Neurogenically evoked cerebral artery constriction is mediated by neuropeptide Y

1994 ◽  
Vol 72 (9) ◽  
pp. 1086-1088 ◽  
Author(s):  
Ismail Laher ◽  
Peter Germann ◽  
John A. Bevan
Keyword(s):  
Neuropeptide Y ◽  
Cerebral Artery ◽  
Basilar Artery ◽  
Cerebral Arteries ◽  
Immune Serum ◽  
Nerve Endings ◽  
Transmural Stimulation ◽  
Basilar Arteries ◽  
Neurogenic Vasoconstriction ◽  
Stimulation Of

We examined the proposal that neuropeptide Y (NPY) released from nerve endings constricts cerebral arteries. Neurogenic vasoconstriction of rabbit basilar arteries is of adrenergic origin but is resistant to blockade by classical α-adrenoceptor antagonists. Tetrodotoxin-sensitive contractions of the rabbit basilar artery were elicited by transmural stimulation of nerves. The contractions were inhibited by incubation of tissues with an antiserum to NPY (0.32 μL undiluted immune serum/mL); addition of prazosin (0.1 μM) did not further attenuate the nerve-mediated contraction. The antiserum to NPY also antagonized vasoconstriction due to exogenously administered NPY and was without effect on responses due to histamine or angiotensin. Our results indicate that neurogenic vasoconstriction of the rabbit basilar artery is largely due to the release of NPY and that it is unlikely that other vasoconstrictors contribute significantly to the increased tone.Key words: cerebral artery, nerves, neuropeptide Y, norepinephrine.

scholarly journals Cerebrovascular responses in mice deficient in the potassium channel, TREK-1

2010 ◽  
Vol 299 (2) ◽  
pp. R461-R469 ◽  
Author(s):  
Khodadad Namiranian ◽  
Eric E. Lloyd ◽  
Randy F. Crossland ◽  
Sean P. Marrelli ◽  
George E. Taffet ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Linolenic Acid ◽  
Basilar Artery ◽  
Cerebral Arteries ◽  
K Channel ◽  
Whole Cell ◽  
Middle Cerebral Arteries ◽  
Basilar Arteries ◽  
Cerebrovascular Smooth Muscle Cells ◽  
Pore Domain

We tested the hypothesis that TREK-1, a two-pore domain K channel, is involved with dilations in arteries. Because there are no selective activators or inhibitors of TREK-1, we generated a mouse line deficient in TREK-1. Endothelium-mediated dilations were not different in arteries from wild-type (WT) and TREK-1 knockout (KO) mice. This includes dilations of the middle cerebral artery to ATP, dilations of the basilar artery to ACh, and relaxations of the aorta to carbachol, a cholinergic agonist. The nitric oxide (NO) and endothelium-dependent hyperpolarizing factor components of ATP dilations were identical in the middle cerebral arteries of WT and TREK-1 KO mice. Furthermore, the NO and cyclooxygenase-dependent components were identical in the basilar arteries of the different genotypes. Dilations of the basilar artery to α-linolenic acid, an activator of TREK-1, were not affected by the absence of TREK-1. Whole cell currents recorded using patch-clamp techniques were similar in cerebrovascular smooth muscle cells (CVSMCs) from WT and TREK-1 KO mice. α-linolenic acid or arachidonic acid increased whole cell currents in CVSMCs from both WT and TREK-1 KO mice. The selective blockers of large-conductance Ca-activated K channels, penitrem A and iberiotoxin, blocked the increased currents elicited by either α-linolenic or arachidonic acid. In summary, dilations were similar in arteries from WT and TREK-1 KO mice. There was no sign of TREK-1-like currents in CVSMCs from WT mice, and there were no major differences in currents between the genotypes. We conclude that regulation of arterial diameter is not altered in mice lacking TREK-1.

scholarly journals Transcranial Doppler Enhanced Thrombolysis for Embolic Occlusion of Major Cerebral Arteries

2003 ◽  
Vol 9 (1_suppl) ◽  
pp. 129-132
Author(s):  
T. Yamanome ◽  
M. Sasoh ◽  
Y. Kubo ◽  
Y. Nishikawa ◽  
H. Endoh ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Basilar Artery ◽  
Transcranial Doppler ◽  
Cerebral Arteries ◽  
Ultrasound Irradiation ◽  
Haemorrhagic Transformation ◽  
Good Outcome

For the treatment of 11 patients with hyperacute embolic occlusion of major cerebral arteries (ten with occlusion of middle cerebral artery and one with occlusion of basilar artery), TCD-enhanced thrombolysis (TCDET) was performed in combination with ultrasound irradiation, using diagnostic transcranial Doppler (TCD) (TC2-64B: 2MHz, 100mW/cm2, pulsed wave) (TCDET group), and the effectiveness of this procedure was compared with that of local intra-arterial fibrinolysis (LIF) in 45 patients with embolic occlusion of the middle cerebral artery (LIF group). Regarding dose of TPA, the LIF group used 1046.7 ± 607.8 units and the TCDET group 700.0 ± 431.3 units (p < 0.05). Regarding time technically required to attain recanalization, the LIF group required 68.2 minutes, and the TCDET group 28.6 minutes. A good outcome was noted in 60.8% of the LIF group and 64% of the TCDET group. Haemorrhagic transformation was observed in 7.8% of the LIF group and in 0% of the TCDET group. No complications due to TCD irradiation were observed in the TCDET group. These findings suggest that TCDET can be an effective method of achieving recanalization.

Mechanism underlying the response to vasodilator nerve stimulation in isolated dog and monkey cerebral arteries

1990 ◽  
Vol 259 (5) ◽  
pp. H1511-H1517 ◽  
Author(s):  
N. Toda ◽  
T. Okamura
Keyword(s):  
Nitric Oxide ◽  
Electrical Stimulation ◽  
Coronary Artery ◽  
Substance P ◽  
Nerve Stimulation ◽  
Cerebral Arteries ◽  
Inhibitory Effect ◽  
Synthesis Inhibitor ◽  
Transmural Stimulation ◽  
Stimulation Of

Relaxant responses to transmural electrical stimulation and nicotine of cerebral artery strips obtained from dogs and Japanese monkeys were abolished by tetrodotoxin and hexamethonium, respectively, and suppressed by treatment with NG-monomethyl-L-arginine (L-NMMA), a nitric oxide (NO) synthesis inhibitor. The inhibitory effect was prevented and reversed by L-arginine but not by D-arginine. The relaxations suppressed by L-NMMA were not increased by exogenously applied NO. Endothelium denudation did not alter the response to transmural stimulation and nicotine or the inhibitory effect of L-NMMA. D-NMMA did not inhibit the response to vasodilator nerve stimulation. Dog coronary artery relaxations caused by transmural stimulation were not inhibited by L-NMMA but reversed to contractions by propranolol. Relaxations caused by substance P of dog cerebral arteries treated with indomethacin were dependent on endothelium and inhibited by L-NMMA, whereas those by NO and nitroglycerin, endothelium-independent relaxations, were unaffected. It is concluded that chemical and electrical stimulation of vasodilator nerves relaxes dog and monkey cerebral arteries, possibly by a mediation of NO rather than a stimulating action of NO on the release of vasodilator transmitter. Endothelium-dependent relaxations by substance P of dog cerebral arteries appear to be mediated by NO.

Stretching releases Ca2+ from intracellular storage sites in canine cerebral arteries

1994 ◽  
Vol 72 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Yoshio Tanaka ◽  
Shinzo Hata ◽  
Hiromi Ishiro ◽  
Kunio Ishii ◽  
Koichi Nakayama
Keyword(s):  
Phospholipase C ◽  
Cerebral Artery ◽  
Basilar Artery ◽  
Cerebral Arteries ◽  
Mechanical Stretch ◽  
Inositol 1,4,5 Trisphosphate ◽  
Intracellular Ca ◽  
Canine Basilar Artery ◽  
Intracellular Storage

Mechanical stretch applied to canine cerebral artery produced myogenic contraction. The contraction of the artery in response to quick stretch was dependent on not only the transmembrane influx of Ca2+ through 1,4-dihydropyridine-sensitive Ca2+ channels but also the release of Ca2+ from intracellular storage sites: the stretch-produced contractile component that was resistant to 0.1 μM nicardipine, a Ca2+-channel antagonist, was inhibited by about 50% after treatment with ryanodine, and was almost completely suppressed by 0.1 mM 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate, a putative phospholipase C inhibitor, or by lowering the temperature from 35 to 20 °C. The results suggest that in addition to transmembrane influx of Ca2+ through L-type Ca2+ channels, the release of Ca2+ from both ryanodine-sensitive and -insensitive intracellular storage sites, which increases intracellular Ca2+, accounts for the stretch-induced contraction of canine basilar artery. It seems also possible that inositol 1,4,5-trisphosphate is a common mediator for the release of Ca2+ from both types of intracellular storage sites.Key words: stretch-induced contraction, cerebral artery, phospholipase C, ryanodine, Ca2+ storage sites, inositol 1,4,5-trisphosphate, Ca2+ release, Ca2+-channel antagonist.

scholarly journals Study of Posterior Cerebral Artery in Human Cadaveric Brain

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
S. A. Gunnal ◽  
M. S. Farooqui ◽  
R. N. Wabale
Keyword(s):  
Cerebral Artery ◽  
Basilar Artery ◽  
Posterior Cerebral Artery ◽  
Cerebral Arteries ◽  
Occipital Lobe ◽  
Common Trunk ◽  
Branching Pattern ◽  
Morphological Variations ◽  
Left Posterior ◽  
Mean Diameter

Objective. Basilar artery (BA) terminates in right and left posterior cerebral arteries (PCAs). Each PCA supplies respective occipital lobe of the cerebrum. The present study is designed to know the morphology, morphometry, branching pattern, and symmetry of PCA. Methods. The study included 340 PCAs dissected from 170 human cadaveric brains. Results. Morphological variations of P1 segment included, aplasia (2.35%), hypoplasia (5.29%), duplication (2.35%), fenestration (1.17%), and common trunk shared with SCA (1.76%). Morphological variations of origin of P2 segment included direct origin of it from BA (1.17%) and ICA (2.35%). Unusually, two P2 segments, each arising separately from BA and ICA, were observed in 1.17%. Unilateral two P2 segments from CW were found in 0.58%. Morphological variations of course of P2 were duplication (0.58%), fenestration (0.58%), and aneurysm (1.76%). Unilateral P2 either adult or fetal was seen in 4.71%. The group II branching pattern was found to be most common. Asymmetry of P2 was 40%. Morphometry of P2 revealed mean length of 52 mm and mean diameter of 2.7 mm. Conclusion. The present study provides the complete anatomical description of PCA regarding morphology, morphometry, symmetry, and its branching pattern. Awareness of these variations is likely to be useful in cerebrovascular procedures.

Stimulation of α2Adrenoceptors Dilates the Rat Middle Cerebral Artery

1996 ◽  
Vol 85 (1) ◽  
pp. 82-90 ◽  
Author(s):  
Robert M. Bryan ◽  
M. Y. Eichler ◽  
M. W. G. Swafford ◽  
T. D. Johnson ◽  
M. S. Suresh ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Pertussis Toxin ◽  
Saline Solution ◽  
Cerebral Arteries ◽  
Middle Cerebral Arteries ◽  
Physiologic Saline ◽  
Stimulation Of

Background Because alpha 2 adrenoceptor agonists are used as adjuncts to anesthetics, their effects on the cerebrovascular circulation are of prime importance. We studied changes in the diameter of rat middle cerebral arteries after stimulation of alpha 2 adrenoceptors with UK14,304. Methods Rat middle cerebral arteries were isolated, cannulated at each end with a glass micropipette, and pressurized to 85 mmHg. The middle cerebral arteries were immersed in a bath (37 degrees C) containing physiologic saline solution, and luminally perfused with physiologic saline solution (100 microliters/ min). Changes in vessel diameter were measured after magnification with a microscope. Results Resting diameter of the middle cerebral arteries was 239 +/- 13 microns (n = 8) for the first study. A dose-dependent dilation was produced by addition of UK14,304 to the extraluminal bath; a 10-15% increase in diameter occurred at a concentration of 10(-4)M. The dilations produced by UK14,304 were blocked with selective alpha 2-antagonists, idazoxan and rauwolscine, but not by the selective alpha 1-antagonist, prazosin. The dilations could be blocked by removal of the endothelium, or the nitric oxide synthase inhibitor, N-nitro-L-arginine methyl ester (10(-5) M). The inhibitory effects of N-nitro-L-arginine methyl ester were reversed with the addition of 10(-3) M L-arginine, but not 10(-3) M D-arginine. Furthermore the dilation produced by UK14,304 was completely abolished with pertussis toxin (100 ng/ml). Conclusions It was concluded that the stimulation of alpha 2 adrenoceptors with UK14,304 produced a dilation in the rat middle cerebral artery that (1) was dependent on intact endothelium, (2) involved nitric oxide, and (3) acted via a pertussis toxin-sensitive G protein.

