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  1. Article ; Online: Effects of tetrodotoxin on the mammalian cardiovascular system.

    Zimmer, Thomas

    Marine drugs

    2010  Volume 8, Issue 3, Page(s) 741–762

    Abstract: ... on the systemic cardiovascular effects of TTX in animals and humans, with a special focus on cardiac excitation and performance ... Na(v)1.8, and Na(v)1.9, are resistant to nanomolar concentrations of tetrodotoxin (TTX; IC(50) > or ... nervous system, are highly sensitive to TTX (IC(50) approximately 10 nM). During the last two decades, it has ...

    Abstract The human genome encodes nine functional voltage-gated Na+ channels. Three of them, namely Na(v)1.5, Na(v)1.8, and Na(v)1.9, are resistant to nanomolar concentrations of tetrodotoxin (TTX; IC(50) > or = 1 microM). The other isoforms, which are predominantly expressed in the skeletal muscle and nervous system, are highly sensitive to TTX (IC(50) approximately 10 nM). During the last two decades, it has become evident that in addition to the major cardiac isoform Na(v)1.5, several of those TTX sensitive isoforms are expressed in the mammalian heart. Whereas immunohistochemical and electrophysiological methods demonstrated functional expression in various heart regions, the physiological importance of those isoforms for cardiac excitation in higher mammals is still debated. This review summarizes our knowledge on the systemic cardiovascular effects of TTX in animals and humans, with a special focus on cardiac excitation and performance at lower concentrations of this marine drug. Altogether, these data strongly suggest that TTX sensitive Na+ channels, detected more recently in various heart tissues, are not involved in excitation phenomena in the healthy adult heart of higher mammals.
    MeSH term(s) Animals ; Cardiovascular System/drug effects ; Humans ; Sodium Channel Blockers/toxicity ; Sodium Channels/drug effects ; Sodium Channels/metabolism ; Tetrodotoxin/toxicity
    Chemical Substances Sodium Channel Blockers ; Sodium Channels ; Tetrodotoxin (4368-28-9)
    Language English
    Publishing date 2010-03-19
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2175190-0
    ISSN 1660-3397 ; 1660-3397
    ISSN (online) 1660-3397
    ISSN 1660-3397
    DOI 10.3390/md8030741
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Effects of Tetrodotoxin on the Mammalian Cardiovascular System

    Thomas Zimmer

    Marine Drugs, Vol 8, Iss 3, Pp 741-

    2010  Volume 762

    Abstract: ... This review summarizes our knowledge on the systemic cardiovascular effects of TTX in animals and humans ... Nav1.8, and Nav1.9, are resistant to nanomolar concentrations of tetrodotoxin (TTX; IC50 ≥ 1 μM ... The other isoforms, which are predominantly expressed in the skeletal muscle and nervous system, are highly sensitive ...

    Abstract The human genome encodes nine functional voltage-gated Na+ channels. Three of them, namely Nav1.5, Nav1.8, and Nav1.9, are resistant to nanomolar concentrations of tetrodotoxin (TTX; IC50 ≥ 1 μM). The other isoforms, which are predominantly expressed in the skeletal muscle and nervous system, are highly sensitive to TTX (IC50 ~ 10 nM). During the last two decades, it has become evident that in addition to the major cardiac isoform Nav1.5, several of those TTX sensitive isoforms are expressed in the mammalian heart. Whereas immunohistochemical and electrophysiological methods demonstrated functional expression in various heart regions, the physiological importance of those isoforms for cardiac excitation in higher mammals is still debated. This review summarizes our knowledge on the systemic cardiovascular effects of TTX in animals and humans, with a special focus on cardiac excitation and performance at lower concentrations of this marine drug. Altogether, these data strongly suggest that TTX sensitive Na+ channels, detected more recently in various heart tissues, are not involved in excitation phenomena in the healthy adult heart of higher mammals.
    Keywords Na+ channel ; TTX sensitivity ; cardiac conduction ; TTX poisoning ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2010-03-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article: Effects of bufalin on norepinephrine turnover in canine saphenous vein.

    Cress, L W / Freas, W / Haddy, F / Muldoon, S M

    Hypertension (Dallas, Tex. : 1979)

    1991  Volume 18, Issue 4, Page(s) 516–522

    Abstract: ... on the cardiovascular system may play a role in the etiology of hypertension. ... inhibited by tetrodotoxin, which suggests a dependence of this response on Na+ influx through the neuronal ... compounds, as a model of the mammalian compound. In vitro experiments in canine saphenous veins showed ...

    Abstract Abundant experimental data suggest that an endogenous digitalislike factor is responsible for some essential hypertension. Some forms of hypertension have also been associated with increased levels of catecholamines. We therefore designed experiments to investigate the role of digitalislike factors in the regulation of norepinephrine turnover in the neurovascular junction. We chose bufalin, an amphibian-derived compound that shares many of the physiological properties postulated as characteristic of digitalislike compounds, as a model of the mammalian compound. In vitro experiments in canine saphenous veins showed that, in addition to inhibiting norepinephrine uptake, bufalin increased norepinephrine overflow by an amount larger than could be explained solely by uptake inhibition. The effect of bufalin on norepinephrine overflow is inhibited by tetrodotoxin, which suggests a dependence of this response on Na+ influx through the neuronal membranes. We propose that Na+,K(+)-ATPase inhibition resulting in neuronal depolarization is responsible for the augmented norepinephrine turnover caused by bufalin and that these indirect effects of norepinephrine on the cardiovascular system may play a role in the etiology of hypertension.
    MeSH term(s) Animals ; Blood Vessels/metabolism ; Bufanolides/pharmacology ; Dogs ; Electric Stimulation ; In Vitro Techniques ; Norepinephrine/metabolism ; Potassium/pharmacology ; Saphenous Vein/metabolism ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors ; Tetrodotoxin/pharmacology
    Chemical Substances Bufanolides ; Tetrodotoxin (4368-28-9) ; Sodium-Potassium-Exchanging ATPase (EC 3.6.3.9) ; Potassium (RWP5GA015D) ; bufalin (U549S98QLW) ; Norepinephrine (X4W3ENH1CV)
    Language English
    Publishing date 1991-10
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/01.hyp.18.4.516
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1488: Show issues Location:
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  4. Article: Vasoconstrictive effects of native tachykinins in the rainbow trout, Oncorhynchus mykiss.

    Kågström, J / Holmgren, S / Olson, K R / Conlon, J M / Jensen, J

    Peptides

    1996  Volume 17, Issue 1, Page(s) 39–45

    Abstract: The role of trout substance P (tSP) and neurokinin A (tNKA) in cardiovascular regulation was ... and tNKA, respectively). Tetrodotoxin did not affect the tSP-induced hypertension. Increases ... increased both systemic and coeliac vascular resistances, leading to hypertension and bradycardia ...

    Abstract The role of trout substance P (tSP) and neurokinin A (tNKA) in cardiovascular regulation was investigated in the rainbow trout, Oncorhynchus mykiss, in vivo and in vitro. In vivo, the coeliac arterial and ventral aortic relative blood flows were measured with Doppler flow probes, and blood pressure was measured via a cannula inserted into the dorsal aorta. tSP (0.1 and 1 nmol kg-1) and tNKA (1 nmol kg-1) increased both systemic and coeliac vascular resistances, leading to hypertension and bradycardia. In addition, cardiac output was decreased. The mammalian NK1 tachykinin receptor antagonist CP-96,345 did not affect the responses to tSP or tNKA. In vitro perfusions of the dorsal aortic and coeliacomesenteric vascular beds were performed using peristaltic pumps. The dorsal aortic vascular resistance was dose-dependently increased following infusion of the two peptides (pD2 values 7.6 +/- 0.1 and 7.3 +/- 0.1 for tSP and tNKA, respectively). Tetrodotoxin did not affect the tSP-induced hypertension. Increases in coeliac vascular resistance caused by tSP was correlated with stomach contractions when measurement of intragastric pressure was made using an inserted balloon. In conclusion, native SP and NKA are potent vasoconstrictors of rainbow trout vasculature, a property quite unusual to tachykinins compared with the vasodilation normally seen in mammals.
    MeSH term(s) Amino Acid Sequence ; Animals ; Cardiovascular Physiological Phenomena ; Cardiovascular System/drug effects ; Mammals ; Molecular Sequence Data ; Neurokinin A/genetics ; Neurokinin A/pharmacology ; Neurokinin A/physiology ; Oncorhynchus mykiss/physiology ; Perfusion ; Species Specificity ; Substance P/genetics ; Substance P/pharmacology ; Substance P/physiology ; Tachykinins/genetics ; Tachykinins/pharmacology ; Tachykinins/physiology ; Vasoconstriction/drug effects ; Vasoconstriction/physiology ; Vasoconstrictor Agents/pharmacology
    Chemical Substances Tachykinins ; Vasoconstrictor Agents ; Substance P (33507-63-0) ; Neurokinin A (86933-74-6)
    Language English
    Publishing date 1996
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 769028-9
    ISSN 1873-5169 ; 0196-9781
    ISSN (online) 1873-5169
    ISSN 0196-9781
    DOI 10.1016/0196-9781(95)02065-9
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1649: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
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  5. Article: Effects of Tetrodotoxin on the Mammalian Cardiovascular System

    Thomas Zimmer

    Abstract: ... This review summarizes our knowledge on the systemic cardiovascular effects of TTX in animals and humans ... Nav1.8, and Nav1.9, are resistant to nanomolar concentrations of tetrodotoxin (TTX; IC50 ≥ 1 μM ... The other isoforms, which are predominantly expressed in the skeletal muscle and nervous system, are highly sensitive ...

