Activation of Veratridine Sensitive Sodium Channels, But not Electrical Field Stimulation, Dilates Porcine Retinal Arterioles with Preserved Perivascular Tissue.

Purpose: Disturbances in retinal blood flow are a prominent feature of vision threatening retinal diseases. The regulation of tone in retinal resistance vessels involves the perivascular retinal tissue, but it is unknown to what extent neurons or glial cells contribute to the effect. Therefore, the purpose of the present study was to study the contribution of neurons in the perivascular retina to vascular tone during activation of voltage-gated sodium channels with veratridine and electrical field stimulation (EFS).

Hypoxia-induced relaxation of porcine retinal arterioles in vitro depends on inducible NO synthase and EP4 receptor stimulation in the perivascular retina.

Purpose: Hypoxia-induced relaxation of porcine retinal arterioles has been shown to be reduced during inhibition of prostaglandin synthesis and nitric oxide synthase (NOS). The purpose of this study was to identity the specific prostaglandin receptor(s) and source(s) of NO mediating this effect.

Methods: Porcine retinal arterioles with preserved perivascular retinal tissue were mounted in a myograph and were exposed to hypoxia in the presence of one of the following: the general NO synthase inhibitor L-NAME, the selective iNOS inhibitor 1400W, the selective nNOS inhibitor 7-nitroindazole, the general cyclooxygenase (COX) inhibitor ibuprofen or an antagonist to the FP- (AL 8810), DP- (BWA868C), EP1 - (SC-19220), EP2 - (PF-044189) or EP4 receptors (GW627368X).

Dorzolamide-induced relaxation of porcine retinal arterioles in vitro depends on nitric oxide but not on acidosis in vascular smooth muscle cells.

The carbonic anhydrase inhibitor dorzolamide can induce relaxation of retinal arterioles with a consequent increase in blood flow and oxygenation of the retina. It has been shown that the mechanisms underlying this relaxation are independent of extracellular acidosis and CO2. The purpose of the present study was to investigate the possible involvement of nitric oxide (NO) and intracellular acidosis in dorzolamide-induced relaxation of retinal arterioles.

Relaxation of porcine retinal arterioles during acute hypoxia in vitro depends on prostaglandin and NO synthesis in the perivascular retina.

Purpose: Disturbances in retinal oxygenation influence retinal function, but are also accompanied by changes in the tone of retinal arterioles. However, the mechanisms underlying these tone changes have not been studied in detail.

Materials And Methods: Porcine retinal arterioles were mounted in a wire myograph, and the vasoactive effects of hypoxia and hyperoxia were studied before and after removal of the perivascular retinal tissue.

Neurogenic contractions in intraocular porcine ciliary arteries are mediated by α₂-adrenoceptors and NPY₁ receptors and are inhibited by prostaglandin E₂ acting on prejunctional EP₄ receptors.

Prostaglandin analogues and adrenergic drugs are used to reduce the intraocular pressure in glaucoma, which may partly be due to an effect on the tone of the intraocular arteries supplying the ciliary body. The aim of the present study was to investigate the interaction between prostaglandins and autonomic nervous activity induced by electrical stimulation of the tone in these ciliary vessels. The intraocular part of porcine ciliary arteries were isolated and mounted in a microvascular myograph for isometric tension recordings, and the effect of prostaglandin E(2) on electrically induced contractions was studied in the presence of selective EP receptor antagonists.