z-logo
Premium
The role of A 3 adenosine receptors in central regulation of arterial blood pressure
Author(s) -
Stella Luigi,
Novellis Vito,
Marabese Ida,
Berrino Liberato,
Maione Sabatino,
Filippelli Amelia,
Rossi Francesco
Publication year - 1998
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0702126
Subject(s) - blood pressure , adenosine , receptor , adenosine receptor , chemistry , medicine , endocrinology , cardiology , neuroscience , pharmacology , biology , agonist
1 Pharmacological studies have suggested that A 3 receptors are present on central neurons. Recently this adenosine receptor subtype has been identified in the rat and its presence in the central nervous system has been confirmed. 2 In this study we investigated the effects of acute intracerebroventricular (i.c.v.) injections of N 6 ‐2‐(4‐aminophenyl)‐ethyladenosine (APNEA), a non‐selective A 3 adenosine receptor agonist, on arterial blood pressure (ABP) and heart rate (HR), after treatment with 8‐cyclopentyl‐1,3‐dipropylxanthine (DPCPX), a selective antagonist of A 1 adenosine receptors. 3 Anaesthetized rats, after DPCPX (12 μg −1  kg i.c.v.), were treated with APNEA (0.4–4 μg kg −1 i.c.v.) resulting in a transitory and dose‐dependent decrease in arterial blood pressure without a change in heart rate. APNEA also induced hypotensive responses after i.c.v. pretreatment with aminophylline, at a dose of 20 μg kg −1 . In contrast, pretreatment 48 h before, with 4 μg kg −1 i.c.v. of pertussis toxin reduced the hypotensive effect induced by APNEA. Administration of APNEA at a higher dose (20 μg kg −1 i.c.v.), after DPCPX, induced a decrease in ABP of −66±5.4 mmHg and after 3 min a decrease in heart rate of −62±6.0 beats min −1 . Transection of the spinal cord abolished this significant fall in ABP, but not the decrease of HR. 4 These results suggest that a population of A 3 ‐receptors is present in the CNS, whose activation induces a decrease in blood pressure with no change of heart rate.British Journal of Pharmacology (1998) 125 , 437–440; doi: 10.1038/sj.bjp.0702126

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom