Lipids and nitric oxide in porcine retinal and choroidal blood vessels.
Lipid profiles of porcine retina, and retinal and choroidal vessels were analyzed using the gas chromatography/mass spectrometry (GC/MS) technique. The retina and both isolated retinal and choroidal vessels contained saturated fatty acid stearic acid and polyunsaturated fatty acids, including arachidonic (C20:4, AA), a precursor for vasoactive prostaglandin (PG-2) series, and W-6 docosahexaenoic acids (C22:6, DHA). However, eicosapentaenoic acid (C20:5, EPA), a precursor for PG-3 series, was not detected in these vessels. When stearic acid was used for normalization of tissue sample, the retina contained relatively higher amounts of DHA than AA, retinal vessels had equal amounts of AA and DHA, while choroidal vessels contained higher amounts of AA than DHA. We also examined the endogenous synthesis of vasoactive endothelial-derived factors like PGs and nitric oxide (NO). Since vasoactive angiotensin II (Ang II) releases these products from blood vessels, this polypeptide was used in a porcine retinal circulation model. The porcine retinal central artery was perfused with oxygenated/heparinized physiological salt solution at 37 degrees C. Changes in A1 and A2 arteriolar diameters induced by Ang II were determined in the absence and presence of the nitric oxide synthase inhibitor, l-NO Arginine (LNOA), and cyclooxygenase inhibitor, flurbiprofen (FB). The central retinal artery designated as the first order arteriole A1 and subsequent branch was defined as A2. Luminal diameters of Al and A2 arterioles were 35 +/- 2 am and 10 +/- 1 microm, respectively. Topical Ang II (10(-10) M-10(-6) M) caused small vasoconstrictions in a dose-dependent manner. This response was enhanced after inhibition of PG synthesis by (10-6 M) FB. Ang II induced-constrictions were further enhanced in the presence of NO synthase inhibitor, LNOA (10(-7) M). There was slightly more increase in Ang II-induced vasoconstrictions in the presence of both NO and PG inhibitors, suggesting that NO may cause release of PGs from these vessels. This study demonstrates that the porcine retinal arterioles have the ability to regulate vasoconstriction responses induced by Ang II by synthesis and release of endogenous vasodilating PGs and NO (especially NO); and these substances may play a vital role in porcine retinal circulation.
Kulkarni
Prasad
P
Department of Ophthalmology and Visual Science, University of Louisville School of Medicine, Kentucky Lions Eye Research Center, 40292, USA. pskulk01@louisville.edu
Cai
Jian
J
Hurst
Harrell E
HE
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000378:metabolism / Q000502:physiology; D002829:Choroid / Q000098:blood supply / Q000378:metabolism* / Q000502:physiology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000502:physiology; D005227:Fatty Acids / Q000378:metabolism*; D008401:Gas Chromatography-Mass Spectrometry; D066298:In Vitro Techniques; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D009569:Nitric Oxide / Q000096:biosynthesis*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D010477:Perfusion; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012171:Retinal Vessels / Q000378:metabolism* / Q000502:physiology; D013552:Swine; D014661:Vasoconstriction / Q000187:drug effects
D016861:Cyclooxygenase Inhibitors; D005227:Fatty Acids; D000804:Angiotensin II; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase