Page 449 - Anatomy and Physiology of Farm Animals, 8th Edition

434 / Anatomy and Physiology of Farm Animals

Collecting ducts begin in the renal Polyuria and Polydipsia
cortex but extend into and through the
VetBooks.ir renal medulla, where the interstitial fluids Polyuria is the passage of larger volumes

are hypertonic. Also, because of the
transport in the loop of Henle, the tubu- of urine than normal. Animals that cannot
generate hypertonic urine when necessary
lar fluid entering the cortical portion of a become polyuric. Polydipsia is excessive
collecting duct is dilute or hypotonic, and thirst, and polyuric animals are often able
this is always true regardless of the water to maintain water balance by increasing
balance status of the animal. If ADH is water intake. The increased intake is con-
not present, the water permeability of the sidered to be a sign of excessive thirst.
collecting duct is relatively low, and the Polyuria and polydipsia (often abbre-
hypotonic fluid entering the collecting viated PU/PD) may develop in animals
ducts passes through and is excreted as a with unregulated diabetes mellitus and
hypotonic urine. Because water is not significant increases in blood glucose.
reabsorbed from the water‐impermeable The renal tubules cannot reabsorb the
collecting duct, the volume is also rela- abnormally large amounts of glucose in
tively large (Fig. 23‐11A). If ADH is pre- the glomerular filtrate, and the glucose
sent, the water permeability of the that remains in the renal tubules exerts
collecting duct is increased, and water is an osmotic effect to retain water in the
reabsorbed because the osmolality inside tubules. Increased urine flow results,
the duct is less than that outside. As the and the animal must increase water
tubular fluid passes through the medul- intake to maintain water balance.
lary portion of the collecting duct, more Polyuria and polydipsia may also result
and more water is reabsorbed, and the when ADH is not available (e.g., pituitary
osmolality of the tubular fluid increases tumor preventing its release) or the kidney
further. In these circumstances urine vol- does not respond appropriately to ADH. In
ume is low and urine osmolality is high either case the water permeability of the
(Fig. 23‐11B). collecting ducts remains relatively low, and
water cannot be reabsorbed from the
collecting ducts into the blood. Again, the
Osmotic Regulation of Antidiuretic affected animals must increase water
Hormone intake to maintain water balance. This
condition is diabetes insipidus.
ADH (or arginine vasopressin in most
mammalian species) release from the pos-
terior pituitary can be regulated by changes Sodium, Potassium,
in the extracellular fluid (ECF) osmolality. and Aldosterone
Specific cells (osmoreceptors) in the hypo-
thalamus monitor the osmolality of ECF. In Most of the sodium and potassium in the
response to increases in ECF osmolality, initial glomerular filtrate is reabsorbed by
these cells stimulate increases in ADH the proximal tubule and the loop of Henle.
release, which results in the excretion of a However, the collecting duct is also capable
small volume of a hypertonic urine. The of sodium and potassium transport, and it
elimination of excess particles and conser- is here that the final adjustments are made
vation of water dilutes the ECF, which acts in the regulation of sodium and potassium
as a negative feedback control to inhibit balance. Aldosterone, a steroid hormone
additional releases of ADH. Reductions in from the adrenal cortex, functions as a
ECF osmolality inhibit ADH release, which major regulator of sodium and potassium
results in the excretion of a relatively large transport in the collecting duct.
volume of dilute urine. This eliminates any Aldosterone acts on principal cells of
excess water. the collecting ducts to promote their