Abstract：
:Dysfunctional vascular endothelial nitric oxide synthase (eNOS) has been proposed to play a main pathophysiological role in various ocular diseases. The aim of the present study was to test the hypothesis that the chronic lack of eNOS impairs endothelium-dependent vasodilation in retinal arterioles. The relevance of eNOS for mediating vascular responses was studied in retinal vascular preparations from eNOS-deficient mice (eNOS-/-) and wild-type controls in vitro. Changes in luminal diameter in response to vasoactive agents were measured by videomicroscopy. The thromboxane mimetic, U46619, induced similar concentration-dependent constriction of retinal arterioles in eNOS-/- and wild-type mice. Responses to the endothelium-independent vasodilator, nitroprusside, did not differ between both mouse genotypes, either. In contrast, responses to the endothelium-dependent vasodilator, acetylcholine, were blunted in eNOS-/- mice. Non-isoform-selective blockade of either nitric oxide synthase (NOS) or cyclooxygenase (COX) alone did not affect responses to acetylcholine. However, combined blockade of both enzyme families markedly attenuated cholinergic vasodilation. Also, combined blockade of COX and neuronal NOS (nNOS) blunted acetylcholine-induced vasodilation, while combined COX and inducible NOS (iNOS) inhibition had no effect. Simultaneous NOS and COX-1 blockade did not affect cholinergic vasodilation, whereas combined NOS and COX-2 inhibition markedly reduced vasodilation to acetylcholine. These findings are the first to demonstrate that the chronic lack of eNOS is associated with moderate endothelial dysfunction in retinal arterioles. However, eNOS-deficiency is partially compensated by nNOS and COX-2 metabolites, which are reciprocally regulated.
journal_name
Exp Eye Resjournal_title
Experimental eye researchauthors
Gericke A,Wolff I,Musayeva A,Zadeh JK,Manicam C,Pfeiffer N,Li H,Xia Ndoi
10.1016/j.exer.2019.01.022subject
Has Abstractpub_date
2019-04-01 00:00:00pages
150-156eissn
0014-4835issn
1096-0007pii
S0014-4835(18)30804-2journal_volume
181pub_type
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