Page 61 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Disorders of Sodium and Water: Hypernatremia and Hyponatremia 51

TABLE 3-3 Effectors of Sodium Balance
Effector Stimuli for Release Inhibitors of Release Major Effects

Aldosterone Angiotensin II Dopamine Increased number and activity of luminal
þ
þ
Hyperkalemia ANP Na channels and basolateral Na ,K þ
Adrenocorticotropic hormone ATPase in principal cells of cortical
collecting ducts
Angiotensin II # Renal perfusion pressure* " Renal perfusion pressure* Systemic vasoconstriction
Glomerular arteriolar vasoconstriction
(efferent > afferent)
þ
Stimulates proximal Na reabsorption
Stimulates aldosterone secretion
Atrial natriuretic " Atrial stretch # Atrial stretch Inhibits Na reabsorption in parts of the
þ
peptide (ANP) collecting duct
Directly increases glomerular filtration rate
Catecholamines # Effective circulating volume " Effective circulating Vasoconstriction
volume Glomerular arteriolar vasoconstriction
(efferent > afferent)
þ
Increase proximal tubular Na reabsorption
(a 1 effect)
Stimulate renin release (b 1 effect)
Renin # Perfusion pressure in Angiotensin II ANP Not an “effector”—an enzyme that converts
juxtaglomerular apparatus angiotensinogen to angiotensin I
Sympathetic nervous system Antidiuretic hormone
activity
Decreased Cl delivery to
macula densa
*Via release and action of renin.

PHE GLN antidiuresis, urea may constitute more than 40% of the
medullary solute. During diuresis, however, it may con-
TYR ASN 17,98
Desmopressin stitute less than 10% of the medullary solute. The uri-
CYS S S CYS (1–desamino-8-D-arginine nary concentrating mechanism is discussed in Chapter 2.
vasopressin) (DDAVP ® )
H PRO Stimuli for Vasopressin Release

D–ARG The major stimulus for vasopressin release is hypertonic-
ity of plasma reaching the osmoreceptors of the hypothal-
GLY NH 2
amus. The threshold for vasopressin release in humans
corresponds to a plasma osmolality of 280 mOsm/kg,
PHE GLN and similar or slightly higher threshold values have been
TYR ASN Vasopressin observed in healthy experimental dogs. 31,135,137 Below
(antidiuretic hormone) this osmolality, vasopressin release is suppressed, and
CYS S S CYS (Pitressin ) urine is maximally diluted. One hour after oral adminis-
®
NH 2 PRO tration of water at 40 mL/kg, normal dogs developed a
L–ARG mean urine osmolality of 132 mOsm/kg (range, 68 to
244 mOsm/kg). 67 In humans, the release of vasopressin
GLY NH 2
is maximal at a plasma osmolality of 294 mOsm/kg, and
Figure 3-4 Comparison of the chemical structures of
desmopressin and vasopressin. PHE, Phenylalanine; TYR, tyrosine; at this plasma osmolality the thirst mechanism becomes
137
operative. Thus, changes in plasma osmolality as small
GLN, glutamine; ASN, asparagine; CYS, cysteine; PRO, proline; ARG,
arginine; GLY, glycine. as 1% to 2% above normal lead to maximal vasopressin
release. The gain of the system is such that a 1 mOsm/
kg increase in plasma osmolality leads to an almost 100
solute in chronic polyuric states. Chronic diuresis can lead mOsm/kg increase in urine osmolality. The vasopressin
to depletion of urea from the medullary interstitium by system curtails water excretion, but further defense
suppression of vasopressin release and impaired urea reab- against hypertonicity requires a normal thirst mechanism
sorption in the medullary collecting ducts. During and access to water. The thirst mechanism has both