NDLI: Spontaneous transient depolarizations in lymphatic vessels of the guinea pig mesentery: pharmacology and implication for spontaneous contractility

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Spontaneous transient depolarizations in lymphatic vessels of the guinea pig mesentery: pharmacology and implication for spontaneous contractility

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Spontaneous transient depolarizations in lymphatic vessels of the guinea pig mesentery: pharmacology and implication for spontaneous contractility

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Von Der Weid, Pierre-yves Rahman, Mozibur Imtiaz, Mohammad S. Van Helden, Dirk F.
Description	Author Affiliation: von der Weid PY ( Inflammation Research Network, Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Calgary, 3330 Hospital Dr. NW, Calgary, AB, Canada T2N 4N1. vonderwe@ucalgary.ca)
Abstract	Guinea pig mesenteric lymphatic vessels exhibit rhythmic constrictions induced by action potential (AP)-like spikes and initiated by entrainment of spontaneous transient depolarizations (STDs). To characterize STDs and the signaling mechanisms responsible for their occurrence, we used intracellular microelectrodes, $Ca^{2+}$ imaging, and pharmacological agents. In our investigation of the role of intracellular $Ca^{2+}$ released from $Ca^{2+}$ stores, we observed that intracellular $Ca^{2+}$ transients accompanied some STDs, although there were many exceptions where $Ca^{2+}$ transients occurred without accompanying STDs. STD frequency and amplitude were markedly affected by activators/inhibitors of inositol 1,4,5-trisphosphate receptors $(IP_{3}Rs)$ but not by treatments known to alter $Ca^{2+}$ release via ryanodine receptors. A role for $Ca^{2+}-activated$ $Cl^{−}$ $(Cl_{Ca})$ channels was indicated, as STDs were dependent on the $Cl^{−}$ but not $Na^{+}$ concentration of the superfusing solution and were inhibited by the $Cl_{Ca}$ channel blockers niflumic acid (NFA), anthracene 9-carboxylic acid, and 5-nitro-2-(3-phenylpropylamino)benzoic acid but not by the volume-regulated $Cl^{−}$ blocker DIDS. Increases in STD frequency and amplitude induced by agonist stimulation were also inhibited by NFA. Nifedipine, the hyperpolarization-activated inward current blocker ZD-7288, and the nonselective cation/store-operated channel blockers SKF-96365, $Gd^{3+},$ and $Ni^{2+}$ had no or marginal effects on STD activity. However, nifedipine, 2-aminoethoxydiphenyl borate, NFA, SKF-96365, $Gd^{3+},$ and $Ni^{2+}$ altered the occurrence of spontaneous APs. Our findings support a role for $Ca^{2+}$ release through $IP_{3}Rs$ and a resultant opening of $Cl_{Ca}$ channels in STD generation and confirm the importance of these events in the initiation of lymphatic spontaneous APs and subsequent contractions. The abolition of spontaneous APs by blockers of other excitatory ion channels suggests a contribution of these conductances to lymphatic pacemaking.
File Format	HTM / HTML
ISSN	03636135
e-ISSN	15221539
Journal	AJP: Heart and Circulatory Physiology
Issue Number	5
Volume Number	295
Language	English
Publisher	American Physiological Society
Publisher Date	2008-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Discipline Cardiology Biological Clocks Calcium Signaling Lymphatic Vessels Metabolism Muscle Contraction Muscle, Smooth Action Potentials Animals Drug Effects Calcium Channels, L-type Chloride Channels Guinea Pigs Inositol 1,4,5-trisphosphate Receptors Membrane Transport Modulators Pharmacology Mesentery Time Factors Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Cardiology and Cardiovascular Medicine

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