Complex physiological and biochemical action of aldosterone in toad urinary bladder and mammalian renal collecting duct cells.
Since the discovery of the steroid hormone aldosterone nearly 35 years ago, our knowledge on the cellular actions of aldosterone is still incomplete. Most of the present physiological and biochemical knowledge about the antinatriuretic action was revealed by investigations on amphibian tight epithelia, in particular the toad urinary bladder. Less biochemical information was obtained from mammalian tissue such as microdissected renal tubules and cultured cells. In our opinion, it is questionable whether de novo synthesis of cell proteins-induced by aldosterone-can explain all of the hormonal effects to increase the Na+ transport. In the present paper we try to analyze the wide and contradictory field of biochemical data about the action of aldosterone on the increase in Na+ transport in renal cells in an attempt to incorporate this information into an extended working hypothesis. We suggest distinguishing principally between an early and a late biochemical response phase. We speculate that aldosterone may act by a two-step mechanism: the early and late aldosterone-induced proteins.
Minuth
W W
WW
Department of Anatomy and Cell Biology, University of Heidelberg, FRG.
Steckelings
U
U
Gross
P
P
D000450:Aldosterone / Q000502:physiology*; D000818:Animals; D002025:Bufonidae; D002478:Cells, Cultured; D007684:Kidney Tubules / Q000166:cytology*; D007685:Kidney Tubules, Collecting / Q000166:cytology*; D008745:Methylation; D008928:Mitochondria / Q000201:enzymology; D012964:Sodium / Q000378:metabolism; D015222:Sodium Channels / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D001743:Urinary Bladder / Q000502:physiology*
D015222:Sodium Channels; D000450:Aldosterone; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase