aI., 1970). DUCK and FEINHOLTZ (1968) have shown that injection of mammalian
corticotrophin also increases the rate of secretion of aldosterone into the blood
of bullfrogs but that the injection of mammalian angiotensin fails to produce such
an effect. This could, however, be due to differences in the structures of the mammalian and homologous bullfrog peptides. When the bullfrog were depleted of
sodium by bathing them in distilled water the circulating levels of aldosterone increased. CRABBE (1961 a; 1966) previously found that while circulating levels of
aldosterone were greatly increased in Bufo marinus depleted of sodium, those of
corticosterone increased only slightly. The increased aldosterone secretion was accompanied by a parallel stimulation in the rate of sodium transport across the skin,
urinary bladder and colon of the toads. CRABBE also found that the injection of
both mammalian corticotrophin and angiotensin increased the rate of sodium transport across these membranes. He has suggested that, while corticotrophin injections may initiate secretion of aldosterone, the changes in the levels of hormone
that normally accompany alterations in the available sodium are probably mediated
by the formation of angiotensin.
The adrenocortical tissues in the Amphibia are closely associated with the surface of the kidney, so that adrenalectomy is a difficult procedure that may be accompanied by renal damage. Attempts to perform this operation are thus sparse.
The toad, Bufo arenarum, has been shown to suffer an excessive loss of salt following adrenalectomy (MARENZI and FUSTINONI, 1938). FOWLER and CHESTER
JONES (1955) destroyed the adrenocortical tissue in the frog, Rana temporaria, and
found that while winter frogs survived this operation for prolonged periods, summer frogs died within 2 days. These frogs suffered large losses of sodium and an
accumulation of potassium which is the classical mammalian reaction to adrenocortical insuffiency. When the summer frogs were placed in isoosmotic saline solution they survived (see CHESTER JONES et al., 1959) suggesting that death was
due to faulty electrolyte balance.
Since adrenocortical tissue in frogs is at least partly under the control of the
adenohypophysis, further attempts to elucidate its role have been made by studying
the effects of the simpler operation of hypophysectomy. It has become apparent
recently that this will not completely extinguish corticosteroid secretion as aldosterone levels are little affected by this operation. Hypophysectomy in Rana temporaria results in a progressive loss of sodium and chloride (JORGENSEN, 1947) but
this loss seems to be slower than that following adrenalectomy in this species.
Sodium loss has also been observed in hypophysectomized Rana esculenta (JORGENSEN and ROSENKILDE, 1957) and Bufo marinus (MIDDLER et aI., 1969), though
RIDLEY (1964) failed to observe such an effect in bullfrogs. MIDDLER et al. were
able to prevent this loss of sodium by injecting mammalian corticotrophin into
the toads and this hormone has also been shown to prolong the survival of hypophysectomized Bufo hufo (JORGENSEN and LARSEN, 1963). The sodium loss observed in hypophysectomized anurans seems to be extrarenal i. e. through the skin.
MIDDLER et al. (1969) could detect no changes in renal sodium excretion following
such an operation but this could be due to the continued presence of aldosterone.
This steroid, however, could not be shown to alter renal sodium excretion in toads
adapted to a bathing media of either distilled water or saline. Neither could MAYER
(1963; 1969) detect such an effect in Rana esculenta prepared in this way. A renal
190
corticotrophin also increases the rate of secretion of aldosterone into the blood
of bullfrogs but that the injection of mammalian angiotensin fails to produce such
an effect. This could, however, be due to differences in the structures of the mammalian and homologous bullfrog peptides. When the bullfrog were depleted of
sodium by bathing them in distilled water the circulating levels of aldosterone increased. CRABBE (1961 a; 1966) previously found that while circulating levels of
aldosterone were greatly increased in Bufo marinus depleted of sodium, those of
corticosterone increased only slightly. The increased aldosterone secretion was accompanied by a parallel stimulation in the rate of sodium transport across the skin,
urinary bladder and colon of the toads. CRABBE also found that the injection of
both mammalian corticotrophin and angiotensin increased the rate of sodium transport across these membranes. He has suggested that, while corticotrophin injections may initiate secretion of aldosterone, the changes in the levels of hormone
that normally accompany alterations in the available sodium are probably mediated
by the formation of angiotensin.
The adrenocortical tissues in the Amphibia are closely associated with the surface of the kidney, so that adrenalectomy is a difficult procedure that may be accompanied by renal damage. Attempts to perform this operation are thus sparse.
The toad, Bufo arenarum, has been shown to suffer an excessive loss of salt following adrenalectomy (MARENZI and FUSTINONI, 1938). FOWLER and CHESTER
JONES (1955) destroyed the adrenocortical tissue in the frog, Rana temporaria, and
found that while winter frogs survived this operation for prolonged periods, summer frogs died within 2 days. These frogs suffered large losses of sodium and an
accumulation of potassium which is the classical mammalian reaction to adrenocortical insuffiency. When the summer frogs were placed in isoosmotic saline solution they survived (see CHESTER JONES et al., 1959) suggesting that death was
due to faulty electrolyte balance.
Since adrenocortical tissue in frogs is at least partly under the control of the
adenohypophysis, further attempts to elucidate its role have been made by studying
the effects of the simpler operation of hypophysectomy. It has become apparent
recently that this will not completely extinguish corticosteroid secretion as aldosterone levels are little affected by this operation. Hypophysectomy in Rana temporaria results in a progressive loss of sodium and chloride (JORGENSEN, 1947) but
this loss seems to be slower than that following adrenalectomy in this species.
Sodium loss has also been observed in hypophysectomized Rana esculenta (JORGENSEN and ROSENKILDE, 1957) and Bufo marinus (MIDDLER et aI., 1969), though
RIDLEY (1964) failed to observe such an effect in bullfrogs. MIDDLER et al. were
able to prevent this loss of sodium by injecting mammalian corticotrophin into
the toads and this hormone has also been shown to prolong the survival of hypophysectomized Bufo hufo (JORGENSEN and LARSEN, 1963). The sodium loss observed in hypophysectomized anurans seems to be extrarenal i. e. through the skin.
MIDDLER et al. (1969) could detect no changes in renal sodium excretion following
such an operation but this could be due to the continued presence of aldosterone.
This steroid, however, could not be shown to alter renal sodium excretion in toads
adapted to a bathing media of either distilled water or saline. Neither could MAYER
(1963; 1969) detect such an effect in Rana esculenta prepared in this way. A renal
190