The sites of glucocorticoid action are probably situated in most tissues of the
body , but the liver and muscles are particularly active in this respect. Mineralocorticoid effects are mediated principally by the tetrapod kidney , the skin and
urinary bladder in some of the amphibians, and the gills of certain fishes . Sodium
and potassium exchanges in such tissues as the gut, the salivary glands, the sweat
glands and the various 'salt' glands may also be influenced by corticosteroids. The
relative importance of such sites varies in different species depending on their osmotic problems and methods of regulation. Adrenocortical steroids ma y act on
the kidney by increasing tubular reabsorption of sodium from the glomerular filtrate and by promoting tubular secretion of potassium into this fluid . In some instances the corticosteroids may also facilitate the rate of glomerular filtration.
Sodium uptake from environmental bathing fluids is increased through the skin
of the Amphibia, while urinary sodium loss is reduced by its reabsorption across
the wall of the urinary bladder in this group. Sodium absorption across the wall
of the gut may also be promoted by corticosteroids, while the sodium/potassium
ratio in saliva and sweat can be decreased. Sodium excretion by the nasal 'salt' gland
of birds may be facilitated by such steroids. The gills of some fish are also considered to be sites for the regulatory action of endogenous corticosteroids, and they
ma y increase sodium excretion through the gills of marine fish and increase uptake
of this ion in fre shwater species. These effects will be discussed in later sectio ns.
y) Control of Secretion. The adrenocortical tissue is subject to a number of stimuli
that control its functional integrity (DENTON 1965; GANONG, BIGLIERI, and M ULROW , 1966), and the synthesis and release of its hormones. The secretion of aldosterone and the glucocorticoid hormones are individually controlled, though this
dichotomy is not rigid. Corticotrophin from th e adenohypophysis stimulates the
secretion of both aldo sterone and the glucocorticoids, but only affects the former
in the high part of the physiologically effective dose range. Aldosterone secretion
can be initiated by the direct influence on the adrenal cortex of a reduced plasma
sod ium and/or elevated plasma potassium. A more complex mechanism controlling
mineralocorticoid secretion is provided by the renin-angiotensin system. Renin is
an enzyme secreted into the blood by the juxtaglomerular cells of the kidney in
response to changes in renal arterial blood flow and pressure. This enzyme interacts
in the plasma with an a-2-globulin called angiotensinogen, to produce a decapep -
tide called angiotensin. This decapeptide is then converted by a plasma enzyme
to an octapeptide, angiotensin II (Table 2.3), which has the ability to constrict peripheral blood vessels and also to initiate aldosterone release. The peripheral
vasoconstriction results in elevation of the blood pressure, and in this respect angiotensin II is the most potent substance known, being about 40 times as active
as noradrenaline. The possible physiological role of angiotensin as a vasoactive
agent is uncertain, but in a number of species it undoubtedly influences secretion
of aldosterone. Such a role has been shown in man, th e do g, the Virginia opossum
and the bullfrog, Rana catesbeiana (DAVIS et al., 1967). A note of caution is, however, conveyed in that the evidence for such a role in th e rat is equivocal. Secretion
of renin by the kidney can be shown to reflect sodium metabolism, this being greatest in sodium-depleted animals. The sodium depletion, and associated reduced
blood volume, is thought to promote release of this enzy m e, by wa y of small de76
body , but the liver and muscles are particularly active in this respect. Mineralocorticoid effects are mediated principally by the tetrapod kidney , the skin and
urinary bladder in some of the amphibians, and the gills of certain fishes . Sodium
and potassium exchanges in such tissues as the gut, the salivary glands, the sweat
glands and the various 'salt' glands may also be influenced by corticosteroids. The
relative importance of such sites varies in different species depending on their osmotic problems and methods of regulation. Adrenocortical steroids ma y act on
the kidney by increasing tubular reabsorption of sodium from the glomerular filtrate and by promoting tubular secretion of potassium into this fluid . In some instances the corticosteroids may also facilitate the rate of glomerular filtration.
Sodium uptake from environmental bathing fluids is increased through the skin
of the Amphibia, while urinary sodium loss is reduced by its reabsorption across
the wall of the urinary bladder in this group. Sodium absorption across the wall
of the gut may also be promoted by corticosteroids, while the sodium/potassium
ratio in saliva and sweat can be decreased. Sodium excretion by the nasal 'salt' gland
of birds may be facilitated by such steroids. The gills of some fish are also considered to be sites for the regulatory action of endogenous corticosteroids, and they
ma y increase sodium excretion through the gills of marine fish and increase uptake
of this ion in fre shwater species. These effects will be discussed in later sectio ns.
y) Control of Secretion. The adrenocortical tissue is subject to a number of stimuli
that control its functional integrity (DENTON 1965; GANONG, BIGLIERI, and M ULROW , 1966), and the synthesis and release of its hormones. The secretion of aldosterone and the glucocorticoid hormones are individually controlled, though this
dichotomy is not rigid. Corticotrophin from th e adenohypophysis stimulates the
secretion of both aldo sterone and the glucocorticoids, but only affects the former
in the high part of the physiologically effective dose range. Aldosterone secretion
can be initiated by the direct influence on the adrenal cortex of a reduced plasma
sod ium and/or elevated plasma potassium. A more complex mechanism controlling
mineralocorticoid secretion is provided by the renin-angiotensin system. Renin is
an enzyme secreted into the blood by the juxtaglomerular cells of the kidney in
response to changes in renal arterial blood flow and pressure. This enzyme interacts
in the plasma with an a-2-globulin called angiotensinogen, to produce a decapep -
tide called angiotensin. This decapeptide is then converted by a plasma enzyme
to an octapeptide, angiotensin II (Table 2.3), which has the ability to constrict peripheral blood vessels and also to initiate aldosterone release. The peripheral
vasoconstriction results in elevation of the blood pressure, and in this respect angiotensin II is the most potent substance known, being about 40 times as active
as noradrenaline. The possible physiological role of angiotensin as a vasoactive
agent is uncertain, but in a number of species it undoubtedly influences secretion
of aldosterone. Such a role has been shown in man, th e do g, the Virginia opossum
and the bullfrog, Rana catesbeiana (DAVIS et al., 1967). A note of caution is, however, conveyed in that the evidence for such a role in th e rat is equivocal. Secretion
of renin by the kidney can be shown to reflect sodium metabolism, this being greatest in sodium-depleted animals. The sodium depletion, and associated reduced
blood volume, is thought to promote release of this enzy m e, by wa y of small de76