EFFECTS OF INTRACEREBROVENTRICULAR ADMINISTRATION OF ATRIAL-NATRIURETIC-PEPTIDE (ANP) ON BLOOD-PRESSURE, HEART-RATE AND PLASMA ADH AND CORTICOSTERONE LEVELS IN NORMAL AND DEHYDRATED RABBITS
C. Kallaras et al., EFFECTS OF INTRACEREBROVENTRICULAR ADMINISTRATION OF ATRIAL-NATRIURETIC-PEPTIDE (ANP) ON BLOOD-PRESSURE, HEART-RATE AND PLASMA ADH AND CORTICOSTERONE LEVELS IN NORMAL AND DEHYDRATED RABBITS, Journal of endocrinological investigation, 21(4), 1998, pp. 200-210
In order to investigate the effects of centrally administered Atrial N
atriuretic Peptide (ANP) on plasma ADH and corticosterone levels as we
ll 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 intracerebro
ventricular (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) a
nd those who were dehydrated for 24h (''dehydrated'' group) before blo
od pressure and heart rate recordings and blood sampling for hormonal
determination. Each group's individuals were divided into two subgroup
s of five animals each. Blood samples were collected at 0 min (control
) and 30, 60, 90, 120 min following icy administration of 25 mu l of e
ither artificial cerebrospinal fluid (aCSF) (subgroups ''aCSF'') or hu
man (h) ANP (1 mu g) in aCSF (25 mu l) (subgroups ''hANP''). Blood pre
ssure and heart rate were also recorded at the same times. Plasma ADH
and corticosterone concentrations were determined by RIA. The results
were analysed by ANOVA. Blood pressure and heart rate values were unaf
fected by water deprivation or by ANP administration. Mean plasma cort
icosterone levels at all times (30-120 min) were significantly higher
(p<0.001) than at 0 min time. Plasma corticosterone levels in the ''de
hydrated+aCSF'' group were significantly higher (p<0.05) than in each
of the other groups (''dehydrated+hANP'', ''euhydrated+aCSF'', ''euhyd
rated+hANP''). Plasma corticosterone levels in each of those other gro
ups did not differ significantly from one another. Dehydration resulte
d in an increase in ADH levels (p<0.0001) and icy administration of hA
NP prevented (p<0.05) in ''dehydrated+hANP'' experimental group, the i
ncrease in ADH levels observed in the control ''dehydrated+aCSF'' grou
p from 90 to 120 min. The increase of corticosterone and ADH in the co
ntrol dehydrated groups could possibly be due to the combined stress s
timulus of dehydration and restriction in the restrain box. These resu
lts indicate that centrally administered ANP, at the concentration ach
ieved in the present study, neither affects blood pressure and heart r
ate in conscious restrained euhydrated and 24h-dehydrated NZW rabbits
nor decreases the ADH and corticosterone response to dehydration, but
does apparently modulate ADH and corticosterone responses to Other sti
muli in the dehydrated state. In conclusion, the results of this study
confirm that brain ANP may have an inhibitory effect on stimulated AD
H and corticosterone release.