The structural development of individual nephrons has been investigated in the kidneys of young rats by microdissection. Superficial, intercortical and juxtamedullary nephrons in Wistar-Konarovice rats aged 2 to 60 days have been followed. At two and five days of age the superficial nephrons were in an early stage of anatomical development. At this time intercortical and juxtamedullary nephrons were more developed, and basically resembled similar structures in adult animals with the exception that the loops of Henle did not have a thin ascending limb. At ten days of age all three types of nephrons were differentiated with the exception that the intercortical nephrons did not possess a thin ascending limb of Henle's loop. At selected stages of development there appears to be a direct relation between the length of the superficial nephrons and the weight of the kidney. Since individual segments of these nephrons do not grow at the same proportional rate, this relationship does not hold when compared to kidney weight.
In the early distal tubule of the newt Triturus vulgaris L., 1 nM arginine-vasopressin (AVP) increased water reabsorption; the fractional reabsorption of Na+ was elevated from 46.2 +/- 6.9% to 67.8 +/- 3.9% (P < 0.001), of Cl- from 52.7 +/- 6.7% to 73.1 +/- 3.5% (P < 0.001), of Mg2+ from 48.0 +/- 7.7% to 71.7 +/- 6.3% (P < 0.001). When V1-receptors were blocked by 1 nM peptide V1-antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(O-methyl) Tyr]-[Arg8]vasopressin, 1 nM AVP increased the fractional reabsorption of fluid by 8.9% of Na+ by 10.7% and of Cl- by 11.2%, as compared with the effect of AVP alone. The fractional reabsorption of Ca2+ after addition of AVP did not differ from control; when V1-receptors were blocked in the presence of AVP, the fractional reabsorption of Ca2+ was increased by AVP. The V1-receptor block in the presence of AVP did not change the fractional reabsorption of Mg2+. Experiments on the urinary bladder of the frog Rana temporaria L. showed that 1 nM SR 49059, a non-peptide antagonist of V1a-receptors, like the peptide V1-antagonist, enhanced the AVP effect by 29%. Inhibition of protein kinase C activity by calphostin C (1 nM) mimicked the effect of V1-antagonists; the AVP hydroosmotic effect was increased by 60%. The results obtained indicate that V1-receptors modulate the effects of V2-receptor activation: their block is accompanied by an enhancement of the AVP hydroosmotic effect in the frog urinary bladder and by an increase of Na+ and Cl- reabsorption in the newt early distal tubule. The enhancement of the AVP effect owing to the V1-receptor activation seems to be mediated by a decrease in protein kinase C activity.
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