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  1. Article: Receptor-mediated Ca++ entry in blood vessels.

    Hester, R K

    Microcirculation, endothelium, and lymphatics

    1989  Volume 5, Issue 1-2, Page(s) 31–53

    Abstract: The importance of receptor-mediated Ca++ entry (RMCa++E) relative to Ca++ release and potential ... are pharmacologically distinct Ca++ channels in some blood vessels that are differentially activated ... dependent Ca++ entry (PDCa++E) in agonist-induced responses in rabbit aorta and renal artery was ...

    Abstract The importance of receptor-mediated Ca++ entry (RMCa++E) relative to Ca++ release and potential-dependent Ca++ entry (PDCa++E) in agonist-induced responses in rabbit aorta and renal artery was quantitatively delineated by utilizing a solution without added Ca++ containing low ethyleneglycol bis(beta-aminoethylether)-N,N'-tetraacetic acid (EGTA) plus D600 to inhibit PDCa++E. Adding an approximate ED80 concentration of norepinephrine (NE; 3 x 10(-7) M), histamine (Hist; 3 x 10(-6) M), or serotonin (5HT; 3 x 10(-6) M) to this solution results in a transient increase in developed force that is attributed to release of a limited cellular pool of Ca++. (NE greater than Hist much greater than 5HT). When the concentrations are approximately equipotent (NE, 3 x 10(-7) M; Hist, 3 x 10(-5) M; 5HT, 10(-5) M) the Ca++ release component increases for Hist and 5HT such that NE = Hist greater than 5HT. Subsequent addition of Ca++ results in an increase in developed force that is sustained and represents RMCa++E. In aorta, RMCa++E can account for 91% of the total NE-induced developed force; for an equipotent concentration of Hist, 71%; and for an equipotent concentration of 5HT, only 37%. This capacity for stimulating RMCa++E is inversely related to the sensitivity of these agonists to the PDCa++E blocker, D600 (5HT much greater than Hist greater than NE). Chronic Mg++ potentiates control responses to NE in normal Ca++, but depresses the sensitivity to Ca++ in the RMCa++E concentration response relationship. The sustained response associated with RMCa++E is only minimally relaxed or inhibited by Mg++ (acute) and is completely inhibited or slowly and completely relaxed by La . In renal artery, a similar approximate ED80 concentration of NE (3 x 10(-6) M) results in a NE-induced transient response attributed to Ca++ release that is 60% less than that seen in aorta, whereas the RMCa++E component in renal artery accounts for 78% of the total response (only 10% less than in aorta). Thus, it appears that there are pharmacologically distinct Ca++ channels in some blood vessels that are differentially activated in a selective and potential-independent manner as a result of specific agonist-receptor interactions.
    MeSH term(s) Animals ; Aorta, Thoracic ; Calcium Channel Agonists/pharmacology ; Calcium Channels/metabolism ; Calcium Channels/physiology ; Endothelium, Vascular/physiology ; Female ; Histamine/pharmacology ; Magnesium/physiology ; Male ; Metabolic Clearance Rate/drug effects ; Norepinephrine/metabolism ; Rabbits ; Receptors, Cell Surface/drug effects ; Receptors, Cell Surface/physiology ; Renal Artery ; Serotonin/pharmacology
    Chemical Substances Calcium Channel Agonists ; Calcium Channels ; Receptors, Cell Surface ; Serotonin (333DO1RDJY) ; Histamine (820484N8I3) ; Magnesium (I38ZP9992A) ; Norepinephrine (X4W3ENH1CV)
    Language English
    Publishing date 1989-02
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 632536-1
    ISSN 0740-9451
    ISSN 0740-9451
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  2. Article ; Online: Adaptive increases in expression and vasodilator activity of estrogen receptor subtypes in a blood vessel-specific pattern during pregnancy.

    Mata, Karina M / Li, Wei / Reslan, Ossama M / Siddiqui, Waleed T / Opsasnick, Lauren A / Khalil, Raouf A

    American journal of physiology. Heart and circulatory physiology

    2015  Volume 309, Issue 10, Page(s) H1679–96

    Abstract: ... mechanisms. E2, PPT, DPN, and G1 caused relaxation of Ca(2+) entry-dependent KCl contraction, and the effect ... inhibition of Ca(2+) entry into vascular smooth muscle, supporting a role of aortic and mesenteric arterial ... subtypes in a blood vessel-specific manner. Blood pressure (BP) and plasma E2 were measured in virgin and ...

