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

Abstract

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with adrenaline and noradrenaline, from perfused cat adrenal glands in response to nicotinic stimulation (V. Cenia, unpublished results), favours a role for this dopaminergic receptor in modulating catecholamine release from the chromaffin cell.

Effects of chronic bromocriptine (CB-154) treatment on the plasma glucose and insulin secretion response to neurocytoglucopenia in rats

“…The presence of dopamine D 2 receptors has been shown in the adrenal medulla and administration of D 2 receptor agonists reduced catecholamine secretion induced by nicotine activation (Artalejo et al 1985, Gonzales et al 1986. Therefore, the D 2 agonist inhibition of catecholamine secretion by the adrenal medulla should have facilitated the higher insulin response in bromocriptine-treated rats submitted to i.v.…”

Three types of bovine chromaffin cell Ca2+ channels: facilitation increases the opening probability of a 27 pS channel.

“…Thus any hormone, neurotransmitter or drug that raises cyclic AMP may activate facilitation including dopamine , VIP (Wilson, 1988), adenosine (Chern, Kim, Slakey & Westhead, 1988) and forskolin (Marriott, Adams & Boarder, 1988;Morita, Dohi, Kitayama, Koyama & Tsujimoto, 1987). Thus when VIP is released from the pre-synaptic nerve terminals of the splanchnic nerve (Haycock, Shukla, Wakade & Wakade, 1990) or dopamine is secreted from chromaffin cells in response to depolarizations (Artalejo, Garcia, Montiel & Sanchez, 1985) their primary effect may be to augment catecholamine release from chromaffin cells by the activation of facilitation Ca2+ channels. It will be of considerable interest to determine whether any of the substances secreted by chromaffin cells including noradrenaline, adrenaline and ATP act as negative feedback controllers to curtail catecholamine secretion.…”

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

“…The reversal of the inhibitory effects of dopamine agonists on catecholamine release by specific D2 antagonists such as sulpiride indicates that the D2 receptor subtype is responsible, both in the adrenal gland (Artalejo et al 1985;Gonzalez et al 1986) and in cultured chromaffin cells (Bigornia et al 1988). To date, there is no evidence for D1 receptors in the adrenal medulla and D1 agonists do not inhibit catecholamine release nor do D1 antagonists prevent the inhibitory effect of apomorphine (Bigornia et al 1988).…”

“…Dopaminergic agonists were shown to inhibit secretion of adrenaline and noradrenaline from perfused adrenal glands (Artalejo, Garcia, Montiel & Sanchez-Garcia, 1985; Gonzalez, Artalejo, Montiel, Hervas & Garcia, 1986) and from chromaffin cells maintained in primary culture (Bigornia, Suozzo, Ryan, Napp & Schneider, 1988). The reversal of the inhibitory effects of dopamine by specific D2 antagonists suggests that the effects are mediated by a D2 receptor in the adrenal medulla and the presence of D2 but not D1 dopamine receptors was demonstrated in ligand binding studies on chromaffin cell membrane suspensions (Gonzales et al 1986;Lyon, Titeler, Bigornia & Schneider, 1987;Quick, Bergeron, Mount & Philie, 1987).…”

“…While earlier work demonstrated that dopamine inhibited nicotinic-evoked catecholamine release (Artalejo et al 1985), more recent data suggest that dopamine decreases secretion from adrenal chromaffin cells by altering Ca2+ channel conductance (Bigornia et al 1988). To assess the possible role of voltage-gated Ca2+ channels and of acetylcholine-activated channels in the dopamine-induced inhibition of catecholamine release, we have compared the effect of D2 agonists on Ca2+ and Na+ uptake evoked by different secretagogues.…”