Age-related changes in responses to nerve stimulation and catecholamines in isolated monkey cerebral arteries

1991 ◽  
Vol 260 (5) ◽  
pp. H1443-H1448 ◽  
Author(s):  
N. Toda
Keyword(s):  
Electrical Stimulation ◽  
Cerebral Artery ◽  
Vascular Tone ◽  
Cerebral Arteries ◽  
Mechanical Responses ◽  
Prostaglandin F2 Alpha ◽  
Age Related ◽  
Basilar Arteries ◽  
Median Effective Concentration ◽  
Regulation Of Vascular Tone

Mechanical responses to transmural electrical stimulation, nicotine, norepinephrine, and isoproterenol were compared in cerebral artery strips obtained from Japanese monkeys of different ages (1 mo, 1 yr, 4–7 yr, and greater than 7 yr old). Transmural electrical stimulation produced a contraction in the baby and juvenile monkey arteries contracted with prostaglandin F2 alpha, whereas the older monkey arteries responded to the stimulation with a relaxation. The stimulation-induced contraction was abolished or reversed to a relaxation by phentolamine; the relaxation was not influenced by propranolol and atropine but was abolished by tetrodotoxin, as was the response of the mature monkey arteries. Contractions caused by norepinephrine were greater in baby cerebral arteries than in the older monkey arteries; however, the apparent median effective concentration values did not differ. Middle cerebral artery contractions were greater than those of basilar arteries. The norepinephrine-induced contraction was suppressed by prazosin but not influenced by yohimbine. Isoproterenol (up to 10(-6) M) produced a greater relaxation in the baby arteries than in the older monkey arteries. It is suggested that adrenergic nerves innervating immature monkey cerebral arteries contribute to the regulation of vascular tone predominantly over nonadrenergic, noncholinergic vasodilator nerves, whereas the vasodilator nerves play a major role in the mature monkey arteries. alpha 1-Adrenoceptor subtype appears to be mainly involved in the norepinephrine-induced contraction of baby monkey cerebral arteries, as it is in that of the adult monkey arteries.

scholarly journals Endotoxin Decreases the Contractile Responses of the Porcine Basilar Artery to Vasoactive Substances

1993 ◽  
Vol 13 (4) ◽  
pp. 712-719 ◽  
Author(s):  
Masami Ueno ◽  
Tony J.-F. Lee
Keyword(s):  
Endothelial Cells ◽  
Basilar Artery ◽  
Muscle Tone ◽  
Cerebral Arteries ◽  
Contractile Responses ◽  
Vasoactive Substances ◽  
Basilar Arteries ◽  
Arterial Reactivity ◽  
Lps Treatment

The effects of endotoxin (lipopolysaccharide; LPS) on the reactivity of isolated porcine basilar artery were examined using in vitro tissue bath techniques. The active muscle tone of the basilar arterial rings with or without endothelial cells induced by U46619 (1 μ M) reached a plateau in 15 min, which was stable for the first hour and gradually decreased during the next 5 h. This time-dependent decrease in tone was significantly potentiated in the presence of LPS (20 μg/ml). The potentiation by LPS was blocked by Nw-nitro-l-arginine (l-NNA; 60 μ M), methylene blue (10 μ M), and dexamethasone (1 μ M) but not by hemoglobin (1 μ M). The effect of l-NNA was readily reversed by l-arginine but not by d-arginine. Furthermore, the contractile responses of porcine basilar arterial rings with or without intact endothelium to U46619 and KCl were decreased following incubation with LPS (20 μg/ml) for 4 h. Similar hyporeactivity was observed in cold storage–denervated cerebral arteries incubated with LPS for 4 h. This decrease in contractile responses in LPS-treated rings was reversed by 60 μ M l-NNA and 1 μ M dexamethasone. These results indicate that LPS treatment renders the porcine basilar arteries hyporesponsive to vasoconstrictors. Since effects of LPS were not modified by the presence of endothelial cells and perivascular neurons, the alteration in cerebral arterial reactivity may be due in part to an enhanced formation of nitric oxide from l-arginine in the vascular smooth muscle cells.

Cerebral vasospasm: contractile activity of hemoglobin in isolated canine basilar arteries

1980 ◽  
Vol 53 (6) ◽  
pp. 787-793 ◽  
Author(s):  
Takeo Tanishima
Keyword(s):  
Cerebral Vasospasm ◽  
Basilar Artery ◽  
Contractile Activity ◽  
Cerebral Arteries ◽  
Adenosine Monophosphate ◽  
Active Species ◽  
Exchange Chromatography ◽  
Basilar Arteries ◽  
Chronic Cerebral Vasospasm

✓ Recent studies suggest the possible role of the red blood cell (RBC) in causing chronic cerebral vasospasm. However, the basic action of hemoglobin (Hb), the major component of the RBC, on cerebral arteries remains unknown. The present study was undertaken to analyze the contractile effects of human Hb (purified by ion-exchange chromatography) on canine arteries in vitro. The contractile activity of lysed RBC was shown to be derived from Hb. Hemoglobin in oxygenated form (oxyHb) caused a maximum contraction equal to about 70% of that induced by serotonin in the basilar artery. Ferrous Hb's (oxyHb and carboxyHb) produced much greater contraction than ferric Hb's (methemoglobin and cyanmethemoglobin), suggesting that superoxide radicals, an active species of oxygen, may be related to the contractile activity of Hb. Neither methysergide, phentolamine, mepyramine, nor aspirin inhibited the vasoconstrictive activity of oxyHb. This finding indicates that the activation of serotonergic, alpha-adrenergic, or histaminergic H1 receptors, or prostaglandin synthesis may not be involved in the mechanism of action of oxyHb. The constituents of Hb caused little or no contraction as compared with Hb as a whole. The basilar artery was more highly sensitive to Hb than arteries from other anatomical locations. Cyclic adenosine monophosphate caused a very slight decrease in the Hb-induced contraction. It is concluded that oxyHb can contract cerebral arteries in vitro. These results, coupled with recent reports on the participation of the RBC in producing chronic vasospasm, strongly suggest that oxyHb released from RBC's plays an important role in the pathogenesis of chronic cerebral vasospasm.

Pharmacological comparison of endothelium-dependent relaxation in isolated cerebral and extracerebral arteries

1988 ◽  
Vol 69 (4) ◽  
pp. 580-587 ◽  
Author(s):  
Tadayoshi Nakagomi ◽  
Kazuhiro Hongo ◽  
Neal F. Kassell ◽  
Tomio Sasaki ◽  
R. Michael Lehman ◽  
...  
Keyword(s):  
Basilar Artery ◽  
Cerebral Arteries ◽  
Isometric Tension ◽  
Content Type ◽  
Wide Range ◽  
Basilar Arteries ◽  
The Common ◽  
The Difference ◽  
Endothelium Dependent Relaxation ◽  
Fine Print

✓ Endothelium-dependent relaxation was induced by acetylcholine (ACh), adenosine triphosphate (ATP), and thrombin in isolated cerebral and extracerebral arteries obtained from rabbits and dogs. Using an isometric tension-recording method, the authors then examined the difference in the extent of relaxation between the cerebral and extracerebral arteries. In rabbits, the dose-response curve of the basilar artery for ACh was significantly different (p < 0.05) from curves of the femoral and common carotid arteries. The IC50 value (the concentration inducing a one-half inhibition of the initial contractile tone) for the basilar artery in ACh-induced relaxation was significantly higher (p < 0.05) than for the common carotid artery, although the mean maximum relaxation of the basilar artery to ACh was not significantly different from that seen in extracerebral arteries. The relaxing effect of ACh in dogs was much less in the middle cerebral and basilar arteries than in the common carotid, vertebral, and femoral arteries. On the other hand, both ATP (in rabbits and dogs) and thrombin (in dogs) induced significantly more (p < 0.05) relaxation in the cerebral arteries than in the extracerebral arteries. Endothelium-dependent relaxation induced by ACh or ATP has been demonstrated in a wide range of arteries from a variety of animals. The present results suggest that ATP has a more important role than ACh in the regulation of the vascular tone of the major cerebral arteries in these two species.

Sign in / Sign up

Export Citation Format

Share Document