    Abstract Normal pregnancy is associated with adaptive hemodynamic, hormonal, and vascular changes, and estrogen (E2) may promote vasodilation during pregnancy; however, the specific E2 receptor (ER) subtype, post-ER signaling mechanism, and vascular bed involved are unclear. We tested whether pregnancy-associated vascular adaptations involve changes in the expression/distribution/activity of distinct ER subtypes in a blood vessel-specific manner. Blood pressure (BP) and plasma E2 were measured in virgin and pregnant (day 19) rats, and the thoracic aorta, carotid artery, mesenteric artery, and renal artery were isolated for measurements of ERα, ERβ, and G protein-coupled receptor 30 [G protein-coupled ER (GPER)] expression and tissue distribution in parallel with relaxation responses to E2 (all ERs) and the specific ER agonist 4,4',4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl)-tris-phenol (PPT; ERα), diarylpropionitrile (DPN; ERβ), and G1 (GPER). BP was slightly lower and plasma E2 was higher in pregnant versus virgin rats. Western blots revealed increased ERα and ERβ in the aorta and mesenteric artery and GPER in the aorta of pregnant versus virgin rats. Immunohistochemistry revealed that the increases in ERs were mainly in the intima and media. In phenylephrine-precontracted vessels, E2 and PPT caused relaxation that was greater in the aorta and mesenteric artery but similar in the carotid and renal artery of pregnant versus virgin rats. DPN- and G1-induced relaxation was greater in the mesenteric and renal artery than in the aorta and carotid artery, and aortic relaxation to G1 was greater in pregnant versus virgin rats. The nitric oxide synthase inhibitor N(ω)-nitro-l-arginine methyl ester with or without the cyclooxygenase inhibitor indomethacin with or without the EDHF blocker tetraethylammonium or endothelium removal reduced E2, PPT, and G1-induced relaxation in the aorta of pregnant rats, suggesting an endothelium-dependent mechanism, but did not affect E2-, PPT-, DPN-, or G1-induced relaxation in other vessels, suggesting endothelium-independent mechanisms. E2, PPT, DPN, and G1 caused relaxation of Ca(2+) entry-dependent KCl contraction, and the effect of PPT was greater in the mesenteric artery of pregnant versus virgin rats. Thus, during pregnancy, an increase in ERα expression in endothelial and vascular smooth muscle layers of the aorta and mesenteric artery is associated with increased ERα-mediated relaxation via endothelium-derived vasodilators and inhibition of Ca(2+) entry into vascular smooth muscle, supporting a role of aortic and mesenteric arterial ERα in pregnancy-associated vasodilation. GPER may contribute to aortic relaxation while enhanced ERβ expression could mediate other genomic vascular effects during pregnancy.
    MeSH term(s) Adaptation, Physiological ; Animals ; Aorta, Thoracic/drug effects ; Aorta, Thoracic/metabolism ; Aorta, Thoracic/physiology ; Arteries/drug effects ; Arteries/metabolism ; Arteries/physiology ; Blood Pressure ; Blotting, Western ; Calcium/metabolism ; Carotid Arteries/drug effects ; Carotid Arteries/metabolism ; Carotid Arteries/physiology ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/physiology ; Enzyme Inhibitors/pharmacology ; Estrogen Receptor alpha/agonists ; Estrogen Receptor alpha/metabolism ; Estrogen Receptor beta/agonists ; Estrogen Receptor beta/metabolism ; Estrogens/metabolism ; Female ; Immunohistochemistry ; Mesenteric Arteries/drug effects ; Mesenteric Arteries/metabolism ; Mesenteric Arteries/physiology ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/metabolism ; Muscle, Smooth, Vascular/physiology ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide Synthase/antagonists & inhibitors ; Phenols/pharmacology ; Potassium Channel Blockers/pharmacology ; Pregnancy/metabolism ; Pregnancy/physiology ; Pyrazoles/pharmacology ; Rats ; Receptors, G-Protein-Coupled/agonists ; Receptors, G-Protein-Coupled/metabolism ; Renal Artery/drug effects ; Renal Artery/metabolism ; Renal Artery/physiology ; Tetraethylammonium/pharmacology ; Vasoconstriction/drug effects ; Vasoconstriction/physiology ; Vasodilation/drug effects ; Vasodilation/physiology
    Chemical Substances Enzyme Inhibitors ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Estrogens ; Gper1 protein, rat ; Phenols ; Potassium Channel Blockers ; Pyrazoles ; Receptors, G-Protein-Coupled ; 4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol (0T83Y6JZPF) ; Tetraethylammonium (66-40-0) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Calcium (SY7Q814VUP) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
    Language English
    Publishing date 2015-09-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.00532.2015
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  3. Article ; Online: Transient receptor potential channels function as a coincidence signal detector mediating phosphatidylserine exposure.

