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“…Furthermore, the hyperosmolar media of excess urea failed to influence the angiotensin II-stimulated AVP release from the explants. These results are compatible with the hypothesis that excess glucose has a specific suppressive effect on AVP release from the neurohypophysis.According to the classical concept of the osmoreceptor for the release of arginine vasopressin (AVP), hyperosmolar solutions made with some solutes such as sodium chloride, which is relatively impermeable to the cell membrane, cause AVP release, whereas hyperosmolar solutions made with other solutes such as glucose or urea do not cause AVP re lease [10,13,16,17,19,23,24]. Andersson and Olsson [I, 3], however, challenged this concept and proposed a hypothe sis that a specific sodium sensor was responsible for AVP re lease.…”
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“…Furthermore, the hyperosmolar media of excess urea failed to influence the angiotensin II-stimulated AVP release from the explants. These results are compatible with the hypothesis that excess glucose has a specific suppressive effect on AVP release from the neurohypophysis.According to the classical concept of the osmoreceptor for the release of arginine vasopressin (AVP), hyperosmolar solutions made with some solutes such as sodium chloride, which is relatively impermeable to the cell membrane, cause AVP release, whereas hyperosmolar solutions made with other solutes such as glucose or urea do not cause AVP re lease [10,13,16,17,19,23,24]. Andersson and Olsson [I, 3], however, challenged this concept and proposed a hypothe sis that a specific sodium sensor was responsible for AVP re lease.…”
mentioning