Catecholaminergic control of intracellular free calcium and beta-endorphin secretion of rat pituitary intermediate lobe cells.
Individual melanotropes and intermediate lobes were tested to elucidate the role of alpha- and beta-adrenergic and D-2 dopamine receptors in the regulation of concentration of intracellular free calcium ([Ca2+]i) and release of beta-endorphin. Hormone secretion was studied in a superfusion system, while [Ca2+]i was measured microspectrofluorimetrically. Noradrenaline (1 microM) resulted in a slight decrease, then a marked increase in [Ca2+]i and secretion of beta-endorphin. The nonselective beta-adrenergic agonist isoproterenol (1 microM) increased [Ca2+]i and secretion of beta-endorphin; this effect was blocked by the beta-antagonist propranolol (10 microM). The alpha-adrenergic agonist phenylephrine (1 microM) increased [Ca2+]i and beta-endorphin secretion, but this effect was not blocked by terazosin or prazosin (alpha1-adrenergic antagonists, 1 microM). Administration of the alpha2-adrenergic agonist xylazine (1 microM) increased [Ca2+]i but did not affect secretion of the hormone. Biphasic effect of noradrenaline was tested in presence of adrenergic and dopaminergic antagonists. The noradrenaline-induced rise in [Ca2+]i and beta-endorphin secretion was decreased by propranolol, but this drug did not modify the inhibition. In the presence of 1 microM sulpiride (selective D-2 dopaminergic antagonist), the inhibitory phase of the curve was abolished, and the subsequent increase was reduced. This suggests that activation of dopamine D-2 receptors is involved not only in the inhibition, but also in the subsequent increase, which may originate from a rebound after the termination of the activation of these inhibitory receptors. Our data suggest the presence of several distinct types of catecholamine receptors in the rat intermediate lobe, and the dominant involvement of D-2 and beta-adrenergic receptors in the noradrenaline-induced regulation of melanotropes.
Némethy
Z
Z
Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest.
Horváth
G
G
Makara
G B
GB
Acs
Z
Z
Barna
I
I
D000322:Adrenergic Agonists / Q000494:pharmacology*; D018674:Adrenergic Antagonists / Q000494:pharmacology*; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D018492:Dopamine Antagonists / Q000494:pharmacology; D007424:Intracellular Fluid / Q000378:metabolism; D008297:Male; D008547:Melanophores / Q000187:drug effects / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology*; D010902:Pituitary Gland / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D011942:Receptors, Adrenergic, alpha / Q000502:physiology; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D017448:Receptors, Dopamine D2 / Q000502:physiology; D013469:Sulpiride / Q000494:pharmacology; D001615:beta-Endorphin / Q000378:metabolism*
D000322:Adrenergic Agonists; D018674:Adrenergic Antagonists; D000316:Adrenergic alpha-Agonists; D018492:Dopamine Antagonists; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D017448:Receptors, Dopamine D2; D001615:beta-Endorphin; D013469:Sulpiride; D002118:Calcium; D009638:Norepinephrine