    Harper, Matthew T / Londoño, Juan E Camacho / Quick, Kathryn / Londoño, Julia Camacho / Flockerzi, Veit / Philipp, Stephan E / Birnbaumer, Lutz / Freichel, Marc / Poole, Alastair W

    Science signaling

    2013  Volume 6, Issue 281, Page(s) ra50

    Abstract: ... inappropriate occlusion of blood vessels. Thrombin, which cleaves and activates Gq-coupled ... of the transient receptor potential C (TRPC) family, TRPC3 and TRPC6. These channels principally allowed entry ... a calcium signal that was largely dependent only on store-operated Ca(2+) entry. In contrast, experiments ...

    Abstract Blood platelet aggregation must be tightly controlled to promote clotting at injury sites but avoid inappropriate occlusion of blood vessels. Thrombin, which cleaves and activates Gq-coupled protease-activated receptors, and collagen-related peptide, which activates the receptor glycoprotein VI, stimulate platelets to aggregate and form thrombi. Coincident activation by these two agonists synergizes, causing the exposure of phosphatidylserine on the cell surface, which is a marker of cell death in many cell types. Phosphatidylserine exposure is also essential to produce additional thrombin on platelet surfaces, which contributes to thrombosis. We found that activation of either thrombin receptors or glycoprotein VI alone produced a calcium signal that was largely dependent only on store-operated Ca(2+) entry. In contrast, experiments with platelets from knockout mice showed that the presence of both ligands activated nonselective cation channels of the transient receptor potential C (TRPC) family, TRPC3 and TRPC6. These channels principally allowed entry of Na(+), which coupled to reverse-mode Na(+)/Ca(2+) exchange to allow calcium influx and thereby contribute to Ca(2+) signaling and phosphatidylserine exposure. Thus, TRPC channels act as coincidence detectors to coordinate responses to multiple signals in cells, thereby indirectly mediating in platelets an increase in intracellular calcium concentrations and exposure of prothrombotic phosphatidylserine.
    MeSH term(s) Adult ; Anilides/pharmacology ; Animals ; Benzyl Compounds/pharmacology ; Blood Platelets/drug effects ; Blood Platelets/metabolism ; Calcium/metabolism ; Carrier Proteins/pharmacology ; Female ; Humans ; Immunoblotting ; Male ; Mice ; Mice, Knockout ; Middle Aged ; Models, Biological ; Peptides/pharmacology ; Phosphatidylserines/metabolism ; Signal Transduction/genetics ; Signal Transduction/physiology ; Sodium/metabolism ; Sodium-Calcium Exchanger/antagonists & inhibitors ; Sodium-Calcium Exchanger/metabolism ; TRPC Cation Channels/genetics ; TRPC Cation Channels/metabolism ; TRPC Cation Channels/physiology ; Thiadiazoles/pharmacology ; Thiazolidines/pharmacology ; Thrombin/pharmacology ; Young Adult
    Chemical Substances 2-(4-(4-nitrobenzyloxy)benzyl)thiazolidine-4-carboxylic acid ethyl ester ; 4-methyl-4'-(3,5-bis(trifluoromethyl)-1H-pyrazol-1-yl)-1,2,3-thiadiazole-5-carboxanilide ; Anilides ; Benzyl Compounds ; Carrier Proteins ; Peptides ; Phosphatidylserines ; Sodium-Calcium Exchanger ; TRPC Cation Channels ; TRPC3 cation channel ; Thiadiazoles ; Thiazolidines ; Trpc6 protein, mouse ; collagen-related peptide ; Sodium (9NEZ333N27) ; Thrombin (EC 3.4.21.5) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2013-06-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.2003701
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  4. Article ; Online: Chronic hypoxia upregulates pulmonary arterial ASIC1: a novel mechanism of enhanced store-operated Ca2+ entry and receptor-dependent vasoconstriction.

    Jernigan, Nikki L / Herbert, Lindsay M / Walker, Benjimen R / Resta, Thomas C

    American journal of physiology. Cell physiology

    2011  Volume 302, Issue 6, Page(s) C931–40

    Abstract: ... in elevated receptor-stimulated vasoconstriction following CH which is likely mediated through increased ASIC1 ... vessel wall [Ca(2+)](i) responses to UTP and KCl (depolarizing stimulus) in fura-2-loaded, pressurized ... vessel wall [Ca(2+)](i), but attenuated vasoconstriction and increases in vessel wall [Ca(2+)](i) to UTP ...

    Abstract Acid-sensing ion channel 1 (ASIC1) is a newly characterized contributor to store-operated Ca(2+) entry (SOCE) in pulmonary vascular smooth muscle (VSM). Since SOCE is implicated in elevated basal VSM intracellular Ca(2+) concentration ([Ca(2+)](i)) and augmented vasoconstriction in chronic hypoxia (CH)-induced pulmonary hypertension, we hypothesized that ASIC1 contributes to these responses. To test this hypothesis, we examined effects of the specific pharmacologic ASIC1a inhibitor, psalmotoxin 1 (PcTX1), on vasoconstrictor and vessel wall [Ca(2+)](i) responses to UTP and KCl (depolarizing stimulus) in fura-2-loaded, pressurized small pulmonary arteries from control and CH (4 wk at 0.5 atm) Wistar rats. PcTX1 had no effect on basal vessel wall [Ca(2+)](i), but attenuated vasoconstriction and increases in vessel wall [Ca(2+)](i) to UTP in arteries from control and CH rats; normalizing responses between groups. In contrast, responses to the depolarizing stimulus, KCl, were unaffected by CH exposure or PcTX1. Upon examining potential Ca(2+) influx mechanisms, we found that PcTX1 prevented augmented SOCE following CH. Exposure to CH resulted in a significant increase in pulmonary arterial ASIC1 protein. This study supports a novel role of ASIC1 in elevated receptor-stimulated vasoconstriction following CH which is likely mediated through increased ASIC1 expression and SOCE.
    MeSH term(s) Acid Sensing Ion Channels ; Animals ; Calcium/metabolism ; Calcium Channels, L-Type/metabolism ; Fura-2/pharmacology ; Hypertension, Pulmonary/metabolism ; Hypertension, Pulmonary/physiopathology ; Hypoxia/metabolism ; Hypoxia/physiopathology ; Male ; Muscle, Smooth, Vascular/blood supply ; Muscle, Smooth, Vascular/drug effects ; Nerve Tissue Proteins/antagonists & inhibitors ; Nerve Tissue Proteins/metabolism ; Peptides ; Potassium Chloride/pharmacology ; Pulmonary Artery/drug effects ; Pulmonary Artery/metabolism ; Rats ; Rats, Wistar ; Sodium Channels/metabolism ; Spider Venoms/pharmacology ; Uridine Triphosphate/pharmacology ; Vasoconstriction/drug effects
    Chemical Substances Acid Sensing Ion Channels ; Asic1 protein, rat ; Calcium Channels, L-Type ; Nerve Tissue Proteins ; PcTX1 protein, Psalmopoeus cambridgei ; Peptides ; Sodium Channels ; Spider Venoms ; Potassium Chloride (660YQ98I10) ; Calcium (SY7Q814VUP) ; Fura-2 (TSN3DL106G) ; Uridine Triphosphate (UT0S826Z60)
    Language English
    Publishing date 2011-12-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00332.2011
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  5. Article: Identification of canonical transient receptor potential (TRPC) channel proteins in native vascular smooth muscle cells.

    Albert, Anthony P / Saleh, Sohag N / Large, William A

    Current medicinal chemistry

    2008  Volume 16, Issue 9, Page(s) 1158–1165

    Abstract: Canonical transient receptor potential (TRPC) channels are Ca(2+)-permeable non-selective cation ... pathway and evoke indirect Ca(2+) entry by inducing depolarisation and opening of voltage-gated Ca(2+ ... strong evidence that native vascular myocytes contain diverse TRPC-mediated channels which are usually ...

