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 Type 1 inositol 1,4,5-trisphosphate receptors mediate UTP-induced cation currents, Ca2+ signals, and vasoconstriction in cerebral arteries

2008 ◽  
Vol 295 (5) ◽  
pp. C1376-C1384 ◽  
Author(s):  
Guiling Zhao ◽  
Adebowale Adebiyi ◽  
Eva Blaskova ◽  
Qi Xi ◽  
Jonathan H. Jaggar
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cerebral Artery ◽  
Purinergic Receptor ◽  
Cerebral Arteries ◽  
Muscle Cells ◽  
Physiological Functions ◽  
Inositol 1,4,5 Trisphosphate ◽  
Intracellular Ca

Inositol 1,4,5-trisphosphate receptors (IP3Rs) regulate diverse physiological functions, including contraction and proliferation. There are three IP3R isoforms, but their functional significance in arterial smooth muscle cells is unclear. Here, we investigated relative expression and physiological functions of IP3R isoforms in cerebral artery smooth muscle cells. We show that 2-aminoethoxydiphenyl borate and xestospongin C, membrane-permeant IP3R blockers, reduced Ca2+ wave activation and global intracellular Ca2+ ([Ca2+]i) elevation stimulated by UTP, a phospholipase C-coupled purinergic receptor agonist. Quantitative PCR, Western blotting, and immunofluorescence indicated that all three IP3R isoforms were expressed in acutely isolated cerebral artery smooth muscle cells, with IP3R1 being the most abundant isoform at 82% of total IP3R message. IP3R1 knockdown with short hairpin RNA (shRNA) did not alter baseline Ca2+ wave frequency and global [Ca2+]i but abolished UTP-induced Ca2+ wave activation and reduced the UTP-induced global [Ca2+]i elevation by ∼61%. Antibodies targeting IP3R1 and IP3R1 knockdown reduced UTP-induced nonselective cation current ( Icat) activation. IP3R1 knockdown also reduced UTP-induced vasoconstriction in pressurized arteries with both intact and depleted sarcoplasmic reticulum (SR) Ca2+ by ∼45%. These data indicate that IP3R1 is the predominant IP3R isoform expressed in rat cerebral artery smooth muscle cells. IP3R1 stimulation contributes to UTP-induced Icat activation, Ca2+ wave generation, global [Ca2+]i elevation, and vasoconstriction. In addition, IP3R1 activation constricts cerebral arteries in the absence of SR Ca2+ release by stimulating plasma membrane Icat.

Evaluation of prostaglandin biosynthetic activity in canine basilar artery following subarachnoid injection of blood

1981 ◽  
Vol 55 (5) ◽  
pp. 771-778 ◽  
Author(s):  
Tomio Sasaki ◽  
Sei-itsu Murota ◽  
Susumu Wakai ◽  
Takao Asano ◽  
Keiji Sano
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Cerebral Artery ◽  
Basilar Artery ◽  
Biosynthetic Activity ◽  
Content Type ◽  
Blood Injection ◽  
Canine Basilar Artery ◽  
Subarachnoid Blood ◽  
Fine Print

✓ Transformation of arachidonic acid into prostaglandins was investigated in the basilar artery by incubating sections of artery with carbon-14-labeled arachidonic acid. Thin-layer radiochromatography revealed that, in normal canine basilar arteries, 14C-arachidonic acid was transformed mainly to 6-ketoprostaglandin (PG)F1α, a spontaneous metabolite of prostacyclin (PGI2). Among other prostaglandins, only a small amount of PGF2α was detected, whereas PGD2, PGE2, and thromboxane B2 were not. Arteries removed on Days 3 and 8 after subarachnoid blood injection showed a prostaglandin synthesis profile similar to that in the normal cerebral artery. In borate-buffered saline (0.1M borate buffer, pH 9.0/0.15M NaCl = 1:9, vol/vol), canine basilar artery produced a PGI2-like substance that inhibited adenosine diphosphate (ADP)-induced platelet aggregation. Its anti-aggregatory activity was completely abolished by acidification. Aspirin likewise inhibited production of the anti-aggregatory substance. From these results, it was concluded that the anti-aggregatory activity was due solely to the production of PGI2 by the arterial specimen. Based on the above results, PGI2 biosynthetic activity in the cerebral artery exposed to subarachnoid blood injection was bioassayed by measuring the inhibitory activity of the incubation product upon ADP-induced platelet aggregation following incubation of the arteries in borate-buffered saline for 5 to 30 minutes at 20°C, using synthetic PGI2-Na as a standard. The synthetic activity of PGI2 in the artery exposed to subarachnoid blood injection had diminished remarkably by Days 3 and 8. This diminution of PGI2 synthesis in the cerebral artery may be involved in the pathogenesis of cerebral vasospasm.

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.

scholarly journals Activation of Protein Kinases in Canine Basilar Artery in Vasospasm

1999 ◽  
Vol 19 (1) ◽  
pp. 44-52 ◽  
Author(s):  
Hirokazu Fujikawa ◽  
Eiichi Tani ◽  
Ikuya Yamaura ◽  
Isao Ozaki ◽  
Katsuya Miyaji ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Tyrosine Kinase ◽  
Basilar Artery ◽  
Molecular Mechanisms ◽  
Kinase Inhibitor ◽  
Polyacrylamide Gel Electrophoresis ◽  
Intracellular Ca ◽  
Canine Basilar Artery ◽  
Kinase Pathway

Subarachnoid hemorrhage (SAH) often leads to a long-term narrowing of cerebral artery called vasospasm. To understand the molecular mechanisms in vasospasm, signal transduction of tyrosine kinase pathway and phosphorylation of myosin light chain (MLC) and calponin (CaP) in the basilar artery were studied. Vasospasm was produced in the canine basilar artery by a two-hemorrhage method, and vasocontraction was induced by a local application of KCl or serotonin to the basilar artery after a transclival exposure. Intracellular substrates of tyrosine kinase pathway, including Shc, Raf1, and extracellular-regulated kinases in the basilar artery, were activated after SAH, and the activation of Shc suggests stimulation of signal transductions from tyrosine kinase receptors, G-coupled receptors, or both. The activation of tyrosine kinase pathway in vasospasm also was supported by dose-dependent dilation of the spastic basilar artery on days 0 and 7 by topical application of genistein, a tyrosine kinase inhibitor, and associated marked inhibition of tyrosine phosphorylation of intracellular substrates, including Shc. In addition, the generation of protein kinase M, catalytic fragment of protein kinase Cα (PKCα), in vasospasm on days 0 and 7 was inhibited in response to genistein, indicating an inactivation of μ-calpain. It is suggested, therefore, that the reversal of vasospasm by genistein is closely associated with the restoration of intracellular Ca2+ levels. However, the increased activities of Raf1 and extracellular-regulated kinases in vasospasm were declined on day 7 compared with those on day 0 or 2, suggesting that the activation of tyrosine kinase pathway is more closely associated with the early stage of vasospasm than with the late stage of vasospasm. The analysis by pyrophosphate polyacrylamide gel electrophoresis (PPi-PAGE) demonstrated three MLC bands in vasospasm on days 2 and 7, as well as in KCl- and serotonin-induced vasocontraction. Since PPi-PAGE resolves smooth muscle MLC into three bands in the MLC kinase (MLCK)-mediated phosphorylation and into a single band in the PKC-mediated phosphorylation based on the phosphorylation state, the current results suggest that MLC in vasospasm is phosphorylated by MLCK but not by PKC. In basilar artery, CaP was significantly down-regulated, and in addition, significantly phosphorylated on serine and threonine residues only in vasospasm on days 2 and 7. Although the significance of CaP phosphorylations in vivo still is controversial, CaP down-regulation and phosphorylation may attenuate the inhibition of Mg2+-ATPase activity by CaP and induce a potential enhancement of smooth muscle contractility in delayed vasospasm. Since CaP is phosphorylated vivo by PKC, activated PKC in vasospasm may phosphorylate CaP. Thus, SAH stimulates tyrosine kinase pathway to increase intracellular Ca2+ and activate PKC, and the former activates MLCK to phosphorylate MLC, whereas the latter phosphorylates CaP but not MLC.

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 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.

scholarly journals Systematization, distribution, and territories of the caudal cerebral artery on the surface of the brain in nutria (Myocastor coypus)

2020 ◽  
Vol 40 (6) ◽  
pp. 484-492
Author(s):  
Laura V. Goltz ◽  
Rodrigo C. Azambuja ◽  
Rui Campos
Keyword(s):  
Cerebral Artery ◽  
Basilar Artery ◽  
Cerebral Arteries ◽  
Terminal Branch ◽  
Meat Industry ◽  
Myocastor Coypus ◽  
Middle Cerebral Arteries ◽  
The Right ◽  
Choroidal Artery ◽  
The Brain

ABSTRACT: The nutria (Myocastor coypus) is a medium-sized, semi-aquatic rodent valued by the skin and meat industry. This study aimed to describe and systematize the caudal cerebral artery on the brain surface in nutria, establishing a standard model and its main variations in this species. The thirty animals used were euthanized according to animal welfare rules. The vessels were filled with latex stained with red pigment and the samples were fixed in formaldehyde. In nutria, the brain was vascularized by the vertebral basilar system. The terminal branches of the basilar artery originated the rostral cerebellar, caudal cerebral, rostral choroidal and middle cerebral arteries, and its terminal branch, the rostral cerebral artery. The terminal branch of the basilar artery projected the caudal cerebral artery, which is usually a single medium-caliber vessel, into the transverse fissure of the brain. The caudal cerebral artery was presented as a single (66.7% of the cases to the right and 76.7% to the left) and double vessel (33.3% of the cases to the right and 23.3% to the left). It originated the rostral mesencephalic artery, the proximal component, and the caudal inter-hemispheric artery. The terminal branches of the rostral and caudal tectal mesencephalic arteries formed a typical anastomotic network. The caudal inter-hemispheric artery emitted central branches, the caudal choroidal artery, hemispherical occipital arteries, rostral tectal mesencephalic branches and distal components, and anastomosed “in osculum” with the terminal branches of the rostral inter-hemispheric artery. The caudal choroidal artery anastomosed with the rostral choroidal artery, where it branched out on the thalamic mass, vascularizing all diencephalic structures and the hippocampus. The caudal cerebral artery and its terminal branches anastomosed with the terminal branches of the rostral and middle cerebral arteries in a restricted region of the caudal pole of the cerebral hemisphere. The vascularization area of the caudal cerebral artery and its central branches in the paleopallial of the piriform lobe is extremely restricted, caudomedially.

scholarly journals Arterial vascularization of the brain of the agouti (Dasyprocta aguti Linnaeus, 1766)

2016 ◽  
Vol 37 (2) ◽  
pp. 773-784 ◽  
Author(s):  
Roberto Sávio Bessa da Silva ◽  
◽  
Gleidson Benevides de Oliveira ◽  
Carlos Magno Oliveira Junior ◽  
Ferdinando Vinicius Fernandes Bezerra ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Cerebral Artery ◽  
Basilar Artery ◽  
Cerebral Arteries ◽  
Ventral Surface ◽  
Terminal Branch ◽  
Medial Branch ◽  
Communicating Branch ◽  
Arterial Vascularization ◽  
The Brain

The agouti, a rodent that is geographically distributed throughout South America, is greatly valued for its meat. This paper describes the arterial vascularization of the base of the agouti’s brain, characterizing behavior, and arterial origin and distribution. Ten animals from the Center for the Multiplication of Wild Animals (CEMAS/UFERSA) were used and the study was approved by SISBIO (report number 32413- 1) and the Ethics Committee on Animal Use (CEUA/UFERSA) (protocol 02/2010). After euthanasia, the animals were incised in the thoracic cavity by an injection of red-stained Neoprene latex 650 and the skulls were subsequently opened. The brains were extracted from the skulls for ventral surface analysis and then fixed in an aqueous 10% formaldehyde solution. The agouti’s arterial vascularization of the brain has two main components, namely the carotid and vertebrobasilar systems. The agouti’s carotid system accounts for vascularization of almost the entire forebrain, while the vertebrobasilar system accounts for vascularization of almost the entire posterior brain (medulla oblongata, pyramid, trapezoid body, cerebellum, bridge, and part of the third caudal section of the forebrain) through the caudal cerebral arteries originating from the terminal branches of the basilar artery. The main arteries on the brain surface include the basilar artery, which is unique, and the arterial pairs, specifically the vertebral arteries, cerebellar caudal arteries, trigeminal artery, rostral cerebellar artery, basilar terminal branch artery, cerebral caudal artery, communicating caudal branch of the cerebral carotid artery, cerebral carotid artery, communicating branch rostral cerebral carotid artery, choroidal rostral artery, medial branch of the communicating branch rostral artery, internal ophthalmic artery, middle cerebral artery, and rostral cerebral artery.

