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Involvement of Kallikrein-Kinin System on Cardiopulmonary Alterations and Inflammatory Response Induced by Purified Aah I Toxin from Scorpion Venom.

Inflammation

February 2016

USTHB, Faculty of Biological Sciences, Laboratory Cellular and Molecular Biology, Department Cellular and Molecular Biology, BP32, EL Alia, Bab Ezzouar, 16111, Algiers, Algeria.

Bradykinins are released from kininogen by kallikrein. They increase capillary lung permeability after their binding to β1 and especially β2 receptors before being metabolized by kininase enzyme. This study was performed to evaluate cardiopulmonary damages and inflammatory response on injected rats with Aah I toxin of scorpion venom and the involvement of Kallikrein-Kinin system in this pathogenesis.

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Roots of Premna integrifolia Linn. Mant. (Verbanacea) are important rasayana (Adaptogenic) drugs and are considered to be useful in the treatment of variety of ailments.

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It is known that insect kinins increase diuresis and fluid secretion in the Aedes aegypti Malpighian tubule, causing a rapid drop of the transepithelial resistance and increasing chloride conductance from the hemolymph towards the tubule lumen. The tubule is composed of both principal and stellate cells. The main route for increased chloride influx upon kinin treatment is proposed to be paracellular, with septate junctions acquiring increased chloride selectivity and conductance.

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The D7-related (D7r) proteins of the malaria vector Anopheles gambiae have been shown to bind the biogenic amines serotonin, norepinephrine, and histamine with high affinity. One member of the group (D7r1 or hamadarin) has also been shown to have an anticoagulant/antikinin activity. To understand the mechanistic details of its antihemostatic/anti-inflammatory effects, we have determined the crystal structure of one member of this group, D7r4, along with the structures of ligand complexes with serotonin, tryptamine, histamine, and norepinephrine.

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Pharmacology of peripheral analgesia.

Pain Pract

September 2001

Department of Anesthesiology, University of Alabama at Birmingham, 35233-6810, USA.

Pain may begin in the periphery with activation of nociceptor transducers. The present article reviews the pharmacology of drug action at the level of the primary afferent by discussing the following: [1] agents which block transduction processes (vanilloids, sodium ion channel blockers, antiserotonergic agents, antipurinergic agents); [2] agents inhibiting the transducer site (opioids, cannabinoids, alpha adrenergic agents); [3] agents blocking transducer-based modulation processes (anti-inflammatories, antikinin agents, antitachykinins); and [4] agents which block primary afferent-related modification processes (antineurotrophins). There is a clear role for many of these agents in the treatment of inflammatory pain and they have potential benefits for neuropathic pain with peripheral triggers.

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