Total body water (TBW) is distributed in compartments divided by semi-permeable membranes. In postnatal life, approximately two thirds of TBW is located in the intracellular space and one third is located in the extracellular space. The latter is further divided with a 3:1 ratio in the interstitial and plasma compartments. Passive equilibration of solutes between body compartments is driven by electrochemical gradients and is mediated by a complex system of transport mechanisms that includes pumps, channels, facilitated carriers and selective paracellular pathways. With few exceptions, water diffuses rapidly across epithelia and cell membranes, following osmotic gradients. High transcellular water transport cannot occur through pure lipid bilayers, as these have low osmotic water permeability (∼0.002 cm/s). Water diffusion through cell membranes is therefore mediated by specific water channels, termed aquaporins (AQPs), which enhance osmotic water permeability by 10–1000 fold. Because solutes diffuse less rapidly than their solvent, the relative water content of body compartments is primarily regulated by their solute distribution. This allows the organism to adjust its TBW distribution by regulating the activity of solute transporters located in biological membranes that separate body compartments. During early fetal life, TBW represents approximately 90% of body mass. As pregnancy progresses, TBW decreases progressively, to reach 75–80% of body mass at the end of gestation. These changes are primarily due to a decline in extracellular water, while intracellular water increases. In the first 24–48 h after birth, the extracellular compartment further decreases, as a result of a negative fluid balance in the immediate postnatal period. The fetus constantly regulates its TBW by salt and water exchanges through the placenta membrane. After birth, uptake of water and solutes is limited to gastro-intestinal intakes, while insensible fluid losses increase dramatically. The newborn needs therefore to activate mechanisms that are aimed at controlling water and salt losses. Most of these mechanisms involve the secretion of hormones, which act directly on the kidney. To be efficient, these mechanisms require that sensors, hormone secretion pathways and target organs have reached an appropriate level of maturity. Water excretion or retention is primarily modulated through the regulation of arginine vasopressin (AVP) secretion. Stimulation of thirst has only limited value in newborns, because of their restricted access to free water and immaturity of the central nervous system. Salt retention by the kidney is predominantly achieved by activation of the renin-angiotensin-aldosterone system, which is potentiated by endothelins and adrenergic renal nerve activity. Conversely renal salt losses are stimulated by natriuretic peptides (NPs), prostaglandins, kinins, nitric oxide (NO) and adrenomedullin. In this review, the roles of AVP and NPs in the regulation of body fluid composition during the prenatal and perinatal periods are briefly reviewed. It is important to notice however, that their action is part of a complex network in which all of the above mentioned pathways are synergistically activated or inhibited to maintain body homeostasis.
Renal modulation: arginine vasopressin and atrial natriuretic peptide
ZAFFANELLO, Marco;
2008-01-01
Abstract
Total body water (TBW) is distributed in compartments divided by semi-permeable membranes. In postnatal life, approximately two thirds of TBW is located in the intracellular space and one third is located in the extracellular space. The latter is further divided with a 3:1 ratio in the interstitial and plasma compartments. Passive equilibration of solutes between body compartments is driven by electrochemical gradients and is mediated by a complex system of transport mechanisms that includes pumps, channels, facilitated carriers and selective paracellular pathways. With few exceptions, water diffuses rapidly across epithelia and cell membranes, following osmotic gradients. High transcellular water transport cannot occur through pure lipid bilayers, as these have low osmotic water permeability (∼0.002 cm/s). Water diffusion through cell membranes is therefore mediated by specific water channels, termed aquaporins (AQPs), which enhance osmotic water permeability by 10–1000 fold. Because solutes diffuse less rapidly than their solvent, the relative water content of body compartments is primarily regulated by their solute distribution. This allows the organism to adjust its TBW distribution by regulating the activity of solute transporters located in biological membranes that separate body compartments. During early fetal life, TBW represents approximately 90% of body mass. As pregnancy progresses, TBW decreases progressively, to reach 75–80% of body mass at the end of gestation. These changes are primarily due to a decline in extracellular water, while intracellular water increases. In the first 24–48 h after birth, the extracellular compartment further decreases, as a result of a negative fluid balance in the immediate postnatal period. The fetus constantly regulates its TBW by salt and water exchanges through the placenta membrane. After birth, uptake of water and solutes is limited to gastro-intestinal intakes, while insensible fluid losses increase dramatically. The newborn needs therefore to activate mechanisms that are aimed at controlling water and salt losses. Most of these mechanisms involve the secretion of hormones, which act directly on the kidney. To be efficient, these mechanisms require that sensors, hormone secretion pathways and target organs have reached an appropriate level of maturity. Water excretion or retention is primarily modulated through the regulation of arginine vasopressin (AVP) secretion. Stimulation of thirst has only limited value in newborns, because of their restricted access to free water and immaturity of the central nervous system. Salt retention by the kidney is predominantly achieved by activation of the renin-angiotensin-aldosterone system, which is potentiated by endothelins and adrenergic renal nerve activity. Conversely renal salt losses are stimulated by natriuretic peptides (NPs), prostaglandins, kinins, nitric oxide (NO) and adrenomedullin. In this review, the roles of AVP and NPs in the regulation of body fluid composition during the prenatal and perinatal periods are briefly reviewed. It is important to notice however, that their action is part of a complex network in which all of the above mentioned pathways are synergistically activated or inhibited to maintain body homeostasis.
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