    Abstract The human genome encodes nine functional voltage-gated Na+ channels. Three of them, namely Nav1.5, Nav1.8, and Nav1.9, are resistant to nanomolar concentrations of tetrodotoxin (TTX; IC50 ≥ 1 μM). The other isoforms, which are predominantly expressed in the skeletal muscle and nervous system, are highly sensitive to TTX (IC50 ~ 10 nM). During the last two decades, it has become evident that in addition to the major cardiac isoform Nav1.5, several of those TTX sensitive isoforms are expressed in the mammalian heart. Whereas immunohistochemical and electrophysiological methods demonstrated functional expression in various heart regions, the physiological importance of those isoforms for cardiac excitation in higher mammals is still debated. This review summarizes our knowledge on the systemic cardiovascular effects of TTX in animals and humans, with a special focus on cardiac excitation and performance at lower concentrations of this marine drug. Altogether, these data strongly suggest that TTX sensitive Na+ channels, detected more recently in various heart tissues, are not involved in excitation phenomena in the healthy adult heart of higher mammals.
    Language English
    Document type Article
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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  6. Article: Effet des ciguatoxines sur le système cardio-circulatoire.

    Marquais, M / Sauviat, M P

    Journal de la Societe de biologie

    1999  Volume 193, Issue 6, Page(s) 495–504

    Abstract: ... effect on the contraction of mammalian atrial and ventricular cardiac muscle. These effects were ... which has been attributed to a direct effect of the toxins on tetrodotoxin-sensitive voltage-dependent Na+ ... of the autonomic nervous system present in cardiac tissue. They also exert a slow delayed inotropic effect on the contraction ...

    Title translation Effect of ciguatoxins on the cardiocirculatory system.
    Abstract The aim of the present review was to collect the main observations reported until now concerning the cardio-circulatory effects of polyether toxins, called ciguatoxins, which are involved in an endemic intoxication named ciguatera found in tropical and subtropical countries. Ciguatera is caused by the ingestion of fishes contaminated with the dinoflagellate Gamberdiscus toxicus. Due to both tropical fish exportation destined for food and tourism, the disease has now spread out to temperate areas. Several toxins have been isolated and purified from different fish species living in different geographical areas. They are classified into three main groups by the nature of certain cycles of their carbon skeleton. Clinical reports show evidence that ciguatera intoxication affect both electrocardiograms and blood pressure. In most cases, ciguateric intoxication mainly evoked bradycardia, hypotension, and the alteration of S-T segment in the electrocardiogram. Isolated and purified ciguatoxins strongly altered the morphology of cardiac tissue inducing swelling of the cells and alterations of cellular organelles. These toxins impair the conduction of cardiac nerves and increase the opening probability of Na+ channels in intracardiac ganglions. Depending on the concentration applied, the substances exerted either a fast positive inotropic effect or a negative inotropic effect on the contraction of mammalian atrial and ventricular cardiac muscle. These effects were attributed to a release of noradrenaline and acetylcholine from neural terminals of the autonomic nervous system present in cardiac tissue. They also exert a slow delayed inotropic effect on the contraction which has been attributed to a direct effect of the toxins on tetrodotoxin-sensitive voltage-dependent Na+ channels of cardiac membranes. Ciguatoxins depolarized the membrane of mammalian atrial and ventricular preparations and shifted the threshold of sodium current activation to more negative membrane potentials. In conclusion, the inotropic effects of ciguatoxins on cardiac tissues mainly depend on the toxin concentration sensitivity of autonomic nerve terminals, which released noradrenaline and/or acetylcholine, while the ciguatoxin-induced increase of the sodium influx could be involved in the cardiac cell swelling which coincides with reports in which ciguatoxins induced a mannitol-inhibited swelling of the Node of Ranvier.
    MeSH term(s) Animals ; Bradycardia/chemically induced ; Cardiovascular System/drug effects ; Cell Size/drug effects ; Ciguatoxins/adverse effects ; Ciguatoxins/chemistry ; Ciguatoxins/classification ; Ciguatoxins/pharmacology ; Electrocardiography/drug effects ; Guinea Pigs ; Heart/drug effects ; Heart Conduction System/drug effects ; Humans ; Hypotension/chemically induced ; Membrane Potentials/drug effects ; Mice ; Molecular Structure ; Myocardial Contraction/drug effects ; Ranidae ; Rats ; Sodium Channels/drug effects ; Synaptic Transmission/drug effects
    Chemical Substances Sodium Channels ; Ciguatoxins (11050-21-8)
    Language French
    Publishing date 1999
    Publishing country France
    Document type English Abstract ; Journal Article ; Review
    ZDB-ID 1476234-1
    ISSN 1760-6128 ; 1295-0661
    ISSN (online) 1760-6128
    ISSN 1295-0661
    Database MEDical Literature Analysis and Retrieval System OnLINE

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