| Research Abstract |
To overcome hyperosmotic stress in a marine environment, elasmobranchs maintain their plasma slightly hyperosmotic to surrounding seawater primarily through the retention of urea. In the kidney, nearly all filtered urea is reabsorbed from primary urine, thereby reducing urinary loss of urea. However, a mechanism of urea reabsorption has not been clarified yet, largely due to the complexity of kidney structure. In this study, we attempted to clarify the mechanism by means of comprehensive analyses of transporting molecules. We isolated a cDNA encoding a facilitative urea transporter (UT) from a dogfish shark, Triakis scyllium. Immunohistochemistry using specific antibodies raised against the cloned UT revealed that the UT is expressed exclusively in the final segment of the bundle zone, that is, in the collecting tubule. Based on the above results together with localization of other important transporting molecules, including Na+/K+-ATPase and water channels, we proposed a model that the collecting tubule is responsible for the reabsorption of urea in the marine elasmobranch kidney. Other countercurrent segments may contribute to production of a driving force for facilitative diffusion of urea through the urea transporter. Meanwhile, we examined structures and salinity-dependent secretion of neurohypophysial hormones (NH), since NHs are plausible candidates for regulatory hormones of the kidney function. We identified three NHs from the hypothalamus of T.scyllium : vasotocin, asvatocin and a novel oxytocin-family peptide, phasitocin. In the hypothalamus, vasotocin mRNA levels significantly increased after transfer to 130% SW, while no change was observed in mRNA levels of asvatocin and phasitocin. The increase in vasotocin mRNA was reflected in the plasma level of vasotocin. These results suggest that vasotocin is an osmoregulatory effector in dogfish shark, especially when the shark is exposed to a hyperosmotic environment.
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