Cardiorespiratory responses after baroreflex activation in sodium depleted rats

• Grant number: 14/02343-5
• Support Opportunities: Scholarships in Brazil - Master
• Start date: August 01, 2014
• End date: January 31, 2015
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Patricia Maria de Paula
• Grantee: Karine Cristina Borsari
• Host Institution: Faculdade de Odontologia (FOAr). Universidade Estadual Paulista (UNESP). Campus de Araraquara. Araraquara , SP, Brazil

Abstract

Blood volume alterations could be caused by different physiological conditions like vomit, increased of sodium intake, or use of diuretics. The sodium depletion produced by Subcutaneous Injection (sc) of the diuretic furosemide associated by a 24 hours sodium deficient diet causes changes in the body fluid balance, activating behavioral, hormonal and autonomic responses to reclaim such changes and restore the homeostasis of sodium. During the sodium depletion using furosemide, neuroendocrine alterations occur, such as a high level of ngAiotensin (ANG II) and aldosterone, low vascular reactivity and non activating of volume receptors. Studies have shown that in anesthetized dogs as well as non-anesthetized and sodium depleted rats there was a decrease in baroreflex sensitivity. However, none of these studies examined whether the neuroendocrine changes that occur during sodium depletion could alter the cardiorespiratory responses after baroreflex activation. Despite many studies about the involvement of the baroreflex in cardiovascular regulation, the ventilatory changes caused after activation of this reflex are not well known. Studies have reported that activation of the baroreflex demonstrates variable effects on Ventilation (VE), including the decrease in respiratory rate as well as no change in VE. These studies suggest that this variability on VE during activation of the baroreflex depends on the animal species, strain, the type of preparation and anesthesia. The objective of this project is evaluate the sensitivity and cardiorespiratory responses after activation and deactivation of the baroreflex using Intravenous (iv) the vasoconstrictor phenylephrine and vasodilator sodium nitroprusside, respectively, in not anesthetized rats normovolemic, after 24 hours of sodium depletion and full sodium (after 2 hours of 1.8% sodium chloride ingestion and water). (AU)