Investigations on the possible involvement of the dopaminergic system in the modulation of the growth and steroidogenic capacity of the rat adrenal zona glomerulosa: a coupled morphometric and biochemical study.
The effects of metoclopramide (MTC) and bromocriptine (BRC) (two drugs which act as antagonist and agonist of DOPA-receptors, respectively) on the zona glomerulosa of dexamethasone/ACTH-treated rats were investigated by coupled biochemical and morphometric techniques. Short-term (1-h) MTC administration significantly increased the plasma concentration of aldosterone, while long-term (7-day) MTC administration, as well as short- and long-term treatment with BRC did not cause any apparent change. Long-term MTC administration was found to significantly potentiate both the rise in the plasma level of aldosterone and the hypertrophy of the zona glomerulosa and its parenchymal cells induced by a prolonged treatment with angiotensin II (AII), but not those evoked by a chronic sodium deprivation alone or combined with AII infusion. Long-term BRC administration notably counteracted the effects of sodium restriction (coupled or not with AII infusion), but not those induced by the administration of AII alone. Long-term MTC administration partially reversed both the lowering of the plasma concentration of aldosterone and the atrophy of the zona glomerulosa and its parenchymal cells caused by a prolonged sodium-loading (combined or not with captopril infusion), but not those produced by the administration of captopril alone. On the other hand, long-term BRC treatment induced a further significant reduction in the blood level of aldosterone and the volume of zona glomerulosa and its cells only in captopril-treated animals. These findings are consistent with the view that the dopaminergic system exerts a maximal tonic inhibitory effect not only on the secretory activity, but also on the growth and steroidogenic capacity of the rat zona glomerulosa. Furthermore, they suggest that the activity of the dopaminergic system is in turn controlled by the sodium balance, being almost completely suppressed by a prolonged sodium deprivation.
Mazzocchi
G
G
Rebuffat
P
P
Robba
C
C
Belloni
A S
AS
Stachowiak
A
A
Gottardo
G
G
Meneghelli
V
V
Nussdorfer
G G
GG
D000302:Adrenal Cortex / Q000187:drug effects / Q000254:growth & development*; D000450:Aldosterone / Q000097:blood*; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001971:Bromocriptine / Q000494:pharmacology; D002216:Captopril / Q000494:pharmacology; D008297:Male; D008787:Metoclopramide / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000502:physiology*; D012083:Renin / Q000097:blood; D012964:Sodium / Q000502:physiology
D011954:Receptors, Dopamine; D000804:Angiotensin II; D001971:Bromocriptine; D000450:Aldosterone; D002216:Captopril; D012964:Sodium; D012083:Renin; D008787:Metoclopramide