Page 183 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003
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       Salt and Water Regulation       Na content lead to changes in ECF volume. It is
                                       regulated mainly by the following factors:
       Osmoregulation. The osmolality of most body  ! Renin–angiotensin system (RAS) (! p. 184).
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       fluids is about 290 mOsm/kg H 2O. Any increase  Its activation promotes the retention of Na via
       in the osmolality of extracellular fluid (ECF)  angiotensin II (AT II; lowers GFR), aldosterone
       due, for example, to NaCl absorption or water  (! A4) and ADH.
       loss, results in an outflow of water from the in-  ! Atriopeptin (atrial natriuretic peptide; ANP)
       tracellular space, because the intracellular  is a peptide hormone secreted by specific cells
       fluid (ICF) and ECF are in osmotic balance  of the cardiac atrium in response to rises in ECF +
    Kidneys, Salt, and Water Balance  controlled by osmosensors (or osmoreceptors)  reabsorption from the collecting duct.
       (! p. 173; B2, B6). The osmolality of the ECF
                                       volume and hence atrial pressure. ANP pro-
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       must be tightly regulated to protect cells from
                                       motes the renal excretion of Na by raising the
                                       filtration fraction (! p. 152) and inhibits Na
       large volume fluctuations. Osmoregulation is
       found mainly in the hypothalamus, hormones
                                       ! ADH. ADH secretion is stimulated by (a) in-
                                       creased plasma and CSF osmolality; (b) the
       (e.g., antidiuretic hormone = ADH = adiuretin =
                                       Gauer-Henry reflex, which occurs when stretch
       vasopressin) and the kidney, the target organ
       of ADH (! p. 166).
                                       receptors in the atrium warn the hy-
         Water deficit (! A1). Net water losses (hy-
                                       pothalamus of a decrease (" 10%) in ECF
       povolemia) due, for example, to sweating, uri-
                                       volume (~ atrial pressure); (c) angiotensin II
       tonic. Osmolality rises of 1% or more
                                       ! Pressure diuresis (! p. 172), caused by an
       (! 3 mOsm/kg H 2O) are sufficient to stimulate
                                       elevated arterial blood pressure, e.g. due to an
    7  nation or respiration, make the ECF hyper-  (! p. 184).
                                       elevated ECF volume, results in increased ex-
       the secretion of ADH from the posterior lobe of
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       the pituitary (! p. 280). ADH decreases uri-  cretion of Na and water, thereby lowering ECF
       nary H 2O excretion (! p. 166). The likewise hy-  volume and hence blood pressure. This control
       pertonic cerebrospinal fluid (CSF) stimulates  circuit is thought to be the major mechanism
       central osmosensors in the hypothalamus,  for long term blood pressure regulation.
       which trigger hyperosmotic thirst. The percep-  Salt deficit (! A3). When hyponatremia occurs
       tion of thirst results in an urge to replenish the  in the presence of a primarily normal H 2O con-
       body’s water reserves. Peripheral osmosensors  tent of the body, blood osmolality and there-
       in the portal vein region and vagal afferent  fore ADH secretion decrease, thereby increas-
       neurons warn the hypothalamus of water  ing transiently the excretion of H 2O. The ECF
       shifts in the gastrointestinal tract.  volume, plasma volume, and blood pressure
         Water excess (! A2). The absorption of hy-  consequently decrease (! A4). This, in turn,
       potonic fluid reduces the osmolality of ECF.  activates the RAS, which triggers hypovolemic
       This signal inhibits the secretion of ADH, re-  thirst by secreting AT II and induces Na reten-
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       sulting in water diuresis (! p. 166) and nor-  tion by secreting aldosterone. The retention of
       malization of plasma osmolality within less  Na increases plasma osmolality leading to
                                        +
       than 1 hour.                    secretion of ADH and, ultimately, to the reten-
                                       tion of water. The additional intake of fluids in
       Water intoxication occurs when excessive volumes
       of water are absorbed too quickly, leading to symp-  response to thirst also helps to normalize the
       toms of nausea, vomiting and shock. The condition is  ECF volume.
       caused by an undue drop in the plasma osmolality  Salt excess (! A4). An abnormally high NaCl
       before adequate inhibition of ADH secretion has oc-  content of the body in the presence of a normal
       curred.                         H 2O volume leads to increased plasma
                                       osmolality (thirst) and ADH secretion. Thus,
       Volume regulation. Around 8–15 g of NaCl are
       absorbed each day. The kidneys have to excrete  the ECF volume rises and RAS activity is
       the same amount over time to maintain Na +  curbed. The additional secretion of ANP, per-
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       and ECF homeostasis (! p. 168). Since Na is  haps together with a natriuretic hormone with
  170  the major extracellular ion (Cl –  balance is  a longer half-life than ANP (ouabain?), leads to
                                       increased excretion of NaCl and H 2O and, con-
       maintained secondarily), changes in total body
                                       sequently, to normalization of the ECF volume.
       Despopoulos, Color Atlas of Physiology © 2003 Thieme
       All rights reserved. Usage subject to terms and conditions of license.
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