Differential inhibition of noradrenaline release mediated by inhibitory A(1)-adenosine receptors in the mesenteric vein and artery from normotensive and hypertensive rats

• Type: Article in International Scientific Journal
• Date: 2013

Authors

Rocha Pereira, C (Author) Other; Sousa, JB (Author) Other; Vieira Rocha, MS (Author) Other; Fresco, P (Author) FFUP; Goncalves, J (Author) FFUP; Diniz, C (Author) FFUP

Journal

Title: Neurochemistry International

Vol. 62 No. 4

Pages: 399-405

ISSN: 0197-0186

Publisher: Elsevier

Indexing

ISI Web of Knowledge - 6 Citations

Scopus - 7 Citations

Scientific classification

FOS: Medical and Health sciences > Basic medicine

Other information

Authenticus ID: P-005-2QS

DOI: 10.1016/j.neuint.2013.02.010

Abstract (EN): Mesenteric arteries and veins are densely innervated by sympathetic nerves and are crucial in the regulation of peripheral resistance and capacitance, respectively, thus, in the control of blood pressure. Presynaptic adenosine receptors are involved in vascular tonus regulation, by modulating noradrenaline release from vascular postganglionic sympathetic nerve endings. Some studies also suggest that adenosine receptors (AR) may have a role in hypertension. We aim at investigating the role of presynaptic adenosine receptors in mesenteric vessels and establish a relationship between their effects (in mesenteric vessels) and hypertension, using the spontaneously hypertensive rats (SHR) as a model of hypertension. Adenosine receptor-mediated modulation of noradrenaline release was investigated through the effects of selective agonists and antagonists on electrically-evoked [H-3]-noradrenaline overflow. CPA (A(1)AR selective agonist: 1-100 nM) inhibited tritium overflow, but the inhibition was lower in SHR mesenteric vessels. IB-MECA (A(3)AR selective agonist: 1-100 nM) also inhibited tritium overflow but only in WKY mesenteric veins. CGS 21680 (A(2A)AR selective agonist: up to 100 nM) failed to facilitate noradrenaline release in mesenteric veins, from both strains, but induced a similar facilitation in the mesenteric arteries. NECA (non-selective AR agonist: 1,3 and 10 mu M), in the presence of A(1) (DPCPX, 20 nM) and A(3) (MRS 1523, 1 mu M) AR selective antagonists, failed to change tritium overflow. In summary, the modulatory effects mediated by presynaptic adenosine receptors were characterized, for the first time, in mesenteric vessels: a major inhibition exerted by the A(1) subtype in both vessels; a slight inhibition mediated by A(3) receptors in mesenteric vein; a facilitation mediated by A(2A) receptors only in mesenteric artery (from both strains). The less efficient prejunctional adenosine receptor mediated inhibitory effects can contribute to an increase of noradrenaline in the synaptic cleft (both in arteries and veins), which might conduce to increased vascular reactivity.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 7