Atrial natriuretic peptide in dehydrated Long-Evans rats and Brattleboro rats.
Atrial natriuretic peptide ( ANP) was measured by radioimmunoassay in atrial and plasma extracts from normal Long-Evans (LE) rats and Brattleboro-strain diabetes insipidus (DI) rats. LE rats, dehydrated for 72 hours, had an increased plasma osmolality and plasma vasopressin. They also demonstrated a higher atrial immunoreactive ANP (IR- ANP) content than hydrated animals (72 hr dehydration: 178.2 +/- 30.4 micrograms/g wet weight atria, mean +/- SE, control: 60.4 +/- 8.2; P less than 0.001). Plasma IR- ANP in dehydrated LE rats tended to be lower than hydrated LE but this was not statistically significant [72 hr dehydration: 61.9 +/- 5.9 pg/ml, control: 82.4 +/- 8.2]. IR- ANP concentration in atrial extracts from DI rats, without detectable plasma vasopressin levels but with increased plasma osmolality, was not different from that in hydrated LE rats (DI: 100.6 +/- 13.2 micrograms/g). There was also no significant difference between plasma IR- ANP in DI and hydrated LE rats (DI: 100.2 +/- 11.9 pg/ml). The atrial IR- ANP concentration in DI rats was decreased by infusion with either arginine-vasopressin (AVP) or 1-deamino-8-arginine vasopressin (DDAVP), and plasma IR- ANP was increased significantly by both infusions (AVP: 171.3 +/- 18.1 pg/ml, DDAVP: 179.5 +/- 24.6). Thus, changes in atrial and plasma IR- ANP concentration appeared to be associated with changes in water balance but not with plasma AVP levels, indicating that the changes in volume may be a more important factor controlling ANP release in vivo than vasopressin itself.[1]References
- Atrial natriuretic peptide in dehydrated Long-Evans rats and Brattleboro rats. Ogawa, K., Henry, M.A., Tange, J., Woodcock, E.A., Johnston, C.I. Kidney Int. (1987) [Pubmed]
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