Peripheral dopamine receptors: A classification based on potency series and specific antagonism

Goldberg, Leon I.; Kohli, Jai D.

doi:10.1016/0165-6147(83)90289-4

Cited by 113 publications

(44 citation statements)

References 8 publications

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“…The peripheral DA2 receptor is known to be sensitive to micromolar concentrations of dopamine; also, apomorphine (a more selective DA2 receptor agonist) is equipotent with dopamine, and sulpiride behaves as a selective antagonist (Goldberg & Kohli, 1983). Radioligand binding studies and the sensitivity of adrenomedullary adenylate cyclase to different selective dopaminergic agonists and antagonists would help to characterize such a receptor; these studies are being initiated at our laboratory.…”

Section: Discussionmentioning

confidence: 99%

A dopaminergic receptor modulates catecholamine release from the cat adrenal gland.

Artalejo¹,

Garcı́a²,

Montiel³

et al. 1985

The Journal of Physiology

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SUMMARY1. Nicotine evokes the release of catecholamines from perfused cat adrenal glands in a concentration-dependent manner, the median effective concentration for nicotine being 5 /tM. Two 2 min pulses of 5 pM-nicotine, 40 min apart (S. and S,) gave net catecholamine outputs of 7-64 and 3-55 jug/8 min, respectively. The ratio S2/S1 in control glands was 0-5.2. Increasing concentrations of apomorphine (1-10 /tM) markedly inhibited catecholamine release during the second nicotine pulse (A2). At 1 /tM-apomorphine, the release during S2 was significantly reduced to 16 % of S,; with 10 ,uM-apomorphine, the secretary response was reduced further to only 3 % of S,, the ratio S2/S1 being 003.3. The presence of haloperidol, sulpiride or picobenzide (each 0 5 ,/M) during S2, completely reversed the inhibition of catecholamine release produced by apomorphine. Haloperidol itself increased the nicotinic secretary response during S2; so, while the ratio S2/S1 was 0 5 in control conditions, this ratio increased significantly to 0 95 if haloperidol (0 5 /lM) was present during S2, suggesting that the presence of this dopaminergic antagonist removed a negative feed-back mechanism that inhibits nicotine-evoked catecholamine release.4. If present during S2, dopamine (1 fSM) also markedly inhibited catecholamine release evoked by nicotine; this inhibition was again reversed by 0.5 /LM-haloperidol.5. Neither the opiate antagonist naloxone nor the a-adrenoceptor blocking agent phentolamine (at concentrations of 0-5-5 ,/M) affected the inhibition by apomorphine of the secretary response to nicotine. 6. These data strongly suggest that the cat adrenal medulla chromaffin cell membrane contains a dopaminergic receptor which modulates the catecholamine secretary process triggered by stimulation of the nicotinic cholinoceptor. The fact that dopamine is released in measurable amounts, together with adrenaline and noradrenaline, from perfused cat adrenal glands in response to nicotinic stimulation (V. Cenia, unpublished results), favours a role for this dopaminergic receptor in modulating catecholamine release from the chromaffin cell.

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Section: Discussionmentioning

confidence: 99%

A dopaminergic receptor modulates catecholamine release from the cat adrenal gland.

Artalejo¹,

Garcı́a²,

Montiel³

et al. 1985

The Journal of Physiology

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“…According to the classification of Goldberg and Kohli, peripheral dopamine (DA) receptors are of either DA1, or DA2 subtype (Goldberg & Kohli, 1983). Renal vasodilatation induced by dopamine is mediated by vascular DA1 receptors, but it is uncertain whether the natriuresis due to this catecholamine results simply from alterations in renal blood flow, or from the stimulation of specific tubular receptors.…”

Section: Introductionmentioning

confidence: 99%

Domperidone treatment in man inhibits the fall in plasma renin activity induced by intravenous gamma‐L‐glutamyl‐L‐dopa.

Worth¹,

Harvey²,

Brown³

et al. 1986

Brit J Clinical Pharma

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1 The dopamine pro-drug -y-L-glutamyl-L-dopa (gludopa) was administered intravenously to six normal subjects at a dose of 12.5 ,ug min--kg-, either with or without the dopamine antagonist domperidone. A control was provided by the intravenous infusion of domperidone and saline on a separate occasion. 2 Intravenous gludopa produced a significant natriuresis, whether administered alone or in combination with domperidone. 3 After gludopa infusion, there was a significant fall in plasma renin activity, an effect which was attenuated significantly by concomitant treatment with domperidone. 4 These observations suggest that blockade of renal DA2 dopamine receptors has little or no effect on gludopa-induced natriuresis, but that at least part of the dopaminergic inhibition of renin release is mediated by renal DA2 receptors.

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“…Dopamine is produced during this biosynthetic process, and while it has generally been considered that dopamine is used only for the synthesis of catecholamines, evidence obtained from a variety of peripheral nervous system tissues indicates that dopamine may have a functional role in the adrenal medulla (Bell, 1982;Goldberg & Kohli, 1983;Lackovic & Neff, 1983).…”

Section: Introductionmentioning

confidence: 99%

Modulation of secretion by dopamine involves decreases in calcium and nicotinic currents in bovine chromaffin cells.

Sontag

Sanderson

Klepper

et al. 1990

The Journal of Physiology

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SUMMARY1. Catecholamine secretion from cultured bovine adrenal chromaffin cells was decreased in a dose-dependent manner by the D2 dopamine agonists apomorphine and LY 17 1555.2. 45Ca2+ uptake was similarly inhibited and whole-cell Ca2+ currents were reduced by apomorphine.3. These inhibitory effects of D2 agonists depended on the secretagogue used, being much more pronounced for nicotine-evoked responses compared to high K+ stimulation, indicating another possible site of action of apomorphine up-stream of Ca2+ entry.4. Inhibition by apomorphine of nicotine-evoked responses could not be explained by competitive antagonism against nicotine or DMPP (1,1-dimethyl-4-phenylpiperazinium iodide).5. Apomorphine caused reductions of inward whole-cell nicotinic current evoked by ACh and nicotine.6. Inhibition of nicotine-evoked secretion and 22Na+ influx by apomorphine were not affected by tetrodotoxin, and voltage-dependent, whole-cell Na+ currents were unaltered by apomorphine.7. No evidence was obtained for increases in K+ conductance by apomorphine. 8. Action potentials recorded in whole-cell current clamp were blocked by apomorphine when they were triggered by nicotinic depolarization but not when they were elicited by direct electrical stimulation.9. Inclusion ofGDP-,-S in the pipette internal solution did not affect apomorphinedependent inhibition of nicotinic-evoked responses, while the decrease in whole-cell Ca2`current induced by apomorphine was completely inhibited in the presence of GDP-fl-S.

show abstract

Peripheral dopamine receptors: A classification based on potency series and specific antagonism

Cited by 113 publications

References 8 publications

A dopaminergic receptor modulates catecholamine release from the cat adrenal gland.

A dopaminergic receptor modulates catecholamine release from the cat adrenal gland.

Domperidone treatment in man inhibits the fall in plasma renin activity induced by intravenous gamma‐L‐glutamyl‐L‐dopa.

Modulation of secretion by dopamine involves decreases in calcium and nicotinic currents in bovine chromaffin cells.

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