Abstract
DeB old first described the correlative relationship between the incidence of distinct storage granules in atrial cardiocytes and body water/electrolyte balance5. In later studies, DeBold and colleagues6 showed that the injection of atrial granular extracts initiated a rapid and extensive diuresis and natriuresis, and they identified the active substituent as the 28 amino acid peptide, atrial natriuretic peptide (ANP), which is released from the atria by distension or local hypoxiasee2,8,10. Receptors for ANP have been localized in the renal glomerular vasculature, suggesting that the circulating peptide directly modulates kidney function3. The unique physiologic role of ANP as a regulator of volume and electrolyte levels in the periphery led others to postulate parallel functions for this peptide in the central nervous system (CNS). In fact, later studies revealed the presence of ANP15,25 and ANP receptors19.20 in specific CNS sites associated with cardiovascular control. In addition, central administration of ANP was shown to decrease the release of arginine vasopressin (AVP) in dehydrated animals21,22 and to decrease salt-water intake following salt deprivation. Thus, ANP appears to act globally at specific targets both in the CNS and periphery to initiate coordinated adjustments in response to changes in systemic hydration and electrolyte balance.
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Fidone, S.J. et al. (1993). Carotid Sinus Nerve Inhibition Mediated by Atrial Natriuretic Peptide. In: Data, P.G., Acker, H., Lahiri, S. (eds) Neurobiology and Cell Physiology of Chemoreception. Advances in Experimental Medicine and Biology, vol 337. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2966-8_38
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