Systemic nitric oxide synthase inhibition suppresses apelin-induced rise in body temperature in rats

Abstract

Apelin is a peptide involved in the regulation of various physiological processes, including thermoregulation, metabolism, and energy balance. This study investigates the role of nitric oxide (NO) in mediating apelin’s eff ects on body temperature, food intake, and body mass gain in rats. Using the non-selective nitric oxide synthase (NOS) inhibitor LNAME and the selective inducible NOS inhibitor aminoguanidine (AG), we assessed how systemic inhibition of NO synthesis modulates apelin-induced responses. Male Wistar rats were administered intraperitoneal injections of [Pyr1]apelin-13 following pre-treatment with L-NAME or AG. Our results show that both L-NAME and AG suppressed the apelin-induced rise in body temperature, with L-NAME having a more pronounced effect. Additionally, LNAME significantly reduced apelin-induced food intake and body mass gain, while AG had a lesser impact. These findings suggest that NO plays a key role in mediating the apelin’s thermoregulatory and metabolic eff ects. The differential outcomes between L-NAME and AG highlight the potential involvement of multiple NOS isoforms in these processes. Further investigation into the distinct roles of NOS isoforms may provide deeper insights into NO-apelin interactions and their relevance to metabolic regulation, offering potential therapeutic targets for metabolic disorders.