    Abstract Canonical transient receptor potential (TRPC) channels are Ca(2+)-permeable non-selective cation channels, which on stimulation allow influx of Na(+) and Ca(2+) ions into cells. It is proposed that stimulation of TRPC conductances by neurotransmitters and hormones such as noradrenaline, angiotensin II and endothelin-1 have important functions in vascular smooth muscle cells including vasoconstriction, cell growth and proliferation. Moreover constitutive TRPC activity contributes to setting the resting membrane potential of vascular myocytes. Activation of TRPC channels is thought to provide a direct Ca(2+) influx pathway and evoke indirect Ca(2+) entry by inducing depolarisation and opening of voltage-gated Ca(2+) channels and by stimulating the reverse mode of the Na(+)/Ca(2+) exchanger. Therefore identification of native TRPC channel proteins, which underlie these mechanisms, will provide important information on physiological functioning of vascular tissue and these conductances are pharmacological targets for the prevention of cardiovascular diseases such as hypertension. This review focuses on different experimental approaches that have been used to elucidate the molecular identity of TRPCs in native vascular myocytes. It will discuss the advantages and problems associated with using siRNA and anti-sense technologies in primary cell cultures, cell lines and transgenic mice models. In addition we describe recent work, which combines studies on the effect of anti-TRPC antibodies and pharmacological agents on biophysically characterised single cation channel currents to identify TRPC channel proteins in freshly dispersed vascular myocytes. These data provide strong evidence that native vascular myocytes contain diverse TRPC-mediated channels which are usually composed of complex heterotetrameric structures possessing marked pharmacological differences.
    MeSH term(s) Animals ; Blood Vessels/chemistry ; Mice ; Mice, Knockout ; Myocytes, Smooth Muscle/metabolism ; Signal Transduction ; Transient Receptor Potential Channels/metabolism
    Chemical Substances Transient Receptor Potential Channels
    Language English
    Publishing date 2008-11-24
    Publishing country United Arab Emirates
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1319315-6
    ISSN 1875-533X ; 0929-8673
    ISSN (online) 1875-533X
    ISSN 0929-8673
    DOI 10.2174/092986709787581815
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  6. Article ; Online: Store-operated Ca2+ entry (SOCE) induced by protease-activated receptor-1 mediates STIM1 protein phosphorylation to inhibit SOCE in endothelial cells through AMP-activated protein kinase and p38β mitogen-activated protein kinase.

    Sundivakkam, Premanand C / Natarajan, Viswanathan / Malik, Asrar B / Tiruppathi, Chinnaswamy

    The Journal of biological chemistry

    2013  Volume 288, Issue 23, Page(s) 17030–17041

    Abstract: ... on serine residues and prevented protease-activated receptor-1 (PAR-1)-induced Ca(2+) entry. Furthermore ... The Ca(2+) sensor STIM1 is crucial for activation of store-operated Ca(2+) entry (SOCE ... and Ca(2+) entry. Of the three p38 MAPK isoforms expressed in endothelial cells, p38β knockdown ...

    Abstract The Ca(2+) sensor STIM1 is crucial for activation of store-operated Ca(2+) entry (SOCE) through transient receptor potential canonical and Orai channels. STIM1 phosphorylation serves as an "off switch" for SOCE. However, the signaling pathway for STIM1 phosphorylation is unknown. Here, we show that SOCE activates AMP-activated protein kinase (AMPK); its effector p38β mitogen-activated protein kinase (p38β MAPK) phosphorylates STIM1, thus inhibiting SOCE in human lung microvascular endothelial cells. Activation of AMPK using 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) resulted in STIM1 phosphorylation on serine residues and prevented protease-activated receptor-1 (PAR-1)-induced Ca(2+) entry. Furthermore, AICAR pretreatment blocked PAR-1-induced increase in the permeability of mouse lung microvessels. Activation of SOCE with thrombin caused phosphorylation of isoform α1 but not α2 of the AMPK catalytic subunit. Moreover, knockdown of AMPKα1 augmented SOCE induced by thrombin. Interestingly, SB203580, a selective inhibitor of p38 MAPK, blocked STIM1 phosphorylation and led to sustained STIM1-puncta formation and Ca(2+) entry. Of the three p38 MAPK isoforms expressed in endothelial cells, p38β knockdown prevented PAR-1-mediated STIM1 phosphorylation and potentiated SOCE. In addition, inhibition of the SOCE downstream target CaM kinase kinase β (CaMKKβ) or knockdown of AMPKα1 suppressed PAR-1-mediated phosphorylation of p38β and hence STIM1. Thus, our findings demonstrate that SOCE activates CaMKKβ-AMPKα1-p38β MAPK signaling to phosphorylate STIM1, thereby suppressing endothelial SOCE and permeability responses.
    MeSH term(s) AMP-Activated Protein Kinases/genetics ; AMP-Activated Protein Kinases/metabolism ; Aminoimidazole Carboxamide/analogs & derivatives ; Aminoimidazole Carboxamide/pharmacology ; Animals ; Calcium/metabolism ; Calcium Channels ; Calcium-Calmodulin-Dependent Protein Kinase Kinase/genetics ; Calcium-Calmodulin-Dependent Protein Kinase Kinase/metabolism ; Capillary Permeability/drug effects ; Capillary Permeability/physiology ; Cells, Cultured ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Gene Knockdown Techniques ; Humans ; Hypoglycemic Agents/pharmacology ; Lung/blood supply ; Lung/metabolism ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mitogen-Activated Protein Kinase 11/genetics ; Mitogen-Activated Protein Kinase 11/metabolism ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Phosphorylation/drug effects ; Phosphorylation/physiology ; Receptor, PAR-1/genetics ; Receptor, PAR-1/metabolism ; Ribonucleotides/pharmacology ; Stromal Interaction Molecule 1
    Chemical Substances Calcium Channels ; Hypoglycemic Agents ; Membrane Glycoproteins ; Membrane Proteins ; Neoplasm Proteins ; Receptor, PAR-1 ; Ribonucleotides ; STIM1 protein, human ; Stim1 protein, mouse ; Stromal Interaction Molecule 1 ; Aminoimidazole Carboxamide (360-97-4) ; AMPK alpha1 subunit, mouse (EC 2.7.11.1) ; CAMKK2 protein, human (EC 2.7.11.17) ; Calcium-Calmodulin-Dependent Protein Kinase Kinase (EC 2.7.11.17) ; Camkk2 protein, mouse (EC 2.7.11.17) ; Mitogen-Activated Protein Kinase 11 (EC 2.7.11.24) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; AICA ribonucleotide (F0X88YW0YK) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2013-04-26
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M112.411272
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  7. Article: Expression of ryanodine receptor type 3 and TRP channels in endothelial cells: comparison of in situ and cultured human endothelial cells.

    Köhler, R / Brakemeier, S / Kühn, M / Degenhardt, C / Buhr, H / Pries, A / Hoyer, J

    Cardiovascular research

    2001  Volume 51, Issue 1, Page(s) 160–168

    Abstract: ... and thereby of endothelial function in intact human blood vessels. ... mediated Ca(2+) mobilization, Ca(2+) release from ryanodine-sensitive pools and Ca(2+)-influx through TRP ... mediated by activation of Ca(2+)-activated K channels. In EA.hy926, caffeine-induced hyperpolarization was ...

    Abstract Objective: Ca(2+) mobilization plays an important role in endothelial function by stimulating Ca(2+)-dependent synthesis of vasodilating factors. In addition to inositol-1,4,5-trisphosphate (InsP(3)) mediated Ca(2+) mobilization, Ca(2+) release from ryanodine-sensitive pools and Ca(2+)-influx through TRP channels have been suggested to be important in endothelial Ca(2+)-signaling. However, the function and molecular identity of TRP channels and ryanodine receptors in human endothelium in situ are still elusive. We hypothesized that expression of ryanodine-receptors (RyR) and TRP channels differs between human endothelium in situ and in cultured cells.
    Methods: By combining single-cell RT-PCR and patch-clamp techniques, expression of RyR and TRP channels was determined in situ in endothelial cells of human mesenteric artery (HMAECs) obtained from patients undergoing bowel resection and in the endothelial cell line EA.hy926.
    Results: At the single cell level, expression of RyR 3 was detected in 25 and 5% of HMAECs and EA.hy926 samples, respectively. Expression of the RyR 1 and 2 was not detected in either HMAECs or EA.hy926. In patch-clamp experiments in HMAECs, applications of caffeine (0.5 mM) induced sustained hyperpolarization mediated by activation of Ca(2+)-activated K channels. In EA.hy926, caffeine-induced hyperpolarization was not detected. Single HMAECs expressed the TRP genes, TRP1 and TRP3, but not TRP 4 and 6. The TRP1 was the predominantly expressed TRP gene in HMAECs in situ whereas TRP3 expression was rarely detected. EA.hy926 expressed only TRP1. In patch clamp experiments in HMAECs, Ca(2+)-store depletion activated non-selective cation currents leading to Ca(2+) entry.
    Conclusions: Our findings suggest that, in addition to InsP(3) mediated Ca(2+) release, Ca(2+) release from ryanodine-sensitive stores mediated by RyR3 and Ca(2+) entry through TRP1 might represent important components of endothelial Ca(2+) signaling in situ and thereby of endothelial function in intact human blood vessels.
    MeSH term(s) Calcium/metabolism ; Calcium Channels/analysis ; Calcium Channels/metabolism ; Cell Separation ; Colon ; Endothelium, Vascular/metabolism ; Humans ; Membrane Potentials ; Mesenteric Arteries ; Patch-Clamp Techniques ; Reverse Transcriptase Polymerase Chain Reaction ; Ryanodine Receptor Calcium Release Channel/analysis ; TRPC Cation Channels
    Chemical Substances Calcium Channels ; Ryanodine Receptor Calcium Release Channel ; TRPC Cation Channels ; TRPC3 cation channel ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2001-07
    Publishing country England
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1016/s0008-6363(01)00281-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Influence of a receptor reserve on the inhibition by calcium channel blockers of alpha adrenoceptor-mediated responses in rat isolated vascular tissues.

