4. THE CIRCULATORY SYSTEM
155
in the active form of the enzyme glycogen phosphorylase. Cyclic AMP
is known to sensitize actomyosin toward changes in calcium concentration (Mommaerts et a2., 1963). Thus cyclic AMP plays a role in both
the inotropic and glycogenolytic effects of epinephrine. Both the glycogenolytic and inotropic effects are blocked by P-adrenergic blocking
agents in mammals ( Sutherland and Rall, 1960). The p-adrenergic blocking agent, Inderal, blocks the response to epinephrine in the isolated
trout heart and causes a general myocardial depression similar to that
seen in mammals ( Nickerson, 1964). The a-adrenergic blocking agent,
phenoxybenzamine, had no effect on the response of the isolated trout
heart ( Bennion, 1968).
High levels of catecholamines have been found in cyclostome hearts
( Bloom et d., 1961 ) . Much lower levels of adrenaline and noradrenaline
have been demonstrated in the hearts of other fishes (von Euler and
Fange, 196l), and adrenaline usually represents more than 50% of the
total catecholamines present. Catecholamines have been shown to increase the rate and force of contraction of both teleost and elasmobranch
hearts (Ostlund, 1954; Falck et al., 1966), and p-adrenergic receptors
have been demonstrated in the isolated plaice and trout heart. Surprisingly, catecholamines have little effect on the hagfish heart; however,
Chapman et al. (1963) did find that adrenaline restored loss of vigor
caused by the application of reserpine in the hagfish heart.
In the intact animal the activity of the heart is determined by the
sum total of many factors that influence the heart. Johansen (1962) observed an increase in stroke volume when venous return was experimentally increased in the cod, Gadus morhua; no rate changes were observed.
Labat et a2. (1961) observed an increase in heart rate in the catfish when
the temperature was increased or if saline was injected into the hepatic
vein, increasing venous return to the heart. Laffont and Labat (1966)
found that below 8°C epinephrine injections caused a decrease in heart
rate, The bradycardia recorded by Laffont and Labat may have been
the result of an increase in vagal tone, resulting from a change in blood
pressure caused by the action of epinephrine on the circulatory system
(Randall and Stevens, 1967).
When trout swim there are large changes in cardiac output which
are the result of small increases in heart rate and large increases in stroke
volume ( Stevens and Randall, 1967b ) ; also the total peripheral resistance to flow dccreases. There is no vagal tone to the heart of trout
during rest or exercise as long as the fish is in well-aerated water;
thereforc, any changes that occur during activity cannot be explained
in terms of a decrease in vagal tone to the heart. The level of circulating
catecholamines increases during cxercise in trout ( Nakano and Tomlinson, 1967). There are p-adrenergic receptors in the heart ( Bennion,
155
in the active form of the enzyme glycogen phosphorylase. Cyclic AMP
is known to sensitize actomyosin toward changes in calcium concentration (Mommaerts et a2., 1963). Thus cyclic AMP plays a role in both
the inotropic and glycogenolytic effects of epinephrine. Both the glycogenolytic and inotropic effects are blocked by P-adrenergic blocking
agents in mammals ( Sutherland and Rall, 1960). The p-adrenergic blocking agent, Inderal, blocks the response to epinephrine in the isolated
trout heart and causes a general myocardial depression similar to that
seen in mammals ( Nickerson, 1964). The a-adrenergic blocking agent,
phenoxybenzamine, had no effect on the response of the isolated trout
heart ( Bennion, 1968).
High levels of catecholamines have been found in cyclostome hearts
( Bloom et d., 1961 ) . Much lower levels of adrenaline and noradrenaline
have been demonstrated in the hearts of other fishes (von Euler and
Fange, 196l), and adrenaline usually represents more than 50% of the
total catecholamines present. Catecholamines have been shown to increase the rate and force of contraction of both teleost and elasmobranch
hearts (Ostlund, 1954; Falck et al., 1966), and p-adrenergic receptors
have been demonstrated in the isolated plaice and trout heart. Surprisingly, catecholamines have little effect on the hagfish heart; however,
Chapman et al. (1963) did find that adrenaline restored loss of vigor
caused by the application of reserpine in the hagfish heart.
In the intact animal the activity of the heart is determined by the
sum total of many factors that influence the heart. Johansen (1962) observed an increase in stroke volume when venous return was experimentally increased in the cod, Gadus morhua; no rate changes were observed.
Labat et a2. (1961) observed an increase in heart rate in the catfish when
the temperature was increased or if saline was injected into the hepatic
vein, increasing venous return to the heart. Laffont and Labat (1966)
found that below 8°C epinephrine injections caused a decrease in heart
rate, The bradycardia recorded by Laffont and Labat may have been
the result of an increase in vagal tone, resulting from a change in blood
pressure caused by the action of epinephrine on the circulatory system
(Randall and Stevens, 1967).
When trout swim there are large changes in cardiac output which
are the result of small increases in heart rate and large increases in stroke
volume ( Stevens and Randall, 1967b ) ; also the total peripheral resistance to flow dccreases. There is no vagal tone to the heart of trout
during rest or exercise as long as the fish is in well-aerated water;
thereforc, any changes that occur during activity cannot be explained
in terms of a decrease in vagal tone to the heart. The level of circulating
catecholamines increases during cxercise in trout ( Nakano and Tomlinson, 1967). There are p-adrenergic receptors in the heart ( Bennion,