Vasopressin and hypercalciuria in enuresis: a reappraisal

OBJECTIVE: To test the hypotheses that vasopressin deficiency or hypercalciuria are important in polyuric and non-polyuric bedwetting, as nocturnal polyuria is a pathogenetic factor in enuresis responsive to antidiuretic therapy with desmopressin. SUBJECTS AND METHODS: Vasopressin deficiency has been implicated as a cause of nocturnal polyuria, but measurements of vasopressin in plasma have given contradictory results, because the hormone is released in pulses. Urinary levels reflect the secretion over longer periods. Hypercalciuria has also been proposed as a pathogenetic factor. Twenty-eight enuretic children who responded to desmopressin therapy with or without added anticholinergic agents (diuresis-dependent enuresis, DE), 15 children with therapy-resistant enuresis (not diuresis-dependent, NDE) and 51 continent controls were assessed. Urinary vasopressin, calcium and osmolality were measured in the morning after a 12-h thirst provocation. Urine production was recorded for 2 days. RESULTS: Because most data were not normally distributed, the values are expressed as the median (range). There were no differences in urine osmolality; i.e. con-trols 919 (636-1232), DE 849 (462-1149), NDE 968 (664-1191) mOsml/kg); vasopressin, controls 34 (8-983), DE 26 (9-295), NDE 50 (9-116) pmol/L; or calcium excretion (expressed as the calcium/creatinine ratio), controls 0.16 (0.01-0.71), DE 0.14 (0.04-0.67), and NDE 0.23 (0.03-0.69). The DE group produced more urine, at 18.4 (9.2-52.5) mL/kg/day, than the other groups, i.e. control 12.7 (8.3-42.8) and NDE 12.1 (6.3-36.8) mL/kg/day (P = 0.008). CONCLUSION: All enuretic children with nocturnal polyuria do not have vasopressin deficiency. The urinary calcium excretion does not differ between enuretic and dry children.     

Vasopressin and diabetes mellitus

In diabetes mellitus (DM), the urine flow rate is increased, and the fluid turnover in the body is accelerated because of the glucose-induced osmotic diuresis. On the other hand, plasma vasopressin (VP) is elevated in both type 1 and type 2 DM. This elevation seems to be due to a resetting of the osmostat. A high VP level is beneficial in the short term because it limits to some extent the amount of water required for the excretion of a markedly enhanced load of osmoles (mainly glucose). However, in the long run, it may have adverse effects by favoring the development of diabetic nephropathy. VP has been shown in normal rats to induce kidney hypertrophy, glomerular hyperfiltration, and an increase in urinary albumin excretion (features also occurring in association in the period preceding diabetic nephropathy). Moreover, VP has been shown to participate in the progression of renal failure in rats with five-sixths reduction in renal mass. In recent studies, we have shown (1) that creatinine clearance, albuminuria and renal mass increased much less during experimental DM in Brattleboro rats unable to secrete VP than in their VP-replete Long-Evans controls, and (2) that albuminuria was prevented during experimental DM in Wistar rats when a VP nonpeptidic, highly selective V2 receptor antagonist was administered chronically for 9 weeks. Taken together, these results strongly suggest that VP plays a crucial role in the onset and aggravation of the renal complications of DM. The mechanisms by which VP exerts these adverse V2-dependent effects are not yet elucidated. They are most likely indirect and may involve several intermediate steps comprising VP-induced changes in the composition of the tubular fluid in the loop of Henle (due to solute recycling in the renal medulla associated with improved concentrating activity of the kidney), inhibition of the tubuloglomerular feedback control of glomerular function, and alterations in glomerular hemodynamics by the intrarenal renin-angiotensin system.     

血管加压素在心肺复苏中的应用

动物实验表明在心肺复苏期间静脉给予血管加压素能有效增加心、脑和肾上腺的血流量 ,促进促肾上腺皮质激素和皮质醇的分泌 ,明显提高复苏成功率 ,且气管内和骨内给药同样有效。初步临床研究发现血管加压素能提高短期内自主循环恢复率。