The action of ATP in the guinea-pig heart

Hopkins, Sondra V.

doi:10.1016/0006-2952(73)90414-0

Cited by 32 publications

(18 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The effects of some coronary dilators are due to a calcium antagonistic action (Fleckenstein, (Burnstock, 1972;Hopkins, 1973a). This idea is compatible with the present finding that adenosine was about 3 times more potent than ATP.…”

Section: Discussionsupporting

confidence: 84%

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

Fujita

Ishida

Izumi

et al. 1980

British J Pharmacology

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionsupporting

confidence: 84%

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

Fujita

Ishida

Izumi

et al. 1980

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Numerous reports indicate that bath-applied ATP causes negative chronotropic effects when applied to the mammalian heart (see Versprille, 1966;Hopkins, 1973).…”

mentioning

confidence: 99%

Effects of sympathetic nerve stimulation on the sino‐atrial node of the guinea‐pig.

Choate

Edwards

Hirst

et al. 1993

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. The effects of sympathetic nerve stimulation on the generation of pacemaker action potentials, recorded from the sino-atrial node of the guinea-pig, were determined by using intracellular recording techniques.2. Trains of stimuli applied to the right stellate ganglion led to an increase in heart rate after a delay of a few seconds. During the initial phase of the tachyeardia the rate of discharge of pacemaker action potentials increased and the rate of diastolic depolarization increased, but both the peak diastolic potential and the maximum rate of rise of the action potentials were reduced. During the later phase of the tachycardia the peak diastolic potential, the amplitude of the action potentials, the maximum rate of rise and the rate of repolarization of the action potentials were increased.3. When membrane potential recordings were made from sino-atrial node cells, in which beating had been abolished by adding the organic calcium antagonist nifedipine, sympathetic nerve stimulation initiated excitatory junction potentials (EJPs) which had time courses similar to those of the tachycardias recorded from beating preparations.4. Although both the tachyeardias produced by either sympathetic nerve stimulation or added noradrenaline were largely abolished by fl-adrenoceptor antagonists, the membrane potential changes recorded during the responses to sympathetic nerve stimulation or added noradrenaline were different. Bath-applied noradrenaline caused a tachycardia which was associated with an increase in the amplitudes of pacemaker action potentials, an increase in the peak diastolic potential and a shortening in the duration of pacemaker action potentials.5. The addition of agents which cause the accumulation of cyclic AMP in the cytoplasm of the cells produced a tachycardia which was associated with a similar sequence of changes in the membrane potentials to those produced by added noradrenaline; again the membrane potential changes produced by these agents differed from those produced by sympathetic nerve stimulation.6. The results are discussed in relation to the idea that neurally released noradrenaline activates a set of receptors which cause tachycardia by increasing

show abstract

“…The heart is sensitive to adenyl compounds (see Drury & Szent-Gyorgyi, 1929;Green & Stoner, 1950;Burnstock, 1976;1980); these compounds have negative inotropic and chronotropic effects on the heart of both mammals (Hollander & Webb, 1957;James, 1965;Hopkins, 1973a;Fujita, Ishida, Izumi, Moritoki, Ohara & Takei, 1980) and frogs (Versprille & Van Duyn, 1966;Hartzell, 1979). In addition, an initial positive inotropic and chronotropic effect of adenosine 5 '-triphosphate (ATP) has been reported in the frog heart (Versprille, 1963;Flitney, Lamb & Singh, 1977;Goto, Yatani & Tsuda, 1977).…”

Section: Introductionmentioning

confidence: 99%

DISTRIBUTION OF P₁ AND P₂‐PURINOCEPTORS IN THE GUINEA‐PIG AND FROG HEART

Burnstock

Meghji

1981

British J Pharmacology

View full text Add to dashboard Cite

1 The effects of adenyl compounds were examined on the guinea-pig and frog heart in terms of the Pl/P2-purinoceptor hypothesis. 2 The effects of two slowly degradable adenosine 5'-triphosphate (ATP) analogues; ,-Ymethylene adenosine 5'-triphosphate (APPCP) and a,p-methylene adenosine 5'-triphosphate (APCPP) were also examined. 3 Adenosine, adenosine 5 '-monophosphate (AMP), adenosine 5 '-diphosphate (ADP), ATP and APPCP produced inhibitory effects in guinea-pig atria. These inhibitory effects were antagonized competitively by theophylline and potentiated by dipyridamole. APCPP did not produce a similar inhibitory response. 4 Guinea-pig ventricles were insensitive to adenyl compounds. 5 ATP and ADP produced initial excitatory effects in frog atria which were followed by inhibitory effects. Adenosine and AMP produced inhibitory effects alone whereas APCPP produced excitatory effects only. The inhibitory effects were antagonized competitively by theophylline and potentiated by dipyridamole. 6 ATP, ADP, APPCP and APCPP evoked excitatory responses in frog ventricles. These responses were not affected by theophylline or dipyridamole. Adenosine and AMP were inactive on frog ventricles.

show abstract

The action of ATP in the guinea-pig heart

Cited by 32 publications

References 8 publications

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

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

Effects of sympathetic nerve stimulation on the sino‐atrial node of the guinea‐pig.

DISTRIBUTION OF P₁ AND P₂‐PURINOCEPTORS IN THE GUINEA‐PIG AND FROG HEART

Contact Info

Product

Resources

About

The action of ATP in the guinea-pig heart

Cited by 32 publications

References 8 publications

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

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

Effects of sympathetic nerve stimulation on the sino‐atrial node of the guinea‐pig.

DISTRIBUTION OF P1 AND P2‐PURINOCEPTORS IN THE GUINEA‐PIG AND FROG HEART

Contact Info

Product

Resources

About

DISTRIBUTION OF P₁ AND P₂‐PURINOCEPTORS IN THE GUINEA‐PIG AND FROG HEART