Nociceptin-Induced Antinatriuresis is Affected by the Renin-Angiotensin-Aldosterone System
Kundel, Mitchell A.
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Nociceptin (Orphanin FQ) is an endogenous peptide whose structure is similar to that of endogenous opioid peptides (Meunier, et aI., 1995; Rienscheid, et al., 1995). Nociceptin has generated interest because of its therapeutic possibilities and because of its diverse pharmacology that both resembles and is different from that of classical opioid systems. Physiological studies have demonstrated that nociceptin evokes significant cardiovascular and renal responses, including bradycardic (lowered heart rate) and depressor (lowered blood pressure) responses and diuretic and antinatriuretic (sodium retentive) responses (Kapusta, et al., 1997). While these effects have been thoroughly described, much is unknown of the mechanisms through which nociceptin acts. This study aimed to analyze the role of the renin-angiotensin-aldosterone system (RAAS) in the antinatriuretic response. Three experimental groups were used consisting of rats subjected to chronic aldosterone blockage, as well as chronic and acute angiotensin IT blockage. While clear results were not found in the aldosterone study, rats subjected to chronic angiotensin IT blockage showed a blunted antinatriuresis as compared to rats only treated with nociceptin. The acute angiotensin IT blockage rats recovered to normal urinary sodium excretion levels after nociceptin injection more quickly than control rats. Together, these results indicate that the RAAS, especially via angiotensin IT, plays a role in modulating nociceptin-evoked antinatriuresis.With honors.