Intracerebroventricular administration of atrial natriuretic peptide prevents increase of plasma ADH, aldosterone and corticosterone levels in restrained conscious dehydrated rabbits.

In order to investigate the effects of centrally administered ANP on plasma ADH, aldosterone and corticosterone levels as well as on blood pressure and on heart rate, 20 male New Zealand White (NZW) rabbits were used. Measurements were made on restrained conscious animals one week after the implantation of an indwelling intracerebroventricular (icv) cannula and two indwelling intravascular catheters (intracarotid and intrajugular). Animals were classified into two main groups, those with water available ad libitum ("euhydrated" group) and those who were dehydrated for 24 h ("dehydrated" group) before blood pressure and heart rate recordings and blood sampling for hormonal determination. Each group's individuals were divided into two subgroups of five animals each. Blood samples were collected at 0 min (control) and 30, 60, 90, 120 min following icv administration of 25 microl of either artificial cerebrospinal fluid (aCSF) (subgroups "aCSF") or human (h) ANP (1 microg) in aCSF (25 microl) (subgroups "hANP"). Blood pressure and heart rate were also recorded at the same times. Plasma ADH, aldosterone and corticosterone concentrations were determined using RIA. The results were analysed by analysis of variance (ANOVA). Blood pressure and heart rate values were unaffected by water deprivation or by ANP administration. Mean plasma corticosterone levels at all times (30-120 min) were significantly higher (p<0.001) than those at 0 min time. Plasma corticosterone levels in the "dehydrated+aCSF" group were significantly higher (p<0.05) than in each of the other groups ("dehydrated+hANP", "euhydrated+aCSF", "euhydrated+hANP"). Plasma corticosterone levels in each of those other groups did not differ significantly from one another. Dehydration resulted in a tendency to increase in aldosterone levels (p<0.07), and icv administration of hANP tended (p<0.08) to prevent in the "dehydrated+hANP" experimental group the increase in aldosterone levels observed in the control "dehydrated+aCSF" group from 30 to 120 min. Dehydration resulted in an increase in ADH levels (p<0.0001), and icv administration of hANP prevented (p<0.05) in "dehydrated+hANP" experimental group the increase in ADH levels observed in the control "dehydrated+aCSF" group from 90 to 120 min. The increase of corticosterone and ADH and the tendency towards increase in aldosterone in the control dehydrated groups could possibly be due to the combined stress stimulus of dehydration and restriction in the restrain box. These results indicate that centrally administered ANP, at the concentration achieved in the present study, neither affects blood pressure and heart rate in conscious restrained euhydrated and 24 h-dehydrated NZW rabbits nor decreases the ADH, aldosterone and corticosterone response to dehydration, but does apparently modulate ADH, aldosterone and corticosterone responses to other stimuli in the dehydrated state. In conclusion, the results of this study confirm that brain ANP may have an inhibitory effect on stimulated ADH, aldosterone and corticosterone release.