Abstract
There is no doubt that the renin-angiotensin-aldosterone system (RAAS) can have a major influence on salt intake but the conditions used to demonstrate this are rare outside the laboratory. Changes in RAAS activity do not explain the voluntary intake of NaCl solution shown by non-deprived rats or the preference for salty foods shown by humans. As a first attempt to investigate an alternative mechanism, my colleagues and I are studying the effects of dietary calcium on salt appetite. Even though calcium-deprived rats have normal RAAS activity, they show a striking increase in NaCl intake, which can surpass the effects of the most severe manipulations of the RAAS. The physiological mechanism underlying this behavior is unknown but it probably involves an adrenal factor, perhaps corticosterone. Whatever the mechanism, the calcium-deprived rat and other low-renin models of salt intake provide a promising approach to help understand the physiological basis of excess salt consumption by humans.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: 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.
