Neural control of free and forced diving
bradycardia and peripheral resistance was studied in the muskrat (Ondatra zibethicus) by means of acute pharmacological blockade with the
muscarinic blocker
atropine, the alpha-
adrenergic blocker phentolamine and the
beta-adrenergic blockers nadolol and
propranolol. Saline injection was used as a control. Heart rate in control animals increased before voluntary dives and dropped markedly as soon as the animals submerged. Heart rate started increasing towards the end of voluntary dives and reached pre-dive values within the first 5 s of recovery. Pre-dive and post-dive
tachycardia were reduced in beta-blocked animals, emphasizing the role of the sympathetic system during the preparatory and recovery periods of voluntary dives. Diving
bradