(gecko, horned toad and Galapagos lizard), the urine sodium level was always about
100 m-equiv/l, even when the animals had been hydrated. Solute reabsorption from
the renal tubule varied from less than 50% in the Galapagos lizards to 85% in the
geckos. The ability of many reptiles to restrict urinary sodium loss is not impressive, and may be subject to some adaptation (genetic or physiological?) commensurate with the environmental conditions to which the animals are normally
subjected.
By analogy with other vertebrates, it appears likely that in the reptiles adrenocortical steroids may increase the reabsorption of sodium across the renal tubule
and facilitate tubular secretion of potassium. However, there is little evidence available to indicate that this is so. Some experiments to elucidate the role of such steroids on urinary excretion of these ions in reptiles are clearly needed. Injections
of vasotocin not only decrease urinary water loss in reptiles, but in the snake, Natrix
sipedon, they also increase renal tubular absorption of sodium while at the same
time facilitating potassium secretion (DANTZLER, 1967 a). This peptide thus mimics
the actions of corticosteroids on the mammalian renal tubule. The action of vasotocin seems to be too rapid for it to be acting by releasing such steroids in the snake,
so it would appear to have a direct effect. The physiological significance, if any,
of this interesting response is not known.
Many reptiles, especially species that live in the sea, may gain excessive quantities of solutes. The reptile kidney has a limited ability to regulate the concentrations of electrolytes, especially sodium, in the body fluids, as the concentration of the urine never exceeds that of the plasma. Indeed, when hyperosmotic solutions are administered to reptiles like the lizard, Trachysaurus rugosus,
or the desert tortoise, Gopherus agassizii, they may become anuric and completely
fail to excrete any of the solute (BENTLEY, 1959 b; DANTZLER and SCHMIDT-NIELSEN, 1966). Even hypoosmotic solutions of sodium chloride are poorly excreted;
when 100 mM NaCl solutions are given to Trachysaurus rugosus they excrete less
than 20% of this through the kidney in 24 hours. The renal responses to potassium
chloride are slightly more rapid and this may be due to the ability to secrete potassium across the renal tubule (SHOEMAKER et al., 1966). The latter response may be
important in herbivorous reptiles that gain excess potassium from their diet.
The relative inability of the reptilian kidney to excrete salts, may be compensated for in two ways. As will be described shortly, many reptiles have the ability to excrete sodium and potassium extrarenally through cephalic 'salt' glands .
In other reptiles, which lack such accessory excretory glands, an ability to withstand considerable increases in the solute concentrations of the body fluids may
exist. As we have seen, this has been shown in natural conditions in the Australian
lizards, Trachysaurus rugosus and Amphibolurus ornatus. Such animals retain electrolytes and await the arrival of more adequate supplies of water which they then
utilize for the renal excretion of such solutes. BRADSHAW and SHOEMAKER (1967)
found that the plasma sodium levels of Amphibolurus could rise to as much as 300
m-equiv/l during periods of summer drought. During a summer rainstorm these
lizards were observed to dart about and drink the water rapidly as it fell; ten hours
later plasma samples were collected and the electrolyte concentrations were found
to have returned to normal. Diamondback terrapins kept in sea-water accumulate
sodium, but when they are placed in fresh water they drink and rapidly excrete
150
100 m-equiv/l, even when the animals had been hydrated. Solute reabsorption from
the renal tubule varied from less than 50% in the Galapagos lizards to 85% in the
geckos. The ability of many reptiles to restrict urinary sodium loss is not impressive, and may be subject to some adaptation (genetic or physiological?) commensurate with the environmental conditions to which the animals are normally
subjected.
By analogy with other vertebrates, it appears likely that in the reptiles adrenocortical steroids may increase the reabsorption of sodium across the renal tubule
and facilitate tubular secretion of potassium. However, there is little evidence available to indicate that this is so. Some experiments to elucidate the role of such steroids on urinary excretion of these ions in reptiles are clearly needed. Injections
of vasotocin not only decrease urinary water loss in reptiles, but in the snake, Natrix
sipedon, they also increase renal tubular absorption of sodium while at the same
time facilitating potassium secretion (DANTZLER, 1967 a). This peptide thus mimics
the actions of corticosteroids on the mammalian renal tubule. The action of vasotocin seems to be too rapid for it to be acting by releasing such steroids in the snake,
so it would appear to have a direct effect. The physiological significance, if any,
of this interesting response is not known.
Many reptiles, especially species that live in the sea, may gain excessive quantities of solutes. The reptile kidney has a limited ability to regulate the concentrations of electrolytes, especially sodium, in the body fluids, as the concentration of the urine never exceeds that of the plasma. Indeed, when hyperosmotic solutions are administered to reptiles like the lizard, Trachysaurus rugosus,
or the desert tortoise, Gopherus agassizii, they may become anuric and completely
fail to excrete any of the solute (BENTLEY, 1959 b; DANTZLER and SCHMIDT-NIELSEN, 1966). Even hypoosmotic solutions of sodium chloride are poorly excreted;
when 100 mM NaCl solutions are given to Trachysaurus rugosus they excrete less
than 20% of this through the kidney in 24 hours. The renal responses to potassium
chloride are slightly more rapid and this may be due to the ability to secrete potassium across the renal tubule (SHOEMAKER et al., 1966). The latter response may be
important in herbivorous reptiles that gain excess potassium from their diet.
The relative inability of the reptilian kidney to excrete salts, may be compensated for in two ways. As will be described shortly, many reptiles have the ability to excrete sodium and potassium extrarenally through cephalic 'salt' glands .
In other reptiles, which lack such accessory excretory glands, an ability to withstand considerable increases in the solute concentrations of the body fluids may
exist. As we have seen, this has been shown in natural conditions in the Australian
lizards, Trachysaurus rugosus and Amphibolurus ornatus. Such animals retain electrolytes and await the arrival of more adequate supplies of water which they then
utilize for the renal excretion of such solutes. BRADSHAW and SHOEMAKER (1967)
found that the plasma sodium levels of Amphibolurus could rise to as much as 300
m-equiv/l during periods of summer drought. During a summer rainstorm these
lizards were observed to dart about and drink the water rapidly as it fell; ten hours
later plasma samples were collected and the electrolyte concentrations were found
to have returned to normal. Diamondback terrapins kept in sea-water accumulate
sodium, but when they are placed in fresh water they drink and rapidly excrete
150