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P<P, published online ahead of print October 22, 2009
(Investigative Ophthalmology and Visual Science. )
© 2009 by The Association for Research in Vision and Ophthalmology, Inc.
doi:10.1167/iovs.09-4391
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Divergent Roles of Nitric Oxide and Rho Kinase in Vasomotor Regulation of Human Retinal Arterioles

Travis W Hein,1 Robert H Rosa,2 Zhaoxu Yuan,3 Elizabeth Roberts,4 and Lih Kuo5

1Departments of Ophthalmology and Surgery, Scott & White Eye Institute, Temple, United States 2Departments of Ophthalmology and Surgery, Scott & White Eye Institute, Temple, United States 3Department of Ophthalmology, Scott & White Eye Institute, Temple, United States 4Department of Ophthalmology, Scott & White Eye Institute, Temple, United States 5Department of Systems Biology and Translational Medicine, Texas A&M Health Science Center, Temple, United States

Correspondence: Travis Hein, Email: thein{at}tamu.edu

Abstract

Purpose: Although the arteriolar segment contributes to flow regulation, there is sparse information at the single microvessel level on how vasomotor function is regulated in the human retina. We have previously reported vasoreactivity and its underlying mechanisms in isolated porcine retinal arterioles. Herein, we studied human retinal arterioles for comparison.

Methods: Retinal tissues were obtained from 7 patients undergoing enucleation at the Scott &amp; White Eye Institute after written informed consent with Institutional Review Board approval. Human and porcine retinal arterioles were isolated and pressurized to 55 cmH2O luminal pressure for vasoreactivity study using videomicroscopic techniques.

Results: Isolated human and porcine retinal arterioles developed myogenic tone and dilated dose-dependently to bradykinin, adenosine, and sodium nitroprusside. Stepwise increases in luminal flow produced graded dilation with ~60% dilation at the highest flow tested. Nitric oxide (NO) synthase inhibitor L-NAME nearly abolished dilations to bradykinin and flow, and attenuated the adenosine-induced dilation without altering the response to nitroprusside. Endothelin-1 caused dose-dependent constriction. Rho kinase (ROCK) inhibitor H-1152 blocked both myogenic tone and endothelin-1-induced constriction. Responses of retinal arterioles to all agonists and increased flow were similar between pigs and humans.

Conclusions: Isolated human retinal arterioles dilate to bradykinin and increased flow in an NO-dependent manner. NO contributes, in part, to adenosine-induced vasodilation. Conversely, ROCK activation mediates myogenic tone and endothelin-1-induced vasoconstriction. Similarities in these vasoactive responses and the underlying mechanisms between human and porcine retinal arterioles support the latter as a viable experimental model of the human retinal microcirculation.

Key Words: retinal blood flow • endothelins • microcirculation • nitric oxide • retinal arterioles






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