ATP-Induced Relaxation of Porcine Retinal Arterioles Depends on the Perivascular Retinal Tissue and Acts Via an Adenosine Receptor

Abstract

The relaxation of porcine retinal arterioles induced by purinergic compounds is modulated by the perivascular retinal tissue.

Purinergic Mechanisms and Prostaglandin E Receptors Involved in ATP-Induced Relaxation of Porcine Retinal Arterioles in vitro

“…The present study confirms previous reports that ATP can induce relaxation of retinal arterioles in vitro which is more pronounced in the presence of retinal tissue implying that the effect is both induced directly by ATP and is mediated through the perivascular retinal tissue [6]. This interpretation is supported by the fact that the perivascular retinal tissue had a similar influence on the relaxing effect of the ATP analogue ATP-γS which is a P 2 purinergic agonist that can substitute ATP in kinase reactions yielding thiophosphorylated proteins resistant to protein phosphatases [21].…”

“…The purine adenosine triphosphate (ATP) is a carrier of energy in the intermediary metabolism [2] but has also been shown to act as an extracellular signalling molecule [3] and to participate in the regulation of retinal vascular tone by stimulation of purine P 2 receptors [4,5,6]. ATP metabolism is known to be disturbed, and concentrations are increased in the vitreous body in diabetic patients [7,8,9,10], which supports that ATP may be involved in the pathophysiology of diabetic retinopathy.…”

“…ATP metabolism is known to be disturbed, and concentrations are increased in the vitreous body in diabetic patients [7,8,9,10], which supports that ATP may be involved in the pathophysiology of diabetic retinopathy. The vaso-active effects of ATP may depend on ATP-induced ATP release, as shown in cardiac vessels [11,12], or be mediated by purinergic receptors [13] stimulated by degradation products of ATP [6] or through the release of other vaso-active compounds such as cyclo-oxygenase (COX) products [14,15]. However, the relative contribution of these mechanisms and the extent to which the mechanisms are active in the retinal vascular wall or depend on the perivascular retinal tissue are unknown.…”

Interaction between flicker-induced vasodilatation and pressure autoregulation in early retinopathy of Type 2 diabetes

“…However, since the retinal vascular system has no autonomic nervous supply, the arteriolar diameter is regulated by local factors from the vascular lumen, the vascular wall, and the perivascular retinal tissue [1][2][3][4]. Clinically, two types of local regulation of the diameter of retinal arterioles can be observed, i.e., pressure autoregulation (which is changes in the diameter of retinal arterioles that ensure a constant perfusion of the capillary bed when the blood pressure changes) and metabolic autoregulation (which is adjustments in the diameter of the retinal arterioles to balance the supply of nutrients and drainage of metabolic waste products when the retinal metabolism changes).…”

The Diameter of Retinal Arterioles Is Unaffected by Intravascular Administration of the Adenosine A_2A Receptor Agonist Regadenoson in Normal Persons

“…Previous studies have shown that adenosine has affinity to a number of adenosine receptor types [21] and that the dilating effect of the compound requires functional Na-K pumps and K ATP channels [22]. Additionally, adenosine may be a final common mediator of other compounds with vasodilating properties such as glutamate and ATP [23, 24]. Alternatively, the lack of effect on retinal vessels may be related to the route of administration of regadenoson.…”