A species difference in the uptake of adenosine by heart

Hopkins, Sondra V.; Goldie, Roy G.

doi:10.1016/0006-2952(71)90440-0

Cited by 73 publications

(20 citation statements)

References 14 publications

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“…This is in contrast to the guinea-pig, where the effects of adenosine are potentiated by dipyridamole (Stafford, 1966, Kolassa et al, 1971Burnstock & Meghji, 1981). It has been shown that less adenosine is taken up in rat hearts than in guineapig hearts (Hopkins & Goldie, 1971 Goldie (1971) and Kolassa et al (1971) have shown, with the use of ['4C]-adenosine, that the adenosine uptake process in rats, unlike the guinea-pig, was not blocked by dipyridamole. It is likely that these observations account for the inability of dipyridamole to potentiate adenosine actions in the rat heart.…”

Section: Discussionmentioning

confidence: 96%

The effect of adenyl compounds on the rat heart

Burnstock

Meghji

1983

British J Pharmacology

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1 The effects of adenyl compounds were examined on the rat atrium and ventricle. 2 Adenosine, adenosine 5'-monophosphate, adenosine 5'-diphosphate, adenosine 5'-triphosphate (ATP) and 1, y-methylene ATP (APPCP) produced negative inotropic effects on the rat atrium. These inhibitory effects were antagonized by 8-phenyltheophylline (8-PT), a P1-purinoceptor antagonist, and potentiated by erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA), an adenosine deaminase inhibitor, but were not affected by dipyridamole, which blocks adenosine uptake.3 a, P-Methylene ATP (APCPP), which is resistant to degradation, did not produce a similar inhibitory response in the rat atrium. 4 Adenosine did not affect the basal developed force of the rat ventricle nor did it affect the 3-adrenoceptor-mediated positive inotropic effect. 5 Very high concentrations of ATP (0.1-3 mM) produced negative inotropic effects in the rat ventricle. APPCP (0.3 mM) also produced an inhibitory response, which was significantly smaller than that produced by ATP (0.3 mM). APCPP elicited excitation rather than the expected inhibitory response.6 The inhibitory effect of ATP in the rat ventricle was not blocked by indomethacin, 8-PT or atropine. 7 It ispossible that the action of ATP in the rat ventricle is mediated via P2-purinoceptors and that the lack of inhibitory action of APCPP on the rat ventricle is due to the difference in structural conformation between ATP and APCPP. 8 It seems likely that inhibitory P1-purinoceptors are present in the rat atrium and that the inhibitory responses produced by ATP in the rat ventricle may be mediated via P2-purinoceptors.

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Section: Discussionmentioning

confidence: 96%

The effect of adenyl compounds on the rat heart

Burnstock

Meghji

1983

British J Pharmacology

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“…It has been shown that the coronary vasodilator, dipyridamole, potentiates the coronary vascular response to adenosine, possibly by preventing degradation of adenosine in the tissue or erythrocytes (Jacob & Berne, 1960;Bunag et al, 1964), or by inhibiting the uptake of adenosine into erythrocytes (Koss, Beisenherz & Maerkisch, 1962) and tissue (Afonso & O'Brien, 1967;Pfleger, Volkmer & Kolassa, 1969;Kalsner, 1975) or by inhibiting the phosphorylation of adenosine (Hopkins & Goldie, 1971) and thus preventing its uptake.…”

Section: Introductionmentioning

confidence: 99%

Potentiation by Dilazep of the Negative Inotropic Effect of Adenosine on Guinea‐pig Atria

Fujita

Ishida

Izumi

et al. 1980

British J Pharmacology

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IDilazep, a coronary dilator, has been reported to potentiate the negative inotropic and negative chronotropic responses of guinea-pig atria to adenosine. Studies were made on the mechanism of the potentiating action of dilazep with special reference to the degradation and uptake of adenosine. 2 The negative inotropic actions of adenosine and adenine nucleotides, such as ATP, ADP, AMP and cyclic AMP, on guinea-pig atria were selectively and dose-dependently augmented by dilazep at concentrations insufficient to produce any effect alone (0.01 to 1 tM). 4 Adenosine (10 pM to 10 mM) was degraded to inosine and hypoxanthine during incubation with atrial tissue; dilazep (0.1 to 10 pM) retarded the disappearance of adenosine and the formation of inosine and hypoxanthine. 5 These results suggest that dilazep potentiates the negative inotropic effect of adenosine on guineapig atria by preventing both its accumulation by atrial tissue and degradation by deaminase.

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“…Rat tissues have been shown to be less sensitive to dipyridamole than tissues from other species, particularly guinea-pig, when adenosine potentiation (Hopkins & Goldie, 1971), inhibition of nucleoside transport or inhibition of NBMPR binding is measured . Additionally, some CNS membrane preparations with apparently uniform populations of NBMPR binding sites show biphasic dipyridamole inhibition of NBMPR binding (Hammond & Clanachan, 1984;.…”

Section: Methodsmentioning

confidence: 99%