Catecholaminergic Medullary Pathways and Cardiovascular Responses to Expanded Circulating Volume and Increased Osmolarity
- PMID: 24829998
- Bookshelf ID: NBK200976
Catecholaminergic Medullary Pathways and Cardiovascular Responses to Expanded Circulating Volume and Increased Osmolarity
Excerpt
Maintaining the composition and volume of the extracellular fluid (ECF) and intracellular fluid (ICF) within a restricted range of variation is critical for normal tissue perfusion and cellular function (Strange 1993). The ECF is primarily composed by the vascular and extravascular (interstitial) fluid, and has sodium as a determinant ion of its osmolarity and volume. The ECF/plasma volume ratio is of utmost importance for maintaining vascular capacitance and, consequently, venous return, cardiac output, and arterial pressure (Ramsay 1991). Maintaining the variability of the ECF volume within a strict range is a central goal of homeostatic mechanisms.
The central nervous system (CNS) is informed about alterations in volume and tonicity of the ECF through the activity of peripheral and central sensory receptors. Receptors that respond to alterations in the volume of ECF are sensitive to the degree of mechanical distension of blood vessels or cardiac chamber (reviewed by Bourque 2008). They are located in the wall of the atrium and pulmonary vessels (cardiopulmonary receptors), and in the adventitia of the aortic arch/carotid sinus (arterial baroreceptors), or renal afferent arterioles (renal baroreceptors). These receptors mediate central autonomic reflexes through primary connections to the nucleus of the solitary tract (NTS) or mediate renorenal reflexes. Receptors that respond to alterations in ICF are sensitive to ECF tonicity or effective osmotic concentration (Bourque 2008; Kuramochi and Kobayashi 2000; McKinley et al. 1992). They are located in renal, intestinal, and hepatic vessels, in the wall of the gastrointestinal tract and oropharyngeal cavity and in brain circumventricular organs, notably area postrema, subfornical organ (SFO), and organum vasculosum of the lamina terminalis (OVLT). Efferent responses to the activation of these receptors include renal sympathetic nerve activity, hormone secretion [atrial natriuretic peptide (ANP), oxytocin, vasopressin, renin–angiotensin II], and hemodynamic changes. Such responses culminate in controlled alterations of renal sodium and water excretion.
Among these several mechanisms and responses, we would like to call attention to those associated with ECF volume expansion. Dehydration is a menace to immediate survival, but volume expansion is associated with long-term changes that affect health, particularly hypertension and heart failure (reviewed by Antunes-Rodrigues et al. 2004; Toney and Stocker 2010; Toney et al. 2010). Conversely, hypertonic NaCl also has a potential therapeutic value to recovery from hemorrhagic shock (Pedrino et al. 2011; Rocha e Silva et al. 1986; Velasco et al. 1980). In this chapter, we will focus on cardiovascular responses to volume expansion and hypertonicity, their sensory afferences, and how these responses are subserved by a brainstem–hypothalamic–preoptic axis and its associated cathecolaminergic pathways.
© 2014 by Taylor & Francis Group, LLC.
Sections
- 8.1. INTRODUCTION
- 8.2. HYPERTONIC VOLUME EXPANSION: NEUROENDOCRINE AND SYMPATHETIC REFLEXES
- 8.3. RECOVERY FROM HEMORRHAGIC SHOCK, HYPERTONICITY, AND CAROTID CHEMORECEPTION
- 8.4. CENTRAL PROCESSING OF NEUROENDOCRINE AND SYMPATHETIC REFLEXES: THE BRAINSTEM–HYPOTHALAMIC/PREOPTIC AXIS
- 8.5. BRAIN NORADRENERGIC CONTROL OF RESPONSES TO VOLUME EXPANSION AND SODIUM LOAD
- ACKNOWLEDGMENTS
- REFERENCES
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