title: Permissive effect of thyroid hormones on induction of rat colonic Na+ transport by aldosterone is not localised at the level of Na+ channel transcription.
abstract: The interrelationship between thyroid hormones and aldosterone has been examined in the regulation of rat colonic amiloride-sensitive Na+ transport which translocates Na+ through apical amiloride-sensitive Na+ channels and basolateral Na+, K+-ATPase. Electrogenic Na+ transport was measured in an Ussing chamber by the short-circuit current and identified by Na+ channel blocker amiloride. Na+-pumping activity of the basolateral Na+,K+-ATPase was investigated in nystatin-treated epithelium by measuring the equivalent short-circuit current after addition of mucosal Na+. The abundance of mRNA coding for alpha, beta and gamma subunits of the Na+ channel (rENaC) was estimated using Northern blot analysis. Hyperaldosteronism was induced by a low-salt diet and hypothyroidism by methimazole. The low-Na+ diet induced electrogenic Na+ transport in euthyroid rats but its effect was almost completely inhibited in hypothyroid animals even if the plasma concentration of aldosterone was high enough to stimulate this transport pathway both in euthyroid and hypothyroid rats. A kinetic study of the basolateral Na+,K+-ATPase revealed a decrease of Na+ transport capacity in hypothyroid rats kept on the low-Na+ diet in comparison with euthyroid animals fed the same diet. No significant differences in steady-state levels of alpha, beta and gamma rENaC mRNA were detected between euthyroid and hypothyroid rats. These data suggest that hypothyroidism decreases the efficacy of the basolateral Na+ pump but fails to inhibit it completely even though it inhibits the transepithelial electrogenic Na+ transport in response to aldosterone. We conclude that the permissive effect of thyroid hormones on the induction of electrogenic Na+ transport by aldosterone is localised beyond the transcriptional step of Na+ channel regulation.
authors.affiliation: Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
authors.forename: L
authors.initials: L
authors.lastname: Mrnka
authors.forename: J
authors.initials: J
authors.lastname: Pácha
mesh_terms: D000450:Aldosterone / Q000378:metabolism*; D000818:Animals; D003106:Colon / Q000378:metabolism*; D006929:Hyperaldosteronism / Q000235:genetics / Q000378:metabolism; D007037:Hypothyroidism / Q000235:genetics / Q000378:metabolism; D066298:In Vitro Techniques; D017136:Ion Transport; D008297:Male; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000378:metabolism*; D015222:Sodium Channels / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013963:Thyroid Hormones / Q000378:metabolism*; D014158:Transcription, Genetic
chemical_list: D012333:RNA, Messenger; D015222:Sodium Channels; D013963:Thyroid Hormones; D000450:Aldosterone; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase