(Hypertension. 1995;25:1069-1074.)
© 1995 American Heart Association, Inc.
Articles |
Cerebral ATP-Sensitive Potassium Channels During Acute Reduction of Carotid Blood Flow
From the Department of Clinical Laboratory and Medicine, Kyoto Prefectural University of Medicine, Kamigyo-ku, Kyoto; and the Department of Clinical Sciences and Laboratory Medicine, Kansai Medical University, Moriguchi City, Osaka (H.T.), Japan.
Correspondence to Masato Nishimura, MD, Department of Clinical Laboratory and Medicine, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602, Japan.
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Abstract |
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Abstract The ATP-sensitive potassium channels (KATP) are activated either by a decrease in intracellular ATP content or by a lowering of the ATP-ADP ratio such as during stroke. We studied the role of cerebral KATP on arterial pressure during acute reduction of cerebral blood flow in 12-week-old male Wistar rats anesthetized with urethane by recording arterial pressure and heart rate continuously. After bilateral ligation of the common carotid arteries, glibenclamide, a specific blocker of KATP, was injected intracerebroventricularly into the cerebral lateral ventricle. Glibenclamide elicited a sustained vasopressor response in a dose-dependent manner in rats with bilateral carotid artery ligation (10 nmol, +15±2 mm Hg; 1 nmol, +5±1 mm Hg, P<.01 versus vehicle), but hemodynamic alterations were barely recorded with glibenclamide in sham-operated control rats. The abdominal sympathetic discharge was not increased significantly enough to explain the pressor mechanism. Similarly, pretreatments with intravenous injections of bunazosin, an
1-adrenoceptor
antagonist, did not affect the pressor response of
intracerebroventricular glibenclamide. To investigate the vasopressor
mechanism further, we measured plasma and pituitary concentrations of
arginine vasopressin and determined the effects of vasopressin
receptor antagonists. The intracerebroventricular injections of
glibenclamide significantly increased the plasma concentration of
vasopressin (P<.05) and significantly decreased the
pituitary concentration of vasopressin (P<.05) in rats with
bilateral carotid artery ligation. Intravenous pretreatment with the
vasopressin V1 receptor antagonist OPC-21268 abolished the
vasopressor response to intracerebroventricular glibenclamide (+16±2
versus +1±1 mm Hg, P<.01). These findings indicate that
KATP in the brain may inhibit an excess rise in arterial
pressure in part by decreasing the release of vasopressin from the
pituitary during bilateral carotid artery ligation.
Key Words: potassium channels • blood pressure • ligation • carotid artery • vasopressin • hypertension, experimental
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Introduction |
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The ATP-sensitive potassium channels (KATP), 45-kD proteins with ATP-binding domains,1 are thought to play a key role in the glucose-induced release of insulin from pancreatic ß-cells.2 Such activity is inhibited more than 95% by 1 mmol/L ATP3 but is activated by a decrease in the intracellular concentration of ATP or by a lowering of the ratio of ATP to ADP,4 5 which may occur during brain ischemia. KATP are widely distributed in the heart, peripheral vasculature, and the brain as well as in the pancreas3 and are considered to play a specific physiological role in each organ. The activation of KATP shortens the action potential, inhibits the increase in intracellular concentration of Ca2+, and reduces the oxygen consumption in heart muscle cells.6 The activation of KATP also induces vasodilatation by relaxing vascular smooth muscle cells.7 Autoradiographic studies of KATP using the high-affinity ligand revealed that KATP are abundant in the globus pallidus, hippocampus, and anterior pituitary but also broadly in other cerebral regions in the telencephalon, diencephalon, and cerebellum of rats.8 Northern blot analysis in rats showed that signal is detected in the thalamus, hypothalamus, and pituitary of the brain, but no signal is detected in the other brain regions,1 meaning that cerebral KATP may be related to cerebral regulation of cardiovascular and endocrine functions.
Patients with stroke, such as a cerebral thrombosis or hemorrhage, show a fluctuation in arterial pressure, with an elevation seen in the acute phase.9 Bilateral carotid artery ligation of normotensive Wistar rats raises arterial pressure,10 11 although it does not produce pronounced cerebral ischemia. Not only the baroreceptor and chemoreceptor reflexes via the carotid sinus but also hyperactivation of the catecholaminergic system may be the main causes of this rise in arterial pressure during cerebrovascular accidents in humans as well as in rats after ligation of the carotid artery.12 13 Since bilateral ligation of the carotid arteries reduces regional cerebral blood flow in the diencephalon of normotensive Wistar rats,10 11 KATP in the brain may be activated during the ligation. The opening of cerebral KATP may affect arterial pressure during acute cerebral ischemia.
