Increased neural atrial natriuretic factor generation in spontaneously hypertensive rats.
Author(s) -
Waldemar Debinski,
Otto Kuchel,
Gaétan Thibault
Publication year - 1989
Publication title -
hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.986
H-Index - 265
eISSN - 1524-4563
pISSN - 0194-911X
DOI - 10.1161/01.hyp.13.6.804
Subject(s) - prohormone , radioimmunoassay , medicine , endocrinology , chemistry , hypothalamus , peptide hormone , hormone , biology
The increased neural atrial natriuretic factor (ANF) concentrations in spontaneously hypertensive rats compared with Wistar-Kyoto control rats prompted us to examine the basis of this phenomenon. Central and peripheral neural tissues from both strains were processed under rigorous antiproteolytic conditions, which were monitored by degradation of purified and iodo-labeled proANF or synthetic ANF[Ser99, Tyr126]. The extracted material was separated on a reverse-phase high-pressure liquid chromatography system, and eluates were determined for immunoreactive ANF with radioimmunoassays, employing antibodies directed against two different fragments of the ANF prohormone. The chromatographic pattern of immunoreactive-ANF elution showed the clear presence of proANF in all neural tissues studied. This pattern also included an intermediate ANF and COOH-terminal of proANF whose relative varying content was tissue dependent. Superior cervical ganglia contained most of the immunoreactive ANF corresponding to proANF and intermediate ANF. Total immunoreactive ANF in the hypothalamus, brainstem, and upper and lower parts of the spinal cord was always higher in spontaneously hypertensive than in Wistar-Kyoto rats. However, there was no difference in the content of the main molecular forms of ANF in any of their neural tissues. We suggest that the increase in neural ANF in spontaneously hypertensive rats does not arise from posttranslational alterations and may indicate an enhanced ANF synthesis rate or accumulation, or both.
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