NDLI: Role of endothelium in vasomotor responses to endothelin system and protein kinase C activation in porcine retinal arterioles.

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Role of endothelium in vasomotor responses to endothelin system and protein kinase C activation in porcine retinal arterioles.

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Role of endothelium in vasomotor responses to endothelin system and protein kinase C activation in porcine retinal arterioles.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Potts, Luke B. Xu, Wenjuan Hein, Travis W. Bradley, Patrick D. Kuo, Lih
Description	Author Affiliation: Potts LB ( Department of Medical Physiology, Scott & White Healthcare, College of Medicine, Texas A&M Health Science Center, Temple, Texas.)
Abstract	PURPOSE: Endothelial cells synthesize vasodilator nitric oxide (NO) and vasoconstrictor endothelin-1 (ET-1) from NO synthase (eNOS) and endothelin-converting enzyme-1 (ECE-1), respectively. Protein kinase C (PKC) and Rho kinase (ROCK) are major signaling molecules mediating vasoconstriction. Although endothelial cells express eNOS, ECE-1, endothelin B (ET(B)) receptors, PKC, and ROCK, their influences on ET-1-induced vasoconstriction remain elusive. We studied whether these endothelial signaling molecules modulate retinal arteriolar constriction to ET-1. METHODS: Porcine retinal arterioles were isolated and pressurized for vasomotor study, under conditions with intact or denuded endothelium, using videomicroscopic techniques. RESULTS: Retinal arterioles developed similar resting tone (≈45% of maximum diameter) with or without endothelium. Endothelial denudation attenuated vasoconstriction to ET-1 precursor, big ET-1, by almost equal to 50%, but did not affect vasoconstrictions to ET-1, ET(B) agonist sarafotoxin S6c, or PKC activator phorbol-12, 13-dibutyrate (PDBu). The ROCK inhibitor H-1152 caused vasodilation, and abolished vasoconstrictions to ET-1 and PDBu independent of endothelium. With L-type voltage-operated calcium channel (L-VOCC) blocker nifedipine, PDBu-induced vasoconstriction was abolished and converted to NO-mediated vasodilation in the presence of endothelium. The ET-1-induced vasoconstriction was unaffected by NO released from endothelium during flow elevation. CONCLUSIONS: Endothelial and smooth muscle ECE-1 contribute equally to synthesis of vasoactive ET-1 in retinal arterioles, with nominal role of endothelial ETB receptors in vasoconstriction to ET-1. The PKC activation leads to endothelium-dependent NO-mediated vasodilation when smooth muscle contraction is ablated by L-VOCC blockade. Endothelial cells and NO appear to have modest roles in modulating ROCK-dependent vasoconstriction, and are insufficient to counteract smooth muscle contractions to ET-1 and PKC activation.
ISSN	01460404
e-ISSN	15525783
DOI	10.1167/iovs13-13178
Journal	Investigative Opthalmology & Visual Science
Issue Number	12
Volume Number	54
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2013-11-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Endothelin-1 Pharmacology Endothelium, Vascular Physiology Muscle, Smooth, Vascular Protein Kinase C Metabolism Retinal Artery Vasomotor System Drug Effects 1-(5-isoquinolinesulfonyl)-2-methylpiperazine Analogs & Derivatives Animals Arterioles Aspartic Acid Endopeptidases Debridement Enzyme Activation Metalloendopeptidases Phorbol 12,13-dibutyrate Antagonists & Inhibitors Sus Scrofa Vasoconstrictor Agents Vasodilator Agents Viper Venoms Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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