Ohzeki T
Acta Endocrinol (Copenh). 1985 Apr;108(4):485-90. doi: 10.1530/acta.0.1080485.
Urinary adenosine 3',5'-monophosphate (cAMP) excretion before and after administration of aqueous vasopressin (pitressin) and 1-deamino-8-D-arginine vasopressin (DDAVP) was measured in congenital nephrogenic and in vasopressin sensitive diabetes insipidus (VS-DI). Excretion of cAMP into the urine increased markedly in response to pitressin (676%) and to DDAVP (252%) in VS-DI. Nephrogenic diabetes insipidus (N-DI) could be divided into two categories (type 1 and type 2) in respect to urinary cAMP responsiveness. In type 1, cAMP excretion showed no definite change after stimulation with pitressin (102%) or DDAVP (127%). On the other hand, urinary excretion of cAMP was significantly elevated in response to DDAVP in familial cases of N-DI type 2 (1269%) without producing any concentrating effect on the urine. Two different defects are considered to be involved in the pathogenesis of N-DI.
在先天性肾性尿崩症和血管加压素敏感性尿崩症(VS-DI)患者中,测量了给予水剂血管加压素(垂体后叶素)和1-去氨基-8-D-精氨酸血管加压素(DDAVP)前后尿中3',5'-环磷酸腺苷(cAMP)的排泄量。在VS-DI患者中,尿中cAMP的排泄量对垂体后叶素(增加676%)和DDAVP(增加252%)有明显增加。就尿cAMP反应性而言,肾性尿崩症(N-DI)可分为两类(1型和2型)。在1型中,用垂体后叶素(增加102%)或DDAVP(增加127%)刺激后,cAMP排泄无明显变化。另一方面,在2型N-DI家族性病例中,尿中cAMP排泄量对DDAVP有显著升高(增加1269%),但对尿液无任何浓缩作用。N-DI的发病机制被认为涉及两种不同的缺陷。