Ebara stitnultLtcd the gcuiglioii t).y t i i w i i s of clcct,rodes placed one inside
the branchial nac and the ot3hcr out,side and considerable mechanical
stress must have occurred. Similarly in Hunter’s work mechanical stress
occurred and in both cases this is likely to have had very considerable
effects on the heart, beat. h i the case of Perophoru the effect on the
second zooid is a ntltural pint of tho co-ordination found between
neighbouring zooids (Ebara, 1961).
D. Cardio-regulatory drugs
The evidence concerning the effects of cardio-regulatory drugs on
the ascidian heart is very conflicting, but this may in part be due to
differences in the techniques used (Table VIII). Acetylcholine normally
acts to depress cardiac. activity in ajmals. Bacq (1934a, 1935a),
Krijgsmaii and Krijgsman (1959), Scudder et ul. (1963) and Sugi and
Matsunami (1966) found no renponse to acetylcholine while Waterman
(1942, 1943) and Ebara ( 1963a,b) both found different types of cardiac
enhancement. Adrenalin is a cardiac accelerator and Scudder et al. and
Sugi and Matsunatni claim to have found such an effect in ascidians.
Sugi and Matsunami also found that serotonin caused an increase of
beat frequency when applied to the visceral pacemaker but either
reduced the frequency or had no cffect when applied to the hypobranchial pacemaker.
Kriebel (1968d) has criticized all earlier work on the grounds that
whole hearts or even whole animals were being exposed and that the
drugs could not penetrate through the myoendothelial wall because of
the tight junctions between cells. Kriebel tested the effects of adrenalin
and acetylcholine on hearts which had been slit open to allow access
of the drugs ant1 found that both drugs caused a temporary cessation of
heart beat ’when used in pharmacological concentration. The effect of
acetylcholine was inhibited by atropine. Kriebel interprets this to
mean that cardio-accelerator). nerves are absent but that “ the tunicate
heart may receive cardio-inhibitory innervation and this innervation
is cholinergic ”. Although the existence of cholinergic somatic nerves
in ascidians has been clainied by Florey ( 1 963, 1967) the evidence does
not seem to warrant Kriebel’s conclusion. No nervous innervation of
the heart has been demonstrated and all evidence nuggents that it is
under intrinsic and not extrinnio control (p. 54). Furthermore both
Bacq (1 935b) and Florcy (1 951 ) have reported very low conwntrationn
of cholinesterase in ascidians atid Ilurante (1956) statw that it dinappears at nietamorphosis ; under thene circumstance8 it would r w r n
unlikely that acetylcholine could be used a8 an important cardioregulator. The existelice of a pharinacological effect by a drug on t,he
the branchial nac and the ot3hcr out,side and considerable mechanical
stress must have occurred. Similarly in Hunter’s work mechanical stress
occurred and in both cases this is likely to have had very considerable
effects on the heart, beat. h i the case of Perophoru the effect on the
second zooid is a ntltural pint of tho co-ordination found between
neighbouring zooids (Ebara, 1961).
D. Cardio-regulatory drugs
The evidence concerning the effects of cardio-regulatory drugs on
the ascidian heart is very conflicting, but this may in part be due to
differences in the techniques used (Table VIII). Acetylcholine normally
acts to depress cardiac. activity in ajmals. Bacq (1934a, 1935a),
Krijgsmaii and Krijgsman (1959), Scudder et ul. (1963) and Sugi and
Matsunami (1966) found no renponse to acetylcholine while Waterman
(1942, 1943) and Ebara ( 1963a,b) both found different types of cardiac
enhancement. Adrenalin is a cardiac accelerator and Scudder et al. and
Sugi and Matsunatni claim to have found such an effect in ascidians.
Sugi and Matsunami also found that serotonin caused an increase of
beat frequency when applied to the visceral pacemaker but either
reduced the frequency or had no cffect when applied to the hypobranchial pacemaker.
Kriebel (1968d) has criticized all earlier work on the grounds that
whole hearts or even whole animals were being exposed and that the
drugs could not penetrate through the myoendothelial wall because of
the tight junctions between cells. Kriebel tested the effects of adrenalin
and acetylcholine on hearts which had been slit open to allow access
of the drugs ant1 found that both drugs caused a temporary cessation of
heart beat ’when used in pharmacological concentration. The effect of
acetylcholine was inhibited by atropine. Kriebel interprets this to
mean that cardio-accelerator). nerves are absent but that “ the tunicate
heart may receive cardio-inhibitory innervation and this innervation
is cholinergic ”. Although the existence of cholinergic somatic nerves
in ascidians has been clainied by Florey ( 1 963, 1967) the evidence does
not seem to warrant Kriebel’s conclusion. No nervous innervation of
the heart has been demonstrated and all evidence nuggents that it is
under intrinsic and not extrinnio control (p. 54). Furthermore both
Bacq (1 935b) and Florcy (1 951 ) have reported very low conwntrationn
of cholinesterase in ascidians atid Ilurante (1956) statw that it dinappears at nietamorphosis ; under thene circumstance8 it would r w r n
unlikely that acetylcholine could be used a8 an important cardioregulator. The existelice of a pharinacological effect by a drug on t,he