Xenopus skeletal muscle cells when grown in culture develop a slow inward calcium current that is sensitive to dihydropyridines. Acetylcholine (ACh, 10 microM) applied through a puffer pipette caused a large inward current in these cells (at the holding potential) through the nicotinic receptor channels and reduced the inward calcium current (during a step depolarization to 0 mV). After the ACh application was discontinued the holding current rapidly returned to pre-ACh levels (20 s) whereas the calcium current showed a slow, partial recovery to pre-ACh levels. Outward potassium current was also reduced during the application of ACh but recovered completely after ACh was discontinued. The effect of ACh on the calcium current was not mimicked by muscarine (100 microM) and was absent when 10 micrograms/ml alpha-bungarotoxin was added to the bath suggesting that the decrease in calcium current was mediated by current through the nicotinic receptor.

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~4lty qf 'Medic.int., University ($British Columhicr, Vcincouvrr 93, British ('olnmhic~ Received May 3, 1944 VIRGO, N. S., and MILLER, J. R. 1944. Hereditary vasopressin-resistant diabetes insipidus in SWV mice. Can. J. Physiol. Pharmacol. 52,995-101 1.Old female mice s f the SWV strain have an hereditary polydipsia-polyuria defect with a severe increase in water timrnover and with hypotonic urine which contains no glucose, blood, or protein; that is, they have diabetes insipidus. Their responses to exogenous vasopressin (negative) and water deprivation (positive) and the normal amount of neurosecretory material in their posterior pituitaries indicate that they have nephrogenic diabetes insipidus. The females also have a progressive kidney defect which, although it resembles nephronophthisis in some aspects and hypokalemia in others, is unique. There is a progressive anemia. Amyloid kidneys, polycystic kidneys, diabetes mellitus, and nephronophthisis have been ruled out as the cause of the defect but hypokalemia and hypercalcemia are still possibilities. The SWV males have a milder form of the defect which develops at an older age and shows n o signs of histopathology. VIRGO, S. N. et MILLER, J. R. 1944. Hereditary vasopressin-resistant diabetes insipidus in SWV mice. Can. J. Physiol. Pharmacol. 52,995-101 1. Les vieilles souris femelles de la souche SWV prksentent une polydipsie-poiyurie hiriditaire, une importante augmentation du taux de renouvellement de I'eau et tine urine hypotonique ne contenant ni glucose, proteines ou sang. Elles sont atteintes de diabkte insipide. Leur riponse nigative B l'administration de vasopressine, leur rkponse positive $ la privation d'eau ainsi que le taux normal de neurosccrktions cte la pituitaire postkrieure indiqueiit un diabkte insipide d'origine rknale. Les femelles prksentent tgalenient une atteinte progressive du systkme rknal. Rien que cette atteinte soit particulikre, elle est similaire par certains aspects St une nephronophthise, et par d'autres A une hypokalikmie. Nous observons igalen~ent une ankrnie progressive. I,es reins amyloides 011 polycystiques. le diabkte mellitus et la nephronophthise ont 616 iliminks comme causes possibles de cette atteinte par contre, une hypokalikmie et une hypercalcemie restent encore des causes possibles. 1,es mhles de cette souche prisentent kgalement une atteinte semblable mais sous une forme moins grave. Elle se tliveloppe B un Age plus avanci et ne prksente pas de signes histopathologiques. [Traduit par Ie journal] CAN. J . PHYSIOL. PHARMACOL. VOL. 52, 1974Materials and Methods injection. After 3-4 weeks, the mice were returned ~h~ SWV strain of house mice was obtained by to the metabolism cages and a control 24-h run was the central ~~i~~l ~~~~t at the uniLJersity of done (day 0 ) . Then on days 1-3, i.m. injections of British Columbia from the ~~f~~~~ ~~~~~~~h ~~~~d , 0.25 U (0.05 ml) Pitressin tannate in oil ( P a r k , Sufielcl, Alberta, in 1949-~h~ sw *,ice were Davis and Co., Detroit, Mich.) were given, and the maintained...

Females of the SWV mouse strain had an age-dependent nephrogenic diabetes insipidus. The distribution of water intakes in the F1, F2 and backcross to each parental strain indicated that at least the polydipsia was determined by a few major dominant genes; rather than by a polygenic system. The Smirnof and chi square analyses revealed more than one major gene was involved. A hypothesis was presented that there are two dominant genes (one fully dominant and one codominant) which may be linked. The expression of these major genes was influenced multiplicatively by environmental factors and the water intakes approached a continuous distribution. The defect was sex influenced: SWV males had only a very mild urine concentrating defect but the reciprocal crosses showed no X-linkage. The kidney weight of the SWV females correlated significantly (P less than 0.05) with the polydipsia in the F1, BC SWV and F2 progeny and the use of both traits provided a qualitative measure for classification. The polydipsia and enlarged kidneys probably represent pleiotropy.

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