Adrenal corticosteroid action on the thick ascending limb.
Several lines of evidence support the view that corticosteroids stimulate Na+, K+, HCO3-, and H+ transport by the TAL and that modulation of transport contributes to homeostasis of these ions. Although some details of the cellular and molecular mechanisms of corticosteroid action in the amphibian diluting segment are known, little is known about these pathways in TAL cells. In addition, the issue of mineralocorticoid versus glucocorticoid specificity and receptor localization in the TAL is not resolved. We anticipate that these intriguing issues will be addressed using TAL cells in culture and isolated TAL in conjunction with patch clamp, fluorescent probes and molecular biological approaches.
Department of Physiology, Dartmouth Medical School, Hanover, NH 03756.
P
P
Dietl
D
D
Good
B
B
Stanton
D000305:Adrenal Cortex Hormones / Q000502:physiology*; D000818:Animals; D001692:Biological Transport; D006801:Humans; D007473:Ion Channels / Q000378:metabolism; D007671:Kidney Concentrating Ability / Q000502:physiology; D007684:Kidney Tubules / Q000502:physiology*; D008138:Loop of Henle / Q000502:physiology*; D008901:Mineralocorticoids / Q000502:physiology; D011965:Receptors, Glucocorticoid / Q000502:physiology; D018161:Receptors, Mineralocorticoid; D011987:Receptors, Steroid / Q000502:physiology
D000305:Adrenal Cortex Hormones; D007473:Ion Channels; D008901:Mineralocorticoids; D011965:Receptors, Glucocorticoid; D018161:Receptors, Mineralocorticoid; D011987:Receptors, Steroid