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

Citation
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
Citations number
77
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
03914097
Volume
21
Issue
4
Year of publication
1998
Pages
200 - 210
Database
ISI
SICI code
0391-4097(1998)21:4<200:EOIAOA>2.0.ZU;2-W
Abstract
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.