ration to altered environmental conditions. Adrenaline and noradrenaline have
widespread physiological (and pharmacological) actions, each hormone having
some distinctively different actions and potencies from the other. Adrenaline increases the heart rate, constricts the blood vessels of the skin and visceral regions
and dilates vessels in the skeletal muscles, so that the blood pressure is changed
little. Noradrenaline, in contrast, constricts the blood vessels of the muscles in addition to those in the other regions, so that the blood pressure rises, and there is
a reflex slowing of the heart. These hormones also dilate the pupils and bronchi,
and relax the smooth muscle of the gut and urinary bladder, adrenaline being the
more potent in these respects. Metabolic processes, like glycol ysis and mobilization
of fatt y acids in the tissues, along with peripheral utilization of substrates and oxygen are increased, adrenaline again being more active than noradrenaline. Some
effects of adrenaline and noradrenaline are mediated through the formation of a
nucleotide, adenosine, 3',5'-phosphate (cyclic AMP), which is also an intermediary in the actions of a number of other hormones, including those from the
neurohypophysis.
Relationship to osmoregulation. The catecholamines are not of direct ph ysiological
importance in osmoregulatory processes, but they may exert indirect effects in certain environment al, experimental and pharmacological circumstances. By influencing oxygen consumption, and changing the regional distribution of blood
in the skin, kidneys and gills the catecholamines could conceivably influence evaporat ion and diffusion of water, as well as electrolyte transfers. Such effects are probably too transient to have chronic effects on the osmoregulation but could have
an influence over short periods of time .
The actions of catecholamine hormones on kidney function have been explored
repeatedly. Emotional stress may result in a transient antidiuresis in mammals, as
a result of the release of adrenaline, which at the same time inhibits release of ADH
(O'CONNOR and VERNEY, 1945). Injections and infusions of adrenaline may reduce
renal sodium excretion (O'CONNOR, 1962). In large doses it facilitates the release
of ADH and corticotrophin, which in turn can influence water and sodium losses.
The amounts of adrenaline required to initiate the above effects are in con siderable
excess of those that accelerate the heart rate, so that it seems unlikely the y are normally of ph ysiological importance. In fishes, adrenaline dilates the branchial vessels
(KEYS and BATEMAN, 1932) which can influence the exchange of electrol ytes (STEEN
and KRUYSSE, 1964). In the anuran amphibians, injected adrenaline also alters water
and sodium exchange ; water uptake in toads is increased (ELLIOTT, 1968), and in
the isolated frog skin, water and sodium uptake is increased (lARD, BASTIDE, and
MOREL, 1968; BASTIDE and JARD, 1968). These effects are similar to those of the
neurohypophysial hormones, and it would appear that these analogous actions are
both mediated by the formation of cyclic AMP. It is usually considered that such
osmotic effects are normally med iated by neurohypophysial hormone, but it is possible that an interaction with adrenaline could facilitate its action. On the other
hand injections of catecholamines may reduce the action of ADH on the mammalian kidney and produce a diuresis (see for instance FISHER, 1968). Such an antagonism can be demonstrated in vitro on the isolated toad urinary bladder and
appears to be mediated by a-adrenergic effects of the catecholamines (HANDLER,
BENSINGER, and ORL OFF, 1968; BENTLEY, 1971 c). The formation of cyclic AMP
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