
o
he
elec ochemical
d i ing
o ce
o
K+
mo emen .
Single-channel
cu en
ampli ude
(i)
e sus
memb ane
po-
en ial
(VM)
is
plo ed
in
Fig.
iF.
Mean
uni a y
cu en
alues
om
14
expe imen s
a e
ep esen ed
by
do s.
In
hese
ionic
condi ions
(2.7
mM
K+
in
he
ex e nal
solu ion
and
140
mM
K+
in
he
solu ion
a
he
in e nal
ace
o
he
memb ane)
he
i-VM
ela ionship
was
almos
linea
in
he
ange
be ween
-30
and
+50
mV,
yielding
an
es ima e
o
he
single-channel
conduc ance
o
be
20.1
pS.
In
symme ical
140
mM
K+
( iangles)
single-channel
cu en
e e sed
a
0
mV
and
he
uni a y
conduc ance
was
41.5
pS.
These
obse a ions
indi-
ca e
ha
he
channels
we e
highly
selec i e
o
K+.
Ca2+-
2927
The
publica ion
cos s
o
his
a icle
we e
de ayed
in
pa
by
page
cha ge
paymen .
This
a icle
mus
he e o e
be
he eby
ma ked
"ad e isemen "
in
acco dance
wi h
18
U.S.C.
§1734
solely
o
indica e
his
ac .
2928
Neu obiology:
Gan o nina
and
L6pez-Ba neo
A
Cell
1nA
_
B
03-----.
Pa ch
2
pA
c
C
Ensemble
-Jil
E
VM
MV
20
1
i
pA
2-
1-
0-
-1
-
-2-
50
ms
I
I
I
I
.
-40
-20
0
20
40
60
VMmV
FIG.
1.
P ope ies
o
he
02-sensi i e
K+
channels.
(A)
Whole-cell
K+
cu en
elici ed
by
a
200-ms
pulse
om
-80
o
+20
mV.
(B)
Single-channel
e en s
eco ded
du ing
a
simila
ol age
s ep
in
an
ou side-ou
excised
memb ane
pa ch.
(C
and
D)
A e age
cu en
o
23
consecu i e
sweeps
eco ded
om
he
same
pa ch
wi h
simila
pulse
p o ocol
as
in
B
(C)
and
blockade
o
he
cu en
by
he
p esence
o
5
mM
e ae hylammonium
(TEA+)
in
he
ex e nal
solu ion
(D).
(E)
Single-channel
cu en
elici ed
by
ol age
s eps
om
-80
o
0,
+20,
and
+40
mV
in
an
ou side-ou
pa ch
wi h
a
mos
one
open
channel.
Pulse
du a ion
was
200
ms.
(F)
Single-channel
cu en
ampli ude
(i)
e sus
memb ane
po en ial
(VM).
Do s
a e
a e age
cu en s
om
14
pa ches
eco ded
in
asymme ical
K+
concen a ions
and
wi h
an
ex e nal
solu ion
equilib a ed
wi h
he
no mal
Po2
(150
mmHg).
The
s aigh
line
i
has
a
slope
o
20.1
pS.
Open
ci cles
a e
a e age
cu en s
om
i e
pa ches
wi h
he
same
solu ions
bu
wi h
low
02
con en
(be ween
80
and
20
mmHg).
T iangles
a e
a e age
measu emen s
om
wo
pa ches
in
symme ical
K+
concen a ions
and
no mal
Po2.
The
s aigh
line
i
has
a
slope
o
41.5
pS.
Cu en
signals
we e
low-pass- il e ed
a
1
kHz
(8-pole
Bessel)
and
digi ized
wi h
a
sampling
in e al
o
500
,us.
In
all
cu en
aces
linea
ionic
and
capaci y
cu en s
we e
sub ac ed.
Solu ions
in
A-F
(do s
and
open
ci cles)
con ained
he
ollowing
(in
mM):
ex e nal:
140
NaCl,
2.7
KCI,
5
CaC12,
2
MgCl2,
10-3
e odo oxin,
10
Hepes;
in e nal:
80
po assium
glu ama e,
40
KCI,
20
KF,
2
MgCl2,
10
EGTA,
10
Hepes.
In
he
ex e nal
solu ion
o
D
5
mM
NaCl
we e
eplaced
by
5
mM
e ae hylammonium
chlo ide.
In
F
( iangles)
he
ex e nal
solu ion
con ained
he
ollowing
(in
mM):
140
KCI,
5
CaC12,
2
MgCl2,
10
Hepes.
In
all
solu ions
pH
was
be ween
7.3
and
7.4.
Holding
po en ial
was
-80
mV
and
empe a u e
was
22-25°C.
Cu en
calib a ion
in
B
also
applies
o
aces
in
C-E.
dependen
maxi-K+
channels
wi h
uni a y
conduc ance
o
abou
250
pS
(in
symme ical
140
mM
K+
solu ions)
we e
also
p esen
in
ype
I
cells.
Since
he
ac i i y
o
maxi-K+
channels
was
una ec ed
by
changes
in
02
ension
(n
=
14),
hei
ac i a ion
was
p e en ed
in
mos
expe imen s
by
main aining
[Ca2+]
a
he
in e nal
ace
o
he
memb ane
below
1
nM.
The
modula ion
o
he
small
K+
channels
by
Po2
was
in es iga ed
in
excised
memb ane
pa ches
exposed
o
solu-
ions
wi h
educed
02
con en .
Fig.
2
illus a es
he
e ec
o
hypoxia
on
an
ou side-ou
excised
pa ch
ha
ne e
showed
mo e
han
one
open
channel.
Fig.
2A
shows
h ee
se s
o
cu en
aces
eco ded
du ing
ol age
pulses
o
+20
mV
in
a
con ol
solu ion
equilib a ed
wi h
ai
(Po2
=
150
mmHg),
while
exposu e
o
he
pa ch
o
low
Po2
(swi ching
om
150
o
80
mmHg),
and
a e
e u ning
o
he
solu ion
wi h
no mal
Po2
( eco e y
aces).
The
a e age
o
15-30
consecu i e
sweeps
eco ded
in
he
h ee
di e en
expe imen al
condi-
ions
a e
shown
in
Fig.
2B.
Open
p obabili y
o
he
channel,
in eg a ed
h oughou
he
pulse
du a ion,
in
he
con ol
solu ion
(po
=
0.61)
dec eased
ma kedly
du ing
exposu e
o
hypoxia
(po
=
0.28)
and
e u ned
o
a
high
alue
(po
=
0.74)
a e
es o a ion
o
no moxic
condi ions.
The
eco dings
clea ly
show
ha
single-channel
cu en
ampli ude
was
un-
a ec ed
by
low
Po2.
The
a e age
i-VM
alues
om
i e
pa ches
exposed
o
hypoxia
a e
plo ed
in
Fig.
1F
(open
ci cles).
The
da a
poin s
indica e
ha
uni a y
conduc ance
was
iden ical
o
he
con ol
alue.
Simila
quali a i e
esul s
ha e
been
ob ained
in
all
pa ches
(ei he
ou side-ou
o
inside-ou )
whe e
he
e ec
o
hypoxia
was
es ed
(n
=
36).
Al hough
a
de ailed
s udy
o
he
e ec
o
hypoxia
on
he
kine ics
o
he
K+
channel
is
necessa y,
ou
p elimina y
da a
sugges
ha
changes
in
02
ension
speci ically
modi y
ac i-
a ion
a e
cons an s.
Mean
open
ime
(-18
ms
a
+20
mV)
was
he
same
in
con ol
and
in
hypoxic
condi ions,
whe eas
mean
closed
ime
(20
ms
a
he
same
memb ane
po en ial
and
Po2
=
150
mmHg)
inc eased
by
a
leas
a
ac o
o
2.5
on
exposu e
o
hypoxia.
Inac i a ion
ime
cou se,
e alua ed
om
ensemble
a e age
eco dings
in
mul ichannel
pa ches,
seemed
o
be
unchanged
by
low
Po2.
The
e e sible
dec ease
o
K+
channel
open
p obabili y
occu s
oughly
wi h
he
ime
cou se
o
Po2
change
in
he
neighbo hood
o
he
memb ane
pa ch.
Fig.
3A
shows
a
con inuous
elec ical
signal
p opo ional
o
he
a ia ion
o
02
ension
in
he
chambe .
Single-channel
e en s
eco ded
om
an
ou side-ou
excised
pa ch
du ing
1.3-s
ol age
s eps
o
+20
mV
a e
shown
in
Fig.
3B.
The
a ows
in
Fig.
3A
indica e
he
ime
a
which
each
pulse
was
deli e ed.
The
pa ch
seemed
o
con ain
i e
channels
and
he
numbe
o
P oc.
Na l.
Acad.
Sci.
USA
88
(1991)
P oc.
Na l.
Acad.
Sci.
USA
88
(1991)
2929
A
Con ol
I
J
~~"0
h_4 Joj
-
HI~~~~~~~~~~~~~
-I,
B
I-ML
j2pA
10.7
pA
50
ms
FIG.
2.
Modula ion
o
single
K+
channels
by
02
ension.
(A)
Rep esen a i e
cu en
aces
elici ed
by
200-ms
depola iza ions
om
-80
o
+20
mV
in
an
ou side-ou
excised
memb ane
pa ch
ha
con ained
a
mos
one
open
channel.
The
onse
and
he
end
o
he
pulses
a e
indica ed
by
he
a ows.
Reco dings
we e
ob ained
in
he
con ol
ex e nal
solu ion
(equilib a ed
wi h
ai ;
Po2
=
150
mmHg),
in
low
Po2
(swi ching
om
150
o
80
mmHg),
and
a e
e u ning
o
he
solu ion
wi h
no mal
Po2.
Pulses
we e
applied
e e y
5
s.
Cu en
calib a ion
was
2
pA.
(B)
Ensemble
a e ages
o
15-30
consecu i e
sweeps
in
he
di e en
expe imen al
condi ions.
Cu en
calib a ion
was
0.7
pA.
Open
channel
p obabili y
(con ol
=
0.61;
low
Po2
=
0.28;
eco e y
=
0.74)
was
calcula ed
om
he
ime
spen
in
he
open
s a e
di ided
by
he
du a ion
o
he
pulses.
Solu ions
and
o he
expe imen al
a iables
we e
as
in
Fig.
1
B-F.
simul aneous
e en s
ma kedly
dec eased
on
exposu e
o
hypoxia.
The
a e age
open
p obabili y
(p0),
in eg a ed
h oughou
he
pulse
du a ion,
was
0.34
in
no moxic
condi-
ions
(a;
Po2
=
150
mmHg)
bu
only
0.06
(b),
0.09
(c),
and
0.12
(d)
wi h
Po2
alues
o
85,
44,
and
116
mmHg,
espec i ely.
Comple e
eco e y
o
single-channel
ac i i y
(po
=
0.25)
was
ob ained
on
e u ning
o
he
con ol
solu ion
(e,
Po2
=
145
mmHg).
po
(o dina e)
as
a
unc ion
o
02
ension
(abscissa)
is
plo ed
in
Fig.
3C.
Be ween
70
and
150
mmHg,
a
ange
ha
includes
he
no mal
Po2
alues
in
a e ial
blood
o
he
abbi ,
channel
open
p obabili y
dec eased
in
pa allel
o
02
ension.
Lowe ing
Po2
below
70
mmHg
p oduced,
howe e ,
a
ela i e
inc ease
in
p0.
These
esul s
demons a e
a
concen a ion-
dependen
e ec
o
02
on
he
K+
channel.
DISCUSSION
This
epo
shows
ha
a
speci ic
kind
o
K+
channel
o
he
ype
I
cell
plasma
memb ane
is
e e sibly
and
selec i ely
modu-
la ed
by
changes
in
Po2.
Ca2+-dependen
maxi-K+
channels
also
p esen
in
he
same
p epa a ion
a e
una ec ed
by
al e -
a ions
in
02
ension.
The
02-sensi i e
K+
channels,
which
explain
he
modula ion
o
he
mac oscopic
K+
cu en
by
Po2
(3),
a e
mos
likely
key
elemen s
in
he
ansduc ion
o
hypoxic
s imuli
by
ype
I
cells.
These
K+
channels
a e
p obably
in ol ed
in
he
egula ion
o
cell
i ing
and
o
Ca2'
en y
h ough
ol age-ga ed
channels
du ing
mode a e
changes
in
ca o id
a e y
Po2
(2-4).
A e
in oxica ion
o
ype
I
cells
wi h
cyanide
o
unde
ex eme
hypoxia
(wi h
Po2
alues
<40
mmHg)
sec e ion
may
be
also
suppo ed
by
s ong
elease
o
Ca2+
om
mi ochond ia
(9,
10);
howe e ,
hese
condi ions
a e
o
unlikely
physiological
occu ence.
In
ac ,
we
ha e
ob-
se ed
in
mos
expe imen s
a
pa ial
eco e y
o
K+
channel
ac i i y
a
e y
low
Po2
le els
( e .
6
and
Fig.
3
in
his
epo ),
which
may
limi
he
i ing
equency
o
ype
I
cells
and
con ibu e
o
p e en ing
hei
ex ensi e
deg anula ion.
The
inhibi ion
o
K+
channel
opening
by
hypoxia
could
no
be
ela ed
o
he
p esence
o
any
dialyzable
componen
o
he
memb ane.
I
was
epea edly
obse ed
in
a
gi en
pa ch
ega dless
o
he
ime
elapsed
a e
excision
and
was
inde-
penden
o
he
in e nal
[Ca2+]
o
he
p esence
o
MgATP
a
he
in e nal
ace
o
he
memb ane.
Mo eo e ,
he
e e sible
educ ion
o
K+
channel
ac i i y
by
hypoxia
was
no
al e ed
by
he
addi ion
o
20
AM
GTP[y-S]
(n
=
4),
which
is
known
o
abolish
he
e e sibili y
o
G-p o ein-media ed
modula ion
o
ionic
channels
(13,
14).
These
obse a ions
sugges
ha
in
ype
I
cells
02
in e ac s
wi h
he
K+
channels
ei he
di ec ly
o
h ough
a
si e
closely
associa ed
wi h
hem.
In
his
espec
ype
I
cells
di e
om
ol ac o y
o
as e
chemo ecep o
cells
in
which
na u al
s imuli
modula e
ion
channels
h ough
he
ac ion
o
in acellula
cyclic
nucleo ides
(15-17).
In
conclu-
sion,
ou
indings
demons a e
ha
en i onmen al
02
egu-
la es
he
open
p obabili y
o
a
ype
o
K+
channel
in
chemo e-
cep o
cells
o
he
ca o id
body
wi hou
al e ing
he
single-
channel
conduc ance.
02
de ec ion
by
ype
I
cells
seems
o
in ol e
di ec
in e ac ion
wi h
he
K+
channels,
pe haps
h ough
a
heme-like
p os he ic
g oup
bound
o
he
channel
molecule.
This
mechanism,
wi hou
p eceden
in
he
li e a-
u e,
may
no
be
es ic ed
o
he
ca o id
body
bu
i
could
also
pa icipa e
in
o he
physiological
p ocesses- o
exam-
ple,
he
au o egula ion
by
local
02
ension
o
blood
low
in
co ona y,
ce eb al,
and
pulmona y
a e ies.
We
hank
D .
J.
U e ia
o
help
in
compu e
p og aming,
D s.
G.
Al a ez
de
Toledo
and
L.
Taba es
o
commen s
on
he
manusc ip ,
and
J.
R.
L6pez-L6pez
o
his
collabo a ion
in
he
cons uc ion
o
he
02-sensing
mic oelec ode.
Resea ch
was
suppo ed
by
a
g an
om
he
Di ecci6n
Gene al
de
In es igaci6n
Cien ica
y
Tdcnica
(PB-86/0250).
Low
P02
Reco e y
I*
Is.
.
].I
. .
T" ----.
10"I
Is
1%.
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LL
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ww"
I-M-1-1-1-1-- - -
Neu obiology:
Gan o nina
and
L6pez-Bameo
"*Ab lw
A-
F
II
-P
I
MI'
1
-' i
am
--L
PTMT
WV'"
41.
2930
Neu obiology:
Gan o nina
and
Lopez-Bameo
A
c
Po
0.4
0.3
0.2
0.1
B
4-
P02,mmHg
3-
2-
1
_
F150
1-
b
d
L50~~~~~~~~0
2-b
30
s
2-
a
2-
1-d
C
d
50
70
90
110
130
150
1-A
j3pA
P02,mmHg
FIG.
3.
Changes
in
02
ension
and
single
K+
channel
ac i i y
in
a
mul ichannel
ou side-ou
excised
pa ch.
(A)
Time
cou se
o
he
a ia ions
o
Po2
in
he
eco ding
chambe
du ing
a
ansien
exposu e
o
hypoxia.
(B)
Single-channel
ac i i y
eco ded
du ing
1.3-s
ol age
s eps
om
-80
o
+20
mV
a
he
ime
indica ed
by
he
a ows
and
lowe case
le e s
in
A.
Consecu i e
pulses
we e
applied
e e y
30
s
o
allow
o
comple e
eco e y
om
inac i a ion.
A e age
open
channel
p obabili y
(p.)
was
calcula ed
om
p0
=
(1/Ni )-
Id ,
whe e
N
=
numbe
o
channels
in
he
pa ch,
i
=
single-channel
cu en
ampli ude,
=
pulse
du a ion,
and
I
=
ne
cu en
du ing
he
pulse.
po
alues
we e
0.34
(a),
0.06
(b),
0.12
(c),
0.09
(d),
and
0.25
(e).
(C)
Channel
open
p obabili y
(p0,
o dina e)
as
a
unc ion
o
Po2
(abscissa)
in
he
chambe .
Solu ions
and
o he
expe imen al
condi ions
we e
as
in
Fig.
1
B-F.
1.
Eyzagui e,
C.
&
Zapa a,
P.
(1968)
in
A e ial
Chemo ecep o s,
ed.
To ance,
R.
W.
(Blackwell,
Ox o d),
pp.
213-251.
2.
Fidone,
S.
J.
&
GonzAlez,
C.
(1986)
in
Handbook
o
Physiol-
ogy,
The
Respi a o y
Sys em
II,
ed.
Fishman,
A.
(Am.
Physiol.
Soc.,
Washing on),
pp.
247-312.
3.
L6pez-Ba neo,
J.,
L6pez-L6pez,
J.
R.,
U e ia,
J.
&
GonzAlez,
C.
(1988)
Science
241,
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R.,
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C.
&
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J.
(1989)
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Physiol.
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W.
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L.,
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T.
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A.
&
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&
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M.,
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S.
&
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A.
(1981)
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601-628.
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0.
P.,
Ma y,
A.,
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E.,
Sakmann,
B.
&
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F.
(1981)
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A.
G.
(1987)
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615-649.
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A.
M.
&
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L.
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