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NO- and non-NO-, non-prostanoid-dependent vasodilatation in rat sciatic nerve during maturation and developing experimental diabetic neuropathy

Thomsen, Kirsten ; Rubin, Inger ; Lauritzen, Martin

The Journal of physiology, 2002-09, Vol.543 (3), p.977-993 [Periódico revisado por pares]

Oxford, UK: The Physiological Society

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Título:
NO- and non-NO-, non-prostanoid-dependent vasodilatation in rat sciatic nerve during maturation and developing experimental diabetic neuropathy
Autor: Thomsen, Kirsten ; Rubin, Inger ; Lauritzen, Martin
Assuntos: Acetylcholine - pharmacology ; Animals ; Blood Glucose ; Blood Pressure ; Cyclooxygenase Inhibitors - pharmacology ; Diabetic Neuropathies - metabolism ; Diabetic Neuropathies - physiopathology ; Fasting ; Glycated Hemoglobin A - analysis ; Indomethacin - pharmacology ; Male ; Molsidomine - analogs & derivatives ; Molsidomine - pharmacology ; Motor Neurons - physiology ; Neural Conduction ; Neurons, Afferent - physiology ; Nitric Oxide - metabolism ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitric Oxide Synthase - metabolism ; Original ; Potassium Channel Blockers - pharmacology ; Prostaglandin-Endoperoxide Synthases - metabolism ; Prostaglandins - metabolism ; Rats ; Rats, Sprague-Dawley ; Sciatic Nerve - blood supply ; Sciatic Nerve - enzymology ; Sciatic Nerve - growth & development ; Vasodilation - drug effects ; Vasodilation - physiology ; Vasodilator Agents - pharmacology
É parte de: The Journal of physiology, 2002-09, Vol.543 (3), p.977-993
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
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Descrição: This study examined NO- and non-NO-, non-prostanoid-dependent pathways of agonist-induced vasodilatation in streptozotocin (STZ)-induced diabetic rats and their age-matched controls at 1â2, 8â10 and 18â20 weeks after induction of diabetes. Using laser Doppler flowmetry, vasodilatory responses to acetylcholine (ACh; 0.1 mM) and morpholino-sydnonimine (SIN-1) were determined in the presence of Ringer solution, during inhibition of NO synthase (NOS) and cyclo-oxygenase (COX) with N Ï -nitro-L-arginine (L-NNA; 1 mM) + indomethacin (10 â5 M), and during inhibition of K + channels, NOS and COX with tetraethylammonium (TEA; 10 mM) + L-NNA + indomethacin. Basal NOS activity and nerve conduction velocity were also determined. In age-matched controls, SIN-1-induced vasodilatation in the presence of TEA + L-NNA + indomethacin, basal NOS activity and the initial vasodilatory response to ACh during NOS and COX inhibition all decreased with maturation. In STZ-induced diabetics, SIN-1-induced vasodilatation in the presence of TEA + L-NNA + indomethacin was impaired immediately after induction of diabetes, but not at 18â20 weeks. NOS activity in STZ-induced diabetics displayed a transient 2-fold increase at 8â10 weeks, decreasing to age-matched control levels at 18â20 weeks. At 18â20 weeks of STZ-induced diabetes, ACh-induced vasodilatation during NOS and COX inhibition was prolonged due to increased K + channel activity and experimental diabetic sensory neuropathy (EDN) had developed. Thus, in sciatic nerve microcirculation of STZ-induced diabetic rats: (1) diabetic impairment of vasodilatation in response to exogenous NO was transient; (2) non-NO-, non-prostanoid-dependent vasodilatation and K + channel activity were augmented in STZ-induced diabetes; and (3) alterations in NO bioactivity were not related to the development of EDN.
Editor: Oxford, UK: The Physiological Society
Idioma: Inglês

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NO- and non-NO-, non-prostanoid-dependent vasodilatation in rat sciatic nerve during maturation and developing experimental diabetic neuropathy

Thomsen, Kirsten ; Rubin, Inger ; Lauritzen, Martin

Oxford, UK: The Physiological Society

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