    Bognar, I T / Enero, M A

    The Journal of pharmacology and experimental therapeutics

    1988  Volume 245, Issue 2, Page(s) 673–681

    Abstract: ... to elucidate whether differences among blood vessels in their receptor reserves are involved in the different ... The effects of the Ca entry blockers nifedipine and verapamil on the contractions induced ... associated with an effective receptor reserve of about 40%, whereas in the MVB no spare receptors ...

    Abstract The effects of the Ca entry blockers nifedipine and verapamil on the contractions induced by phenylephrine (PHE) in rat isolated aorta and mesenteric vascular bed (MVB) were evaluated. The main goal was to elucidate whether differences among blood vessels in their receptor reserves are involved in the different degrees to which Ca antagonists inhibit alpha adrenergic vasoconstriction. In the two tissues the responses to the full agonist PHE were antagonized by prazosin with an at least 1000-fold greater potency than by yohimbine. The -log KB values for both antagonists in the aorta (11.07 and 7.40, respectively) were significantly higher than those in the MVB (9.77 and 6.43, respectively), thus suggesting receptor heterogeneity between the two tissues. Both nifedipine and verapamil were more effective in reducing the responses in the MVB (maximal inhibition, 54.3 +/- 1.9 and 55.0 +/- 3.5%) than in the aorta (25.2 +/- 5.8 and 30.4 +/- 0.7%). Studies with phenoxybenzamine (PB) indicated that in the latter case the responses were associated with an effective receptor reserve of about 40%, whereas in the MVB no spare receptors for the full agonist were available. Pretreatment of the MVB with PB showed no effect on the inhibitory action of verapamil. Conversely, removal of the spare receptors in the aorta (10(-10) M PB) rendered the responses more susceptible to inhibition by verapamil. Pretreatment of the aortic strips with 10(-9) M PB, however, failed to enhance further the effectiveness of verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)
    MeSH term(s) Animals ; Aorta, Thoracic/physiology ; Calcium/metabolism ; Female ; In Vitro Techniques ; Ion Channels/drug effects ; Ion Channels/physiology ; Male ; Mesenteric Arteries/physiology ; Muscle Contraction/drug effects ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/physiology ; Nifedipine/pharmacology ; Perfusion ; Prazosin/pharmacology ; Rats ; Rats, Inbred Strains ; Receptors, Adrenergic, alpha/drug effects ; Receptors, Adrenergic, alpha/physiology ; Verapamil/pharmacology ; Yohimbine/pharmacology
    Chemical Substances Ion Channels ; Receptors, Adrenergic, alpha ; Yohimbine (2Y49VWD90Q) ; Verapamil (CJ0O37KU29) ; Nifedipine (I9ZF7L6G2L) ; Calcium (SY7Q814VUP) ; Prazosin (XM03YJ541D)
    Language English
    Publishing date 1988-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3106-9
    ISSN 1521-0103 ; 0022-3565
    ISSN (online) 1521-0103
    ISSN 0022-3565
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