y) The Kidney . Large volumes of plasma are filtered across the glomerulus; this
ultrafiltrate passes into the renal tubule, where most of its constituents are reabsorbed. The quantities of solutes filtered are enormous, and usually more than
99.9% of the sodium is reabsorbed back into the plasma. These processes are relatively greater in mammals than in cold-blooded species . If the diet contains an excess of sodium, or if changes in the composition of the body fluids are necessary,
more sodium may be excreted. Most vertebrates can form a hypoosmotic urine
which may contain only afew m-equiv/I of sodium. In animals on a normal diet
such urinary losses are easily replenished, but in some circumstances even these
may be physiologically significant. The formation of large volumes of urine, due
to excessive drinking, or to feeding on a very succulent diet, exaggerates such losses.
The role of the adrenal cortex in renal sodium conservation and potassium excretion
has already been described; aldosterone promotes reabsorption of sodium and secretion of potassium across the wall of the renal tubule. The absence of a functional
adrenal cortex results in an excess loss of sodium in the urine and failure to excrete
adequate potassium. Changes in the sodium content of the diet are reflected in the
sodium content of the urine, and the circulating levels of the adrenocortical hormones, especially aldosterone. Thus, rabbits living in the sodium-poor areas of the
plateau of the Australian Snowy Mountains have urinary sod ium levels as little
as one -thirtieth of those rabbits living in adjacent sodium-replete grasslands (BLAIR
WEST et al., 1968). The adrenal glands of the sodium-deficient rabbits are enlarged
and the levels of aldosterone and renin in the blood are 3 to 6-fold greater than
in the sodium-replete animals. Other hormones that may influence urinary sodium
losses are the thyroid and neurohypophysial hormones. The administration of antithyroid drugs increases renal sodium loss, an action related to its decreased tubular reabsorption, and a decline in the rate of production and the efficacy of aldosterone (FREGLY and TAYLOR, 1964). Injections of vasopressin and oxytocin also may
increase urinary sodium and chloride losses in a number of species, including the
rat , dog, camel and sheep, but not man (see HELLER, 1963; MACFARLANE, 1964).
Such effects of the neurohypophysial hormones are often unpredictable, depending
on such factors as, the urinary concentration and volume, as well as the sodium
content of the diet . In many instances such effects can be related to the vascular
actions of such hormones, which can result in alterations of the glomerular filtration rate. A normal physiological role for the thyroid and neurohypophysis in
the control of urinary salt excretion is doubtful, but in abnormal circumstances
large changes in the circulating levels of such hormones could facilitate loss of
sodium.
(I) The Mammary and Lacrymal Glands. The secretions of these glands are an additional potential source of salt loss.
Human milk, immediately post-partum, contains 20 m-equiv sodium/l and 24
m-equiv potassium/I, but after 120 days the concentration of these salts changes
to 6 and 16 m-equiv/l respectively, the Na/K ratio drops from 0.8 to 0.4, (see THAYSEN, 1960). The young of marsupials are born in a less developed condition than
those of placental mammals, and it is interesting that in the wallaby, Setonix brachyurus, the initial sodium level of the milk is higher than in man (BENTLEY and
SHIELD, 1962), being 40 m-equiv/l while potassium is 20 m-equiv/l (Na/K rat io
95
ultrafiltrate passes into the renal tubule, where most of its constituents are reabsorbed. The quantities of solutes filtered are enormous, and usually more than
99.9% of the sodium is reabsorbed back into the plasma. These processes are relatively greater in mammals than in cold-blooded species . If the diet contains an excess of sodium, or if changes in the composition of the body fluids are necessary,
more sodium may be excreted. Most vertebrates can form a hypoosmotic urine
which may contain only afew m-equiv/I of sodium. In animals on a normal diet
such urinary losses are easily replenished, but in some circumstances even these
may be physiologically significant. The formation of large volumes of urine, due
to excessive drinking, or to feeding on a very succulent diet, exaggerates such losses.
The role of the adrenal cortex in renal sodium conservation and potassium excretion
has already been described; aldosterone promotes reabsorption of sodium and secretion of potassium across the wall of the renal tubule. The absence of a functional
adrenal cortex results in an excess loss of sodium in the urine and failure to excrete
adequate potassium. Changes in the sodium content of the diet are reflected in the
sodium content of the urine, and the circulating levels of the adrenocortical hormones, especially aldosterone. Thus, rabbits living in the sodium-poor areas of the
plateau of the Australian Snowy Mountains have urinary sod ium levels as little
as one -thirtieth of those rabbits living in adjacent sodium-replete grasslands (BLAIR
WEST et al., 1968). The adrenal glands of the sodium-deficient rabbits are enlarged
and the levels of aldosterone and renin in the blood are 3 to 6-fold greater than
in the sodium-replete animals. Other hormones that may influence urinary sodium
losses are the thyroid and neurohypophysial hormones. The administration of antithyroid drugs increases renal sodium loss, an action related to its decreased tubular reabsorption, and a decline in the rate of production and the efficacy of aldosterone (FREGLY and TAYLOR, 1964). Injections of vasopressin and oxytocin also may
increase urinary sodium and chloride losses in a number of species, including the
rat , dog, camel and sheep, but not man (see HELLER, 1963; MACFARLANE, 1964).
Such effects of the neurohypophysial hormones are often unpredictable, depending
on such factors as, the urinary concentration and volume, as well as the sodium
content of the diet . In many instances such effects can be related to the vascular
actions of such hormones, which can result in alterations of the glomerular filtration rate. A normal physiological role for the thyroid and neurohypophysis in
the control of urinary salt excretion is doubtful, but in abnormal circumstances
large changes in the circulating levels of such hormones could facilitate loss of
sodium.
(I) The Mammary and Lacrymal Glands. The secretions of these glands are an additional potential source of salt loss.
Human milk, immediately post-partum, contains 20 m-equiv sodium/l and 24
m-equiv potassium/I, but after 120 days the concentration of these salts changes
to 6 and 16 m-equiv/l respectively, the Na/K ratio drops from 0.8 to 0.4, (see THAYSEN, 1960). The young of marsupials are born in a less developed condition than
those of placental mammals, and it is interesting that in the wallaby, Setonix brachyurus, the initial sodium level of the milk is higher than in man (BENTLEY and
SHIELD, 1962), being 40 m-equiv/l while potassium is 20 m-equiv/l (Na/K rat io
95