EFFECTS OF ADENOSINE AND ADENOSINE-ANALOGS ON MEAN CIRCULATORY FILLING PRESSURE AND CARDIAC-OUTPUT IN ANESTHETIZED RATS

Authors
Citation
R. Tabrizchi, EFFECTS OF ADENOSINE AND ADENOSINE-ANALOGS ON MEAN CIRCULATORY FILLING PRESSURE AND CARDIAC-OUTPUT IN ANESTHETIZED RATS, Naunyn-Schmiedeberg's archives of pharmacology, 356(1), 1997, pp. 69-75
Citations number
36
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00281298
Volume
356
Issue
1
Year of publication
1997
Pages
69 - 75
Database
ISI
SICI code
0028-1298(1997)356:1<69:EOAAAO>2.0.ZU;2-0
Abstract
The effects of adenosine and adenosine analogues, 2-[p-(2-[carboxyethy l) phenethylamino]-5'-N-ethylcarboxamidoadenosine (CGS 21680) and N-6- 2-(4-aminophenyl)-ethyladenosine (APNEA), on mean arterial pressure, c ardiac output, mean circulatory filling pressure, arterial resistance, venous resistance and heart rate in untreated or treated (with gangli on-blockers mecamylamine and atropine) pentobarbital-anesthetized rats were examined. Infusion of adenosine (100, 300 and 900 mu g/kg/min), CGS 21680 (0.1, 0.3 and 0.9 mu g/kg/min) or APNEA (1.0, 3.0 and 9.0 mu g/kg/min) reduced mean arterial pressure and arterial resistance in a ll groups. Adenosine and APNEA also reduced mean circulatory filling p ressure, venous resistance and heart rate in untreated animals. Furthe rmore, APNEA but not adenosine reduced cardiac output. In contrast, CG S 21680 increased cardiac output and heart rate but did not have any e ffect on mean circulatory filling pressure or venous resistance. In ga nglion-blocked rats, APNEA reduced cardiac output, mean circulatory fi lling pressure and heart rate, while adenosine did not have any effect on these parameters. In addition, APNEA and adenosine reduced arteria l resistance but were unable to alter venous resistance while CGS 2168 0 reduced mean circulatory filling pressure and arterial resistance bu t did not further affect cardiac output, heart rate and venous resista nce in ganglion-blocked animals. The results of the present study sugg est that adenosine and APNEA dilate arterioles and vein, whereas CGS 2 1680 causes arterial dilatation but not venodilatation in untreated an imals due to hypotension-induced sympathetic activation. A possible ex planation for the present observations could be differences in the dis tribution of vascular A(2) versus A(3) adenosine receptors in the veno us circulation.