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Impaired Water Excretion (impaired + water_excretion)
Selected AbstractsPathological Role of Aquaporin-2 in Impaired Water Excretion and HyponatremiaJOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2004S. Ishikawa Abstract In the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), inappropriately elevated secretion of vasopressin can result in a reduction of antidiuretic efficacy: a phenomenon known as ,vasopressin escape'. We compared experimental SIADH with 1-deamino-8- d -arginine vasopressin (dDAVP)-excess rats, where both groups received continuous subcutaneous administration of dDAVP by osmotic minipump but the SIADH rats also received a liquid diet that induced hyponatraemia. The SIADH rats, but not the dDAVP excess rats, showed a marked attenuation of urinary concentrating ability. Vasopressin V2 receptor binding capacity and mRNA expression were similar between the two groups, but the SIADH rats showed a diminished up-regulation of aquaporin-2 (AQP-2) mRNA and protein expression. These findings indicate the presence of tonicity-response regions in the AQP-2 promoter gene, and that either hypervolemia or hypotonicity may attenuate the postreceptor signalling of vasopressin in renal collecting duct cells in SIADH rats. [source] Pathophysiological roles of arginine vasopressin and aquaporin-2 in impaired water excretionCLINICAL ENDOCRINOLOGY, Issue 1 2003San-e Ishikawa First page of article [source] Urinary excretion of the aquaporin-2 water channel exaggerated in pathological states of impaired water excretionCLINICAL ENDOCRINOLOGY, Issue 2 2001Takako Saito OBJECTIVE The present study was undertaken to determine whether the hydro-osmotic action of arginine vasopressin (AVP) is exaggerated in pathological states of impaired water excretion by measuring urinary excretion of the aquaporin-2 (AQP-2) water channel. PATIENTS AND MEASUREMENTS Eighteen hyponatraemic patients with impaired water excretion and 12 control subjects were studied during an acute oral water load (20 ml/kg body weight). RESULTS In the patient group plasma AVP levels were 1·6 pmol/l, relatively high compared to plasma osmolality of 279·8 mmol/kg. Urinary excretion of AQP-2 under ad libitum water drinking was 41·1 fmol/umol creatinine in the patient group, a value significantly greater than that of 21·7 fmol/,mol creatinine in the control subjects. The acute water load verified the impairment in water excretion in the patient group, as the excretion of the water load was only 28·2% (control, 77·3%, P < 0·001) and the minimum urinary osmolality was as high as 437·3 mmol/kg (control, 122·9 mmol/kg, P < 0·001). Also, the minimum urinary excretion of AQP-2 was significantly greater in the patient group than that in the control. There was a positive correlation between plasma AVP levels and urinary excretion of AQP-2 in the control subjects (r = 0·56, P < 0·01). In contrast, the urinary excretion of AQP-2 was exaggerated compared to the respective plasma AVP levels in the patient group, and thus the positive correlation disappeared. CONCLUSION These results indicate that hydroosmotic action of AVP is exaggerated more than that expected from plasma AVP levels in pathological states of impaired water excretion, with non-suppressible, but normal, arginine vasopressin levels in spite of the hypo-osmotic condition. [source] | ||||||||||