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Effect of vasopressin administration and deficiency upon 3H-AVP binding sites in the CNS and periphery during
Insights
Early life administration of arginine8-vasopressin (AVP) increases hepatic AVP receptor density in rats. This effect persists into adulthood, indicating early AVP exposure influences liver AVP receptor development.
Area of Science:
- Endocrinology
- Developmental Biology
- Neuroscience
Background:
- Arginine8-vasopressin (AVP) plays crucial roles in physiological regulation.
- The impact of early-life AVP exposure on receptor development is not fully understood.
- Vasopressin (VP) deficiency models offer insights into VP receptor regulation.
Purpose of the Study:
- To investigate the effects of chronic early-life arginine8-vasopressin (AVP) administration on AVP binding sites in rat tissues.
- To examine the influence of VP deficiency on hepatic AVP receptor expression.
- To determine the developmental sensitivity of hepatic AVP receptors to vasopressin.
Main Methods:
- Male Long-Evans (LE) rat pups received daily subcutaneous AVP injections from day 1 to 7 of life.
- 3H-AVP binding assays were conducted on liver, kidney, and septum membranes at postnatal days 8 and 60.
- Binding site density (Bmax) and affinity were assessed in LE, heterozygous Brattleboro (HET-BB), and homozygous Brattleboro (HOM-BB) rats.
Main Results:
- Chronic neonatal AVP treatment significantly increased hepatic 3H-AVP binding site density in both young (day 8) and adult (day 60) rats, without altering affinity.
- Kidney and septum showed no significant changes in AVP binding sites following AVP treatment.
- Homozygous Brattleboro rats (VP deficient) exhibited increased hepatic AVP binding sites compared to LE controls, while heterozygous rats showed decreased binding.
Conclusions:
- Hepatic arginine8-vasopressin (AVP) receptors are highly sensitive to the presence or absence of vasopressin during the early postnatal period.
- Early-life AVP exposure can lead to long-lasting alterations in hepatic AVP receptor density.
- These findings highlight a critical developmental window for AVP receptor regulation in the liver.
Abstract:
Arginine8-vasopressin (AVP, 40 micrograms/100 g b.wt., SC) was administered to male Long-Evans (LE) pups from day 1 to 7 of life and the pups were sacrificed on day 8 or 60. 3H-AVP binding was performed on membranes prepared from the liver, kidney, and septum. No significant changes were observed in the kidney or septum of animals 8 or 60 days old. However, the chronic AVP treatment did result in a significant increase in the density of 3H-AVP binding sites in the liver when compared to control day 8 pups (control 44 +/- 2 vs. AVP 56 +/- 3 fmol/mg protein), with no change in affinity. This effect was maintained into adulthood, as the day 60 AVP-treated LE rats also showed a significant increase in liver 3H-AVP binding sites compared to control (control 186 +/- 9 vs. AVP 239 +/- 14 fmol/mg protein), with no change in affinity. A comparison of 3H-AVP binding sites in 8-day-old LE, heterozygous Brattleboro (HET-BB), and homozygous Brattleboro rats (HOM-BB) was performed to assess the effect of complete (HOM-BB) and partial (HET-BB) VP deficiency on binding sites in the CNS and periphery. The liver again was the only tissue in which a change in 3H-AVP binding characteristics was noted. The HOM-BB rat (Bmax 144 +/- 6 fmol/mg protein) displayed a significant increase in AVP binding sites from the LE rat (Bmax 100 +/- 7 fmol/mg protein), while the 3H-AVP binding sites in the HET-BB rat liver (Bmax 69.8 +/- 9 fmol/mg protein) were significantly lower than LE rats. Thus hepatic AVP receptors appear most sensitive to the presence or absence of vasopressin during the early postnatal period.