scholarly journals Responses of Isolated Feline and Human Cerebral Arteries to Prostacyclin and Some of its Metabolites

1983 ◽  
Vol 3 (2) ◽  
pp. 238-245 ◽  
Author(s):  
Tore Uski ◽  
Karl-Erik Andersson ◽  
Lennart Brandt ◽  
Lars Edvinsson ◽  
Bengt Ljunggren
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Basilar Artery ◽  
Species Differences ◽  
Cerebral Arteries ◽  
Pial Arteries ◽  
Contractile Effect ◽  
Resting Tension ◽  
As Species ◽  
Middle Cerebral Arteries

The effects of prostacyclin (PGI2) were studied in isolated cat basilar and middle cerebral arteries and in human pial arteries. In feline vessels with low resting tension, PGI2 had a contractile effect that reached a maximum of 132% (basilar artery) and 23% (middle cerebral artery) of the potassium-induced (127 m M) contraction. In potassium-contracted feline vessels, PGI2 caused a further contraction. When these vessels were contracted by PGF2α, PGI2 induced relaxation, which was most marked in the middle cerebral artery. PGI2 consistently relaxed the middle cerebral artery contracted by the prostaglandin endoperoxide analogue U-44069, whereas the basilar artery was almost unaffected. In human pial arteries with low resting tension, PGI2 had no effects in concentrations below 10−6 M, whereas higher concentrations induced contractions. In potassium-contracted (35 or 127 m M) preparations, PGI2 in concentrations below 10−6 M produced relaxation; in higher concentrations further contraction was induced. Human pial arteries contracted by PGF2α, U-44069, noradrenaline, or 5-hydroxytryptamine consistently relaxed in response to PGI2 (< 10−6 M). The PGI2 metabolite 6-keto-PGE1 had effects similar to those of PGI2, but proved to be less potent on human pial vessels. 6-Keto-PGF1α was ineffective, whereas 6, 15-diketo-PGF1α had minor relaxant effects. The results suggest that consideration must be given to regional as well as species differences concerning the cerebrovascular effects of PGI2.

scholarly journals The cytosolic sperm factor that triggers Ca2+ oscillations and egg activation in mammals is a novel phospholipase C: PLCζ

Reproduction ◽  
2004 ◽  
Vol 127 (4) ◽  
pp. 431-439 ◽  
Author(s):  
K Swann ◽  
M G Larman ◽  
C M Saunders ◽  
F A Lai
Keyword(s):  
Membrane Fusion ◽  
Phospholipase C ◽  
Potential Role ◽  
Egg Activation ◽  
Specific Factor ◽  
Sperm Protein ◽  
Protein Factor ◽  
Inositol 1,4,5 Trisphosphate ◽  
Intracellular Ca ◽  
Sperm Factor

When sperm activate eggs at fertilization the signal for activation involves increases in the intracellular free Ca2+concentration. In mammals the Ca2+changes at fertilization consist of intracellular Ca2+oscillations that are driven by the generation of inositol 1,4,5-trisphosphate (InsP3). It is not established how sperm trigger the increases in InsP3and Ca2+at fertilization. One theory suggests that sperm initiate signals to activate the egg by introducing a specific factor into the egg cytoplasm after membrane fusion. This theory has been mainly based upon the observation that injecting a cytosolic sperm protein factor into eggs can trigger the same pattern of Ca2+oscillations induced by the sperm. We have recently shown that this soluble sperm factor protein is a novel form of phospholipase C (PLC), and it is referred to as PLCζ(zeta). We describe the evidence that led to the identification of PLCζ and discuss the issues relating to its potential role in fertilization.

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