Τόμος 12 (1998) – Τεύχος 1 & 2 – Άρθρο 4 – Επιθεώρηση Κλινικής Φαρμακολογίας και Φαρμακοκινητικής-Διεθνής Έκδοση – Volume 12 (1998) – Issue 1 & 2 – Article 4 – Epitheorese Klinikes Farmakologias και Farmakokinetikes-International Edition

By | | Άρθρο επισκόπησης - Review Article, Ιωάννης Λιαγκούρης - Ioannis Liangouris, Κωνσταντίνος Καλλιάρας - Constantinos Kaliaras, Κωνσταντίνος Μαυρουδής - Konstantinos Mavroudis, Μιχαήλ Γ. Αποστολάκης - Michael J. Apostolakis, Νικόλας Δ. Αγγελόπουλος - Nicolas D. Angelopoulos, Πλήρες Κείμενο στα Αγγλικά - Full Text in English
Title Effects of intracerebroventricular administration of atrial natriuretic peptide (ANP) on plasma ADH levels in normal and dehydrated rabbits
Authors Constantinos Kaliaras1, Nicolas Angelopoulos1, Michael Apostolakis1, Konstantinos Mavroudis2 and Ioannis Liangouris1

1. Department of Experimental Physiology, Faculty of Medicine, Aristotelion University of Thessaloniki, GR-540Q6, Thessaloniki, Greece

2. 2nd Division of Endocrinology, Alexandra Hospital, Athens, Greece
Citation Kaliaras, C., Angelopoulos, N., Apostolakis, M., Mavroudis, K., Liangouris, I.: Effects of intracerebroventricular administration of atrial natriuretic peptide (ANP) on plasma ADH levels in normal and dehydrated rabbits, Epitheorese Klin. Farmakol. Farmakokinet. 12(3): 23-30 (1998)
Publication Date Received for publication: 10 October 1997

Accepted for publication: 1 November 1997
Full Text Language English
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Keywords ANP, dehydration, intracerebroventricular, plasma ADH, rabbits.
Other Terms review article
Summary In order to investigate the effects of centrally administered Atrial Natriuretic Peptide (ANP) on plasma ADH levels, 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 intravascuiar 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 24h (dehydrated group) before 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 μl of either artificial cerebrospinal fluid (aCSF) (subgroups aCSF) or human (h) ANP (1 μg) in aCSF (25 μl) (subgroups hANP). Plasma ADH concentrations were determined by RIA. The results were analysed by ANOVA. 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 ADH 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, does not decrease in conscious restrained euhydrated and 24h-dehydrated NZW rabbits the ADH response to dehydration, but does apparently modulate ADH response 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 release.
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