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Department of Neurosurgery, University of Mississippi Medical Center, Jackson, Mississippi 39216
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Cl
efflux induces
depolarization and contraction of smooth muscle cells. This study
was undertaken to explore the role of Cl flux in
histamine-induced contraction in the rabbit basilar artery. Male New
Zealand White rabbits (n = 16) weighing 1.8-2.5 kg
were euthanized by an overdose of pentobarbital sodium. The basilar arteries were removed for isometric tension recording. Histamine produced a concentration-dependent contraction that was attenuated by
the H1 receptor antagonist chlorpheniramine
(108 M) but not by the H2 receptor antagonist
cimetidine (3 × 106 M) in normal Cl
Krebs-Henseleit bicarbonate solution (123 mM Cl). The
histamine-induced contraction was reduced by the following manipulations: 1) inhibition of
Na+-K+-2Cl cotransporter with
bumetanide (3 × 105 and 104 M),
2) bicarbonate-free HEPES solution to disable
Cl/HCO
channels with the use of niflumic acid,
5-nitro-2-(3-phenylpropylamino) benzoic acid, and indoleacetic acid 94 R-(+)-methylindazone. In addition, substitution of
extracellular Cl (10 mM) with methanesulfonate acid (113 mM) transiently enhanced histamine-induced contraction. Manipulation of
Cl flux affects histamine-induced contraction in the
rabbit basilar artery.
Cl channels; Na+-K+-2Cl cotransporter; Cl/HCO
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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HISTAMINE, which acts as a neurotransmitter of central neurons, can be released from mast cells distributed throughout the whole brain, predominantly in the perivascular regions (40). Neurons containing histamine have been identified in the posterior hypothalamus (43), and histaminergic fibers have been shown to innervate cerebral blood vessels (37). Thus histamine might play a role in the regulation of cerebrovascular tone under either physiological or pathophysiological conditions (1, 4, 6).
The physiological response to histamine is mediated through four
distinct subtype receptors (H1-H4)
(6, 19). In cerebral arteries, activation of
H1 receptors induces contraction, whereas activation of
H2 receptors leads to relaxation. The vasomotor effects of
histamine are highly dependent on species and vascular region being
investigated (17, 21, 22, 40, 42, 43). In cerebral smooth
muscle cells, histamine induces inositol phospholipid hydrolysis,
mobilizes Ca2+ from intracellular store, or depolarizes
membrane, and promotes Ca2+ entry from voltage-dependent
Ca2+ channels (14, 15, 21, 22). Elevation of
intracellular Ca2+ not only produces contraction, but also
activates Ca2+-dependent K+ channels,
Ca2+-dependent Cl channels, or nonselective
cation channels (15, 14, 42).
Elevation of intracellular Ca2+ is the major source for the
activation of Ca2+-dependent Cl channels
(14, 15). Histamine increases intracellular
Ca2+, activates Ca2+-dependent Cl
channels in the rabbit basilar arteries and produces contraction in the
rabbit middle cerebral arteries (14, 15, 23). However, the
role of Na+-K+-2Cl cotransporter
and HCO exchanger in the
accumulation of intracellular Cl, and the functional
evidence of Cl channels in histamine-induced contraction
in cerebral arteries, remains to be determined. Thus Cl
flux was manipulated by inhibition of
Na+-K+-2Cl cotransporter and
HCO exchanger, substitute of
extracellular Cl concentration (from 123 to 10 mM), and
blockade of Cl channels in the rabbit basilar artery
exposed to histamine.
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MATERIALS AND METHODS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Tissue Preparation
Male New Zealand White rabbits (n = 16) weighing 2-2.5 kg were anesthetized by intravenous injection of acepromazine (5 mg), ketamine (50 mg), and xylazine (25 mg) and euthanized by an overdose of pentobarbital sodium (250 mg). The brain was removed and the basilar arteries were cut into 2-mm-thick rings and placed in an ice-cold modified Krebs-Henseleit biocarbonate solution containing (in mM) 120 NaCl, 4.5 KCl, 1 MgSO4, 27 NaHCO3, 1.2 KH2PO4, 2.5 CaCl2, and 10 dextrose and bubbled with 95% O2-5% CO2.Isometric Tension
The isometric tension study procedures were described previously (7, 23). Briefly, the rings were suspended at 400 mg resting tension (Radnoti Transducer, Radnoti Glass) between stainless steel hooks in 10-ml water-jacketed tissue baths (Radnoti Glass) in modified Krebs-Henseleit bicarbonate solution with 95% O2-5% CO2 at 37°C. The rings were incubated for 90 min until a stable rest tension was achieved. The solution was changed every 20 min to remove metabolites. The tissues were challenged with KCl (60 mM) twice at 30-min intervals before the experiment. Isometric force transducers were connected to arterial rings and the contraction was recorded with an eight-channel MacLab 8E and stored on a Power Macintosh computer. The low Cl
solution was prepared by replacing 120 mM NaCl with 120 mM NaOH and by
titrating the pH of the buffer to 7.4 with the use of methanesulfonate acid (MS).
In all experiments, whereas the extracellular Cl
concentration was being changed, the low-level Cl
solution was prewarmed and preaerated in a 37°C water bath, mixed with the agonists at the designated concentration, and injected slowly
into the water bath. The control group with normal Cl
solution was done in the same way. The HEPES buffer was made by
replacing 27 mM NaHCO3 with 20 mM HEPES and titrating the
pH of the solution to 7.4 using 1 M NaOH solution. The tension
developed by histamine application was shown as a ratio to 60 mM KCl
(except the low-Cl solution-induced contraction was
calculated as the ratio to 90 mM KCl). The measured osmolarity of the
normal Cl buffer and the low concentration
Cl buffer was 284 and 288 mosmol/kg, respectively.
Chemicals
Histamine, d-(+)-chlorpheniramine (H1 receptor antagonist), cimetidine (H2 receptor antagonist), bumetanide (Na+-K+-2Cl
cotransporter inhibitor), and niflumic acid (Ca2+-dependent
Cl channel blocker) were purchased from Sigma
Aldrich. 5-Nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB),
a nonselective Cl channel blocker, and indolacetic
acid 94, R-(+)-methylindazone (IAA-94), a nonselective
Cl channel blocker, were purchased from Tocris and
Alexis, respectively.
Statistics
All data are shown as means ± SE, and n is the number of arterial rings in each group. One-way ANOVA and Student's t-test were used as analysis methods. A value of P < 0.05 was considered to be significantly different.| |
RESULTS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Histamine Induces Contraction via H1 Receptor
Histamine (108-105 M) produced
dose-dependent contraction in the rabbit basilar artery. H1
receptor antagonist d-(+)-chlorpheniramine (108 M) shifted the concentration-dependent response
curve to the right and reduced significantly (P < 0.05, ANOVA) the maximum contraction to histamine (Fig.
1). The 50% effective concentration (EC50) and the maximum normalized response in the absence
of H1 receptor antagonist d-(+)-chlorpheniramine
are 1.70 ± 0.10 µM and 124.84 ± 2.16%, respectively. The
maximum normalized response in the presence of H1 receptor
antagonist d-(+)-chlorpheniramine is 60.28 ± 4.86%.
EC50 value in the presence of
d-(+)-chlorpheniramine was not calculated due to the lack of
maximum contraction.
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Cimetidine (3 × 106 M), a specific H2
receptor antagonist, was used in another series studies (Fig. 1). The
concentration-dependent response curve to histamine remained the same
either in the presence or in the absence of cimetidine. The maximum
contraction to histamine was slightly increased in the presence of
cimetidine (P < 0.05, ANOVA). The EC50 and
the maximum normalized response in the presence of cimetidine was
1.73 ± 1.42 µM and 165.42 ± 20.09% compared with
1.70 ± 0.10 µM and 124.84 ± 2.16% (in the absence of
cimetidine), respectively.
Effect of Bumetanide on Histamine- Induced Contraction
Rings were pretreated with 3 × 105 M
(n = 7) and 104 M (n = 7)
bumetanide (Na+-K+-2Cl
cotransporter inhibitor) for 30 min before application of histamine (Fig. 2, A-C)
from 108 to 105 M. Bumetanide significantly
suppressed the contraction in a concentration-dependent and reversible
manner. The EC50 and the maximum normalized response to
histamine from 108 to 105 M was 0.75 ± 0.14 µM and 84.24 ± 3.39% for bumetanide (30 µM); 0.73 ± 0.04 µM and 62.04 ± 0.50% for bumetanide (100 µM); and 1.70 ± 0.10 µM and 124.84 ± 2.16% for rings
without bumetanide, respectively (Fig. 2D). Bumetanide
reduced significantly the histamine-induced contraction
(P < 0.05, ANOVA).
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Effect of HEPES on Histamine-Induced Contraction
Rings were pretreated in HEPES solution (2 × 102 M, HCO6 M. The HEPES solution significantly (P < 0.05, Student's
t-test) suppressed the contraction induced by histamine
(Fig. 3, A and B).
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Effect of HEPES on KCl- and K-Methanesulfonate-Induced Contraction
To test whether HEPES solution itself has an effect on contractile proteins by changing intracellular pH, we pretreated arterial rings with 20 mM HEPES (2 × 102 M, HCO
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Effect of Low Cl Concentration on Histamine-Induced
Contraction
Direct application.
Prewarmed and preaerated low concentration Cl (10 mM
Cl) buffer, having already mixed with histamine at
106 M, was used to compare with the effect of histamine
at 106 M in normal Cl buffer. The
contractile response to histamine dissolved at 106 M was
enhanced transiently in low-Cl (10 mM Cl)
buffer for 5 to 8 min, followed by a prolonged relaxation toward the
rest tension level (Fig. 5A).
Thus low-Cl (10 mM Cl) buffer enhanced the
initial contraction but reduced plateau contraction induced by
histamine (P < 0.05, Student's t-test, Fig. 5B).
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Change Cl concentration during sustained contraction.
The rings were contracted first in a normal 123 mM Cl
solution by histamine at 106 M for at least 20 min. After
the tension attained stable and plateau phase, the normal
Cl buffer was quickly drained and exchanged for either a
"fresh" normal Cl buffer (123 mM Cl) or
low-Cl (MS, 10 mM Cl) buffer
containing the same concentration of histamine. No marked change in
tension was observed when normal Cl solution was changed
to fresh normal Cl solution (Fig.
6A). In contrast, tension was
markedly and transiently enhanced to its maximum within 5-8 min
after the low-Cl buffer was applied, followed by a rapid
relaxation toward the rest tension level (Fig. 6B).
The low-Cl buffer potentiated histamine-induced
contraction (P < 0.05, Student's t-test)
but reduced sustained contraction (P < 0.05, Student's t-test) of histamine (Fig. 6C).
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Change low-Cl solution into normal Cl
buffer.
To investigate the nature of the transient enhancement by
low-Cl buffer further, low-Cl solution with
histamine (106 M) was applied first and then followed by
histamine (106 M) in normal Cl solution. In
this different sequence, histamine in low-Cl solution
produced a transient contraction, followed by relaxation (Fig.
7A). Restoring normal
Cl produced a slow-developing contraction (Fig.
7A). These studies showed that although low-Cl
solution enhanced transiently of histamine-induced initial peak contraction, extracellular Cl is necessary for the
sustained contractile phase (Fig. 7B).
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Effect of depletion of intracellular Cl on
histamine-induced contraction.
This experiment tested the effect of histamine on contraction when
intracellular Cl was depleted. The arterial rings were
incubated in low-Cl solution (10 mM Cl) for
20 min before histamine (106 M) was applied. The rings
were then incubated in normal Cl solution (123 mM
Cl) for at least 60 min before applying histamine at the
same concentration. Histamine (106 M) produced
significant higher tension in normal Cl solution than in
low-Cl solution (Fig. 8).
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Effect of low-Cl solution on
K-methanesulfonate-induced contraction.
To test whether low-Cl solution has an effect on
intracellular pH or contractile proteins without adding back
Cl to the buffer solution, K-methanesulfonate was used
instead of KCl. K-methanesulfonate was applied first in normal
Cl solution and then washed and applied in
low-Cl solution. There was no significant difference in
K-methanesulfonate (60 mM)-induced contraction either in
low-Cl or normal Cl solutions (Fig.
9).
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Effects of Cl channel blockers on histamine-induced
contraction.
Histamine (106 M) was used first to achieve a sustained
contraction. The relaxant effect of niflumic acid, NPPB, and IAA-94 was
tested (106-104 M) on the sustained
contraction and all inhibitors induced concentration-dependent relaxation. Figure 10,
A-C, showed the original tracings of
contraction by histamine and relaxation by inhibitors. IC50
for the NPPB, IAA-94, and niflumic acid were 50.28 ± 3.05, 10.51 ± 8.65, and 77.23 ± 2.10 µM, respectively (Fig.
10D).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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The present study supports the hypothesis that manipulation of
Cl flux affects histamine-induced contraction in the
rabbit basilar arteries. The
Na+-K+-2Cl cotransporter
inhibitor bumetanide, the HCO channel blockers NPPB, niflumic acid, and
IAA-94 all depressed histamine-induced contraction. Low extracellular
Cl solution transiently enhanced the initial components
of the contraction induced by histamine. However, normal
Cl concentration seems critical in the maintaining of the
plateau phase of the contraction induced by histamine.
Role of
Na+-K+-2Cl
cotransporter in histamine-induced contraction.
The Na+-K+-2Cl cotransporter,
also known as the bumetanide-sensitive cotransporter, is an
electrically neutral pathway for the coupled movement of
Na+, K+, and Cl across the plasma
membrane (3, 33). Transport is bidirectional and is driven
by the transmembrane gradients of all three ions. The
Na+-K+-2Cl cotransporter is one
of the three mechanisms responsible for the accumulation of
intracellular Cl in smooth muscle cells (2, 3, 16,
26-28, 33). The
Na+-K+-2Cl cotransporter in
intact smooth muscle cells was demonstrated first by Deth et al.
(12) in rat and rabbit aortas. In rat femoral arterial
smooth muscle cells, norepinephrine (NE) activates the Na+-K+-2Cl cotransporter to
increase intracellular Cl accumulation and to depolarize
membrane potential (11). Other agonists, such as
angiotension II, phenylephrine, endothelin (ET), and KCl, all acutely
enhance the activity of
Na+-K+-2Cl cotransporter measured
by the flux of 86Rb+ in smooth muscle cells. On
the contrary, vasodilators such as nitric oxide and nitroprusside
inhibited the basal Na+-K+-2Cl
cotransporter-1 activity (2, 3). The
Na+-K+-2Cl cotransporter is more
active functionally in arterial smooth muscles in the
deoxycorticosterone acetate-salt model of hypertension than in
normotensive control rats (5, 8-11). Consequently, the level of intracellular Cl is higher, and the
extracellular Cl is more positive in hypertension, thus
contributing to the hypertensive depolarization and
maintenance. Those studies indicate that the Na+-K+-2Cl cotransporter plays an
important role in the regulation of vascular smooth muscle contraction
by modulation of membrane potentials.
cotransporter that
leads to reduction of intracellular Cl, hyperpolarization
of the membrane potential, and relaxation of NE-induced contraction in
rat aorta (26, 27). The present study showed that
bumetanide depressed histamine-induced contraction, which indicates
consistently that Cl efflux affects the
contractile-response in cerebral arteries. This result is consistent
with our previous study that bumetanide attenuated ET-1-induced
contraction in the rabbit basilar artery (7).
Role of Cl/HCO/HCO above the equilibrium
potential. Accumulating Cl via the
Cl/HCO
cotransporter and the two effects are additive (8, 26). The bicarbonate-free solution (HEPES), which disables
Cl/HCO/HCO/HCO
Role of extracellular Cl concentration in
histamine-induced contraction.
In this study, low-Cl solution potentiated transiently
but significantly histamine-induced contraction, no matter if
low-Cl solution was used initially or was added on the
top of histamine-induced sustained contraction. Regardless of whether
low-Cl solution was used initially or was added on the
top of histamine-induced contraction, low-Cl solution
consistently produced, after a transient contraction, a relaxant
response to a level slightly above the resting tension. After the
extracellular Cl was restored to normal concentration,
the rings gradually developed a sustained contraction to histamine to a
level significantly higher than that induced by histamine in
low-Cl solution. These results obtained in the present
study are somehow different from one of our previous studies.
Low-Cl solution enhanced both the initial and the
sustained components of ET-1-induced contraction in the rabbit basilar
artery (7). Low-Cl solution did not cause
relaxation in the presence of ET-1 (7). Even though the
mechanism for low-Cl solution-induced relaxation in the
presence of histamine is not clear, it seems a unique phenomenon for
histamine-induced contraction in the rabbit basilar artery.
Low-Cl solution did not change KCl or
K-methanesulfonate-induced contraction (Fig. 9), potentiated both the
initial and sustained contraction by ET-1 (7), but
enhanced transiently of the initial contraction and produced relaxation
in the presence of histamine in the rabbit basilar artery. These
studies probably ruled out the possible release of relaxants from
endothelial cells because these relaxants would relax ET-1- or
KCl-induced contractions as well. Consistently, pretreatment of
arterial rings with
NG-nitro-L-arginine methyl ester
changed neither the initial enhancement nor the subsequent relaxant
effect to histamine in the low-Cl solution (preliminary
data). One of the other possibilities for the relaxant effect of low
Cl is that alteration of extracellular Cl
solution may affect the activity of
Na+-K+-2Cl cotransporter and
HCO exchanger. Indeed, in cultured
cortical astrocytes, Cl-free solution greatly decreased
the Na+-K+-2Cl cotransporter
activity (36). Low-Cl solution did not
affect the activity of the nonselective cation channels, although it
has been reported that nonselective cation ion channels are the major
contributors of the sustained contraction phases in the pulmonary
arteries and in the rabbit middle cerebral arteries (14, 15,
42). The contribution of cation conductance to histamine-induced
inward current was presumably small or the distribution of cation
channels is sparse compared with those of Cl channels in
the rabbit basilar artery (23). Apparently, more studies
are needed to clarify this unique relaxant phenomenon of low
Cl in histamine-induced contraction in the rabbit basilar artery.
solution (using 130 mM Na+ glutamate to replace 130 mM NaCl) did not change
either the initial component or the sustained component of
histamine-induced contraction. The apparent discrepancy between these
two studies might be related to the different experimental conditions.
First, in our study, the contractile apparatus was exposed to
low-Cl solution and histamine simultaneously, whereas in
the other study (14), the tissues were treated with
low-Cl solution for 15-30 min before histamine was
applied. In our study, the depletion of intracellular Cl
was avoided and thus a transient enhancement of the histamine-induced contraction occurred at the initial phase of the contraction. This
hypothesis is supported by our experiment that depletion of
intracellular Cl by incubating the arterial rings in
low-Cl solution (10 mM Cl) for 20 min
reduced histamine-induced contraction compared with the contraction by
histamine in normal Cl solution (Fig. 8). Thus long-term
depletion of intracellular Cl might affect contractility.
Indeed, low-Cl solution also produced a relaxant response
in histamine-induced contraction as discussed above. A normal level of
extracellular Cl might be necessary for the sustained
contraction induced by histamine. Second, methanesulfonate ion and
glutamate ion, respectively, were used in these two studies.
Methanesulfonate ion, which is an impermeant Cl channel
anion, was used in our study. Because of its negligible permeability
and apparent lack of interaction with Cl, it is used as
the preferred impermeant Cl substitute in substitution
studies of membrane conductance (26, 27, 34). The
low-Cl buffer replaced with MS potentiated
NE-induced contraction in the rat aorta (26, 27) and
ET-1-induced contraction in the rabbit basilar artery (7).
Role of Ca2+-dependent
Cl channels in histamine-induced contraction.
Histamine activates H1 receptors in the rabbit pulmonary
and the guinea pig tracheal myocytes, releases Ca2+ from
the intracellular caffeine-sensitive Ca2+ store, and
increases membrane conductance to Cl and K+
ion (13, 17, 41, 42). In the rabbit middle cerebral
artery, histamine induces a transient contraction by releasing
Ca2+ from intracellular store, in the presence of
Co2+ (1 mM), which prevents Ca2+ influx through
voltage-dependent Ca2+ channels and nonselective cation
channels (14, 15). Histamine activates an inward current
close to the equilibrated potential for Cl in the rat
basilar artery and Cl channel blocker niflumic acid (100 µM) reversed completely the inward current (23). Thus
histamine releases intracellular Ca2+, activates
Cl channels, and produces contraction in cerebral arteries.
channel blockers, as shown in the present study as
well as reported previously (15, 23). Three
Cl channel blockers were used in the present study and
all achieved a relaxant effect, although IAA-94 seems more potent than
those of NPPB or niflumic acid. Niflumic acid is the only specific
inhibitor for the Ca2+-dependent Cl channels
and it blocks the Ca2+-dependent Cl channels
in smooth muscle, including cerebral vascular smooth muscle cells
(15, 32). Niflumic acid, at the same concentration as used
in this study, reduced histamine-induced inward current in tracheal
myocytes and attenuated ET-1-induced contraction in the pulmonary
artery in the rat (18, 24). Niflumic acid reduced the
amplitude of depolarization and contraction by histamine in the rabbit
middle cerebral artery and the rabbit basilar artery (7, 15,
23). However, due to the poor selectivity of these Cl channel blockers and their other effects on
K+ channels (13, 25, 38) or voltage-dependent
Ca2+ channels (13, 24, 25), both channels are
important to the normal function of cerebral vascular function
(31, 35), the exact type of Cl channels
involved and their possible gating mechanism in the rabbit basilar
artery cannot be determined by the current study.
In conclusion,this is the first investigation to our knowledge of the
effect of Na+-K+-2Cl
cotransporter and HCO exchanger in
histamine-induced contraction in cerebral arteries. Various approaches,
as shown in Fig. 11, were used to
demonstrate that modulation of Cl flux alters
histamine-induced contraction in the rabbit basilar arteries.
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flux in histamine-induced
contraction are presumed that histamine activates H1
receptor, which results in an elevation of intracellular
Ca2+, either by releasing Ca2+ from internal
stores or by promoting Ca2+ entry from extracellular space.
Elevation of intracellular Ca2+ induces contraction and in
the mean time activates Cl channels, especially the
Ca2+-activated Cl channels. The
Na+-K+-2Cl cotransporter and the
HCO exchanger are involved either
in the initial or in the plateau phases of histamine-induced
contraction. Disabling the
Na+-K+-2Cl cotransporter or the
HCO exchanger abolishes the
contractile response of the rabbit basilar artery to histamine.
Although a low extracellular Cl concentration enhances
the initial contraction to histamine, a normal level of
Cl is needed to maintain a sustained contraction.
This study revealed a unique phenomenon: normal level of
Cl is necessary to some extent for a sustained
contraction to histamine in the rabbit basilar artery. The mechanism
underneath this phenomenon remains unclear although relaxants released
from endothelial cells might not be involved. A proper understanding of
Cl flux in histamine-induced contraction in cerebral
arteries might be importance because maintaining a prolonged
contraction is essential for hypertension and cerebral vasospasm for
which we currently need more therapies (20, 30,
39).
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FOOTNOTES |
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Address for reprint requests and other correspondence: J. H. Zhang, Dept. of Neurosurgery, Univ. of Mississippi Medical Center, 2500 N. State St., Jackson, MS 39216 (E-mail: johnzhang3910{at}yahoo.com).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
First published December 13, 2001;10.1152/ajpheart.00837.2001
Received 25 September 2001; accepted in final form 1 December 2001.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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