Abstract
Calcitonin (CT), when administered peripherally, is a potent hypocalcemic agent. This peptide can also exert a variety of profound effects through brain receptors after central injection. We examined the capacity of CT to alter plasma calcium of freely moving conscious rats after intracerebroventricular (i.c.v.) injection. A dose-dependent decrease in plasma calcium was seen after administration of 25 ng, 250 ng or 2500 ng of salmon calcitonin (sCT). The extent and duration of hypocalcemia after central injection was equal to, or greater than, that seen after giving the same doses of peptide intravenously (i.v.). Calcitonin gene-related peptide (CGRP), when administered centrally at a 50-fold molar excess, produced only a transient decrease in plasma calcium. No increase in plasma levels of sCT could be detected by RIA after i.c.v. injection, although measurable levels were obtained by i.v. injection. Centrally administered sCT did not appear to produce hypocalcemia by enhancing the release of endogenous rat CT. In contrast to the rise in rat immunoreactive parathyroid hormone (PTH) seen after i.v. injection of sCT, no significant elevation occurred after central administration of the peptide despite induction of comparable levels of hypocalcemia. Consequently, reduced PTH release may contribute to the central hypocalcemic action of CT. The results indicate that peptides acting through the brain CT receptor may modulate peripheral blood calcium.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.