Centrally induced cardiovascular responses are usually mediated by both sympathetic nervous system activity and release of pituitary hormones such as vasopressin. Arginine vasopressin (AVP), which is supposed to be released from pituitary glands during cerebral ischemia, is reported to block KATP from outside the cell membrane.14 Therefore, AVP may be involved in the regulatory mechanism of the brain KATP and blood pressure.
The aim of the present study was to elucidate the role of cerebral KATP in the possible regulation of arterial pressure and the underlying mechanism during acute reduction of cerebral blood flow by measuring not only blood pressure and heart rate but also peripheral sympathetic discharge and plasma AVP levels in rats with bilateral common carotid arterial ligation.
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Methods |
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Twelve-week-old male Wistar rats (n=109, 257±3 g) were purchased from Oriental Bio-Service Laboratory (Kyoto, Japan). The experimental procedure was authorized by the Committee for Animal Research of Kyoto Prefectural University of Medicine. Rats were anesthetized with urethane (120 mg/100 g IP, Nakarai Tesque). Catheters (PE-50, Clay Adams, Becton-Dickinson) were inserted into the femoral artery for recording of arterial pressure and into the femoral vein for injection of drugs. Arterial pressure was recorded continuously by connecting the catheter to a small-volume displacement pressure transducer (TP-200T, Nihon Kohden). Heart rate (pulse rate, in beats per minute [bpm]) was automatically calculated by triggering the femoral arterial pulse pressure with a tachometer (AT-601G, Nihon Kohden). The trachea was intubated with a cannula (PE-240, Clay Adams, Becton-Dickinson) for artificial ventilation after skeletal muscle was paralyzed by injection of decamethonium bromide (0.2 mg/100 g IV, Sigma Chemical Co).
Bilateral Ligation of Common Carotid Arteries
With rats under urethane anesthesia, bilateral carotid arteries
were dissected free from the vagosympathetic trunks in the neck and
ligated with double sutures (3-0 silk, Nippon Shoji Co). A sham
operation revealed the carotid arteries without ligation. To prevent
respiratory arrest, all experimental rats, including sham-operated
rats, received artificial ventilation with room air during the
experiment. When both arterial pressure and heart rate had become
stable approximately 60 minutes after bilateral ligation of the carotid
arteries, we started the experiments described below.
Intracerebroventricular Injections
A guide cannula (23-gauge stainless steel tube, 30 mm long with
a 30-gauge stylet) was inserted stereotaxically into the right lateral
cerebral ventricle. The stereotaxic coordinates were 1.6 mm right
laterally and 0.8 mm dorsoventrally from the bregma, with the incisor
bar set 3.3 mm below the interaural line. Agents were injected into the
cerebral ventricle (ICV) by insertion of an injection cannula (30-gauge
stainless steel tube) connected to a 25-µL syringe into the guide
cannula. In each injection, 10 µL was delivered manually into the
ventricle over 10 seconds. At the end of each experiment, methylene
blue solution was injected through the injection cannula to verify its
correct placement in the right lateral ventricle.
Recording of Abdominal Sympathetic Nerve Activity
After an extensive transverse dissection of the left lateral
abdominal wall was made, the sympathetic nerve bundle emerging from the
celiac ganglion and accompanied by a superior mesenteric artery was
placed over a bipolar electrode. These methods have been described in
detail elsewhere.15
Radioimmunoassay for AVP
The plasma concentration of AVP and the amount of AVP in the
pituitary glands were measured with a radioimmunoassay kit (Mitsubishi
Medical Science Co). Blood was collected into plastic tubes containing
Na2EDTA (final concentration, 1 mg/mL) at 5 minutes after
ICV and intravenous injections of glibenclamide or vehicle, when the
peak response was recorded. Rats were killed by decapitation, and the
pituitary glands were immediately removed and stored at -20°C. After
determination of the wet weight of the pituitary gland, the tissue was
homogenized (Ultra Disperser, model LK-22, Yamato) with 2 mL of 0.1
mol/L acetate buffer. The homogenate was then boiled for 10 minutes and
centrifuged at 40 000g for 30 minutes. The supernatant was
evaporated with an air stream. The dried residue was redissolved in the
assay buffer for assay. Plasma samples were applied to Sep-Pak C18
columns (Pharmacia Fine Chemicals) and eluted with 1.5 mL methanol. The
extract was evaporated with an air stream. The intra-assay coefficient
of variability was 9.9% (n=10); the interassay coefficient of
variability was 15.3% (n=8).
Measurement of Plasma Glucose Concentration
To exclude the possibility that glibenclamide administration may
induce hypoglycemia, we measured the plasma glucose level of test
animals 30 minutes after injections of glibenclamide or vehicle using
an automatic analyzer (Ektachem 700 analyzer, Eastman Kodak).
Agents
Glibenclamide (Sigma) and bunazosin hydrochloride (Eisai
Pharmaceutical Co) were dissolved in saline (0.9% NaCl), and pH was
adjusted to 7.5 with sodium hydroxide. Physiological saline (0.9%
NaCl, pH 7.5) was used as the control vehicle for glibenclamide and
bunazosin. OPC-21268 (Otsuka Pharmaceutical Co), a nonpeptide blocker
of AVP V1 receptors,16 and OPC-31260 (Otsuka),
an AVP V2 receptor blocker,17 were dissolved
in 0.1 mol/L dimethyl sulfoxide (Sigma), which was used as the control
vehicle for OPC-21268 and OPC-31260 solutions.
Experimental Protocol
We recorded arterial pressure, heart rate, and abdominal
sympathetic nerve activity for no less than 30 minutes after ICV
injections of glibenclamide (1 and 10 nmol) or vehicle into the rats
with or without bilateral ligation of carotid arteries and intravenous
injections of glibenclamide (10 nmol) or vehicle into the rats with
bilateral carotid artery ligation. For measurements of plasma and
pituitary AVP, we killed rats 5 minutes after glibenclamide
administration, when the peak vasopressor response was recorded with
the ICV injection of glibenclamide, and collected 1 mL of blood and
pituitary glands. Intravenous pretreatments with OPC-21268 (5 mg/kg)
and OPC-31260 (10 mg/kg) were performed 5 minutes before the ICV
injections of glibenclamide, and intravenous pretreatments with
bunazosin hydrochloride (50 µg) were performed 10 minutes before ICV
injections of glibenclamide, when arterial pressure was stable.
Statistical Analysis
Data are expressed as mean±SEM. Differences between
experimental and control groups were evaluated by one-way ANOVA
followed by Duncan's multiple range test. A level of P<.05
was accepted as statistically significant.
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Results |
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Effects of Bilateral Ligation of the Carotid Arteries
Arterial pressure was markedly elevated immediately after bilateral ligation of the carotid arteries. Approximately 60 minutes later, mean arterial pressure was still higher in rats with bilateral ligation of the carotid arteries (n=17) than in sham-operated rats (n=10) (134±4 versus 92±10 mm Hg, P<.01). Heart rate did not differ in the two groups (366±24 versus 358±18 bpm).
Cardiovascular Responses to ICV Injections of Glibenclamide
ICV injections of glibenclamide produced a significant and
dose-dependent increase in mean arterial pressure in rats with
bilateral ligation of the carotid arteries compared with ICV injections
of vehicle. The peak pressor response was observed 3 to 5 minutes after
injection of either 1 or 10 nmol glibenclamide. ICV injections of 10
nmol glibenclamide increased arterial pressure for more than 30
minutes. Heart rate was decreased at 25 and 30 minutes after ICV
injections of 10 nmol glibenclamide compared with vehicle; ICV
injections of 1 nmol glibenclamide produced no appreciable change in
heart rate (Figs 1 and 2). ICV injections
of glibenclamide had no influence on abdominal sympathetic nerve
activity in rats with bilateral ligation of the carotid arteries
(changes in abdominal sympathetic nerve activity from baseline, 3
minutes after injection: vehicle, +0.05±0.03 [n=5]; 1 nmol
glibenclamide, +0.05±0.12 [n=5]; 10 nmol glibenclamide, -0.03±0.18
[n=5]; 30 minutes after injection: vehicle, +0.03±0.05 [n=5]; 1
nmol glibenclamide, +0.06±0.13 [n=5]; 10 nmol glibenclamide,
+0.08±0.06 [n=5]).
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ICV injections of 10 nmol glibenclamide in sham-operated rats did not elicit a significant response in mean arterial pressure or heart rate (Figs 1 and 3). Intravenous injections of 10 nmol glibenclamide had no significant effect on mean arterial pressure or heart rate of rats with bilateral ligation of the carotid arteries compared with injection of vehicle (change in mean arterial pressure: vehicle, -2±4 mm Hg [n=5]; 10 nmol glibenclamide, +1±3 mm Hg [n=5]; change in heart rate: vehicle, -4±6 bpm [n=5]; 10 nmol glibenclamide, -2±6 bpm [n=5]).
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ICV and intravenous injections of glibenclamide had no effect on plasma glucose levels in rats with bilateral ligation of the carotid arteries (ICV injection: vehicle, 8.7±0.9 mmol/L [n=7]; 1 nmol glibenclamide, 10.4±2.3 mmol/L [n=6]; 10 nmol glibenclamide, 10.5±2.1 mmol/L [n=7]; intravenous injection: vehicle, 9.4±1.9 mmol/L [n=5]; 10 nmol glibenclamide, 9.7±1.4 mmol/L [n=5]).
Plasma Concentrations and Pituitary Contents of AVP
The Table shows plasma and pituitary concentrations
of AVP after injection of glibenclamide. ICV injections of 10 nmol
glibenclamide significantly increased the plasma AVP concentration in
rats with bilateral ligation of the carotid arteries and produced a
significant decrease in the pituitary AVP content compared with
injection of vehicle. Plasma and pituitary concentrations of AVP were
not significantly affected in sham-operated rats administered 10 nmol
glibenclamide ICV. Intravenous injections of 10 nmol glibenclamide did
not influence AVP levels in rats with bilateral ligation of the carotid
arteries.
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Effects of Intravenous Pretreatment With OPC-21268 on the Pressor
Response to ICV Injections of Glibenclamide
Intravenous administration of OPC-21268 reduced arterial
pressure (control, +2±3 mm Hg [n=6]; OPC-21268, -22±4 mm Hg
[n=6], P<.01) and abolished the vasopressor response to
ICV injections of 10 nmol glibenclamide in rats with bilateral ligation
of the carotid arteries (Figs 4 and 5).
Heart rate was not influenced by intravenous pretreatment with
OPC-21268 (30 minutes after ICV injection of 10 nmol glibenclamide:
control, -56±12 bpm [n=6]; OPC-21268, -64±14 bpm [n=6]).
Intravenous pretreatment with OPC-31260 (10 mg/kg) affected neither
basal arterial pressure (control, +2±3 mm Hg [n=5]; OPC-31260,
-5±5 mm Hg [n=5]) nor vasopressor response to ICV injection of 10
nmol glibenclamide in rats with bilateral ligation of the carotid
arteries (vehicle, +15±3 mm Hg [n=5]; OPC-31260, +16±4 mm Hg
[n=5]).
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Effects of 1-Adrenoceptor Blockade on the Pressor
Responses to Glibenclamide
Intravenous injections of bunazosin hydrochloride (50 µg), an
1-adrenergic blocker, produced a prolonged lowering of
arterial pressure in rats with bilateral ligation of the carotid
arteries (-42±3 mm Hg) (Fig 6). Injections of 10 nmol
glibenclamide ICV produced a marked vasopressor response compared with
vehicle (vehicle, +3±2 mm Hg [n=5]; glibenclamide, +16±3 mm Hg
[n=5], P<.01).
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Discussion |
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We found in the present study that ICV injections of glibenclamide produced a dose-dependent pressor effect in rats with bilateral ligation of the carotid arteries but not in sham-operated rats. Because glibenclamide is a specific and potent blocker of KATP18 and because intravenous administration of glibenclamide did not elicit any cardiovascular response in rats with bilateral ligation of the carotid arteries, this pressor effect must be closely related to inhibition of KATP in the ischemic brain. Intravenous glibenclamide can reach the brain after bilateral ligation of the carotid artery because the residual blood flow still exists, although the amount of glibenclamide must be lower than the ICV injection because of the dilution with blood. A lack of vasopressor effects with intravenous injections of glibenclamide suggests that a large amount of glibenclamide is needed to inhibit KATP in rat brain. Otherwise, glibenclamide may not penetrate the blood-brain barrier.
Although KATP in the peripheral vasculature are the
targets of antihypertensive agents,7 the
relationship between cerebral KATP and the regulation of
arterial pressure has not been previously investigated. Inhibition of
KATP in the substantia nigra reportedly elicits the release
of 
-aminobutyric acid.19 The bradycardia observed after
ICV injections of 10 nmol glibenclamide in rats with bilateral ligation
of the carotid arteries may be explained by the action of
-aminobutyric acid released by glibenclamide.
Both plasma and pituitary AVP concentrations were significantly
increased in rats with bilateral ligation of the carotid arteries
compared with sham-operated rats. ICV injections of 10 nmol
glibenclamide significantly increased the plasma concentrations of AVP
and decreased the pituitary concentrations of AVP. ICV injections of
glibenclamide increased AVP release and turnover rate in the pituitary
glands of rats with bilateral ligation of the carotid arteries. This
finding means that cerebral KATP inhibit AVP release from
the pituitary glands in the hypoperfused brain. This mechanism may
resemble that for KATP in the pancreatic ß-cell, which
inhibits insulin release.2 Since AVP exhibits a marked
vasoconstrictive effect in vascular smooth muscle cells20
and potentiates the vasoconstrictive activity of such vasoactive
peptides as angiotensin II21 and
endothelin,22 the increased synthesis and release of AVP
into the peripheral circulation may be involved in causing the
hypertension that follows ligation of the carotid arteries. In support
of this, the pressor effect produced by injection of glibenclamide ICV
into rats with bilateral ligation of the carotid arteries was abolished
by intravenous pretreatment with OPC-21268 and was unaffected by
pretreatment with either a V2 receptor antagonist or an
1-adrenoceptor blocker. ICV injections of glibenclamide
did not influence abdominal sympathetic nerve activity. Thus, the
pressor response was apparently not mediated by peripheral sympathetic
nerve activity or by the stimulation of AVP V2 receptors
but by activation of AVP V1 receptors in the peripheral
vascular bed. AVP V1 receptors are distributed widely in
the vascular smooth muscle cells and produce vasoconstriction via a
phosphatidylinositol pathway.23 Both plasma and pituitary
concentrations of AVP were increased in rats with bilateral ligation
even by ICV injections of vehicle. Thus, bilateral ligation of the
carotid arteries per se elicited AVP synthesis and release. Intravenous
injections of OPC-21268 reduced arterial pressure in rats with
bilateral ligation of the carotid arteries. These findings suggest that
an elevated level of circulating AVP may participate in the vasopressor
mechanism during bilateral carotid artery ligation via the AVP
V1 receptors. In addition, AVP is reported to block
KATP in peripheral smooth muscle cells.22 Both
the increase in plasma levels of AVP and the blocking of
KATP in peripheral smooth muscle cells may raise arterial
pressure. During the acute reduction of cerebral blood flow, activated
KATP in the brain may inhibit the rise in arterial pressure
by inhibiting the hypersecretion of AVP from the pituitary.
The carotid arteries supply blood exclusively to the cerebral cortex, midbrain, thalamus, and hypothalamus but not to the lower brain stem, as measured by injection of radioactive microspheres into the carotid arteries.24 Bilateral ligation of the carotid arteries in spontaneously hypertensive rats (SHR) causes acute ischemia of the brain areas in which the carotid artery is responsible for the blood supply.10 11 After carotid ligation, cortical blood flow was reduced to less than 10% of the resting level, and thalamic blood flow was decreased to less than 20% in SHR.11 In normotensive Wistar rats, bilateral carotid artery ligation also caused the reduction of regional cerebral blood flow, although its extent was less than in SHR: carotid ligation decreased cortical blood flow to 36% to 38% of the resting level and thalamic blood flow to 40% in Wistar rats.11 Therefore, present bilateral carotid artery ligation is the model of acute reduction of carotid blood flow with the minimum amount of ischemia, which does not always produce cerebral infarction.25
The cardiovascular regulatory roles of cerebral KATP have not been clarified, despite their abundance in the brain. The present report is the first to show that cerebral KATP are involved in cardiovascular regulation during bilateral common carotid artery ligation by inhibiting the secretion of AVP from the pituitary.
Received August 8, 1994; first decision September 8, 1994; accepted December 23, 1994.
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References |
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