title: Effects of arginine vasotocin and mesotocin on the activation and development of amiloride-blockable short-circuit current across larval, adult, and cultured larval bullfrog skins.
abstract: Amphibian skin has osmoregulatory functions, with Na(+) crossing from outside to inside. Na(+) transport can be measured as the short-circuit current (SCC). We investigated the short-term and long-term effects of arginine vasotocin (AVT) and mesotocin (MT) (which modulate Na(+) transport) on the activation and development of an amiloride-blockable SCC (adult-type feature) in larval, adult, and corticoid-cultured larval bullfrog skins. We found: (1) AVT-receptor (AVT-R) and MT-receptor (MT-R) mRNAs could be detected in both larval and adult skins, (2) in the short term (within 60 min), the larval SCC (amiloride-stimulated SCC) was increased by AVT, forskolin, and MT, suggesting that AVT and MT did not activate the inactive ENaC (epithelial sodium channel) protein thought to be expressed in larval skin, (3) in the short term (within 90 min), AVT, forskolin, and MT stimulated the adult SCC (amiloride-blockable SCC), (4) AVT and MT increased both the larval and adult SCC via receptors insensitive to OPC-21268 (an antagonist of the V(1)-type receptor), OPC-31260 (an antagonist of the V(2)-type receptor), and ([d(CH(2))(5),Tyr(Me)(2),Thr(4),Orn(8),des-Gly-NH (2) (9) ]VT) (an antagonist of the oxytocin receptor), (5) culturing EDTA-treated larval skin with corticoids supplemented with AVT (1 microM) or MT (1 microM) for 2 weeks (long-term effects of AVT and MT) did not alter the corticoid-induced development of an amiloride-blockable SCC (adult-type feature). AVT and MT thus have the potential to stimulate SCC though channels that are already expressed, but they may not influence the development of the amiloride-blockable SCC (an adult-type feature) in larval skin.
authors: Department of Physiology, School of Medicine, Saitama Medical University, Moroyama, Iruma-gun, Saitama, 3500495, Japan. makokam@saitama-med.ac.jp
authors: Makoto
authors: M
authors: Takada
authors: Kayo
authors: K
authors: Fujimaki-Aoba
authors: Shigeru
authors: S
authors: Hokari
mesh_terms: D000305:Adrenal Cortex Hormones / Q000494:pharmacology; D000584:Amiloride / Q000494:pharmacology*; D000818:Animals; D065092:Antidiuretic Hormone Receptor Antagonists; D001552:Benzazepines / Q000494:pharmacology; D005576:Colforsin / Q000494:pharmacology; D055724:Electrophysiological Phenomena / Q000187:drug effects / Q000502:physiology; D062686:Epithelial Sodium Channel Blockers; D053503:Epithelial Sodium Channels / Q000378:metabolism*; D004848:Epithelium / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism; D015870:Gene Expression / Q000235:genetics; D007814:Larva / Q000254:growth & development / Q000378:metabolism*; D010121:Oxytocin / Q000031:analogs & derivatives* / Q000494:pharmacology; D010880:Piperidines / Q000494:pharmacology; D015363:Quinolones / Q000494:pharmacology; D011892:Rana catesbeiana; D018045:Receptors, Oxytocin / Q000037:antagonists & inhibitors; D011979:Receptors, Pituitary Hormone / Q000235:genetics; D017483:Receptors, Vasopressin / Q000235:genetics; D012867:Skin / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism*; D014668:Vasotocin / Q000494:pharmacology*
chemical_list: D000305:Adrenal Cortex Hormones; D065092:Antidiuretic Hormone Receptor Antagonists; D001552:Benzazepines; D062686:Epithelial Sodium Channel Blockers; D053503:Epithelial Sodium Channels; D010880:Piperidines; D015363:Quinolones; D018045:Receptors, Oxytocin; D011979:Receptors, Pituitary Hormone; D017483:Receptors, Vasopressin; C116046:mesotocin receptor; C034862:vasotocin receptor; C068644:OPC 21268; C076251:mozavaptan; D005576:Colforsin; C001713:mesotocin; D010121:Oxytocin; D000584:Amiloride; D014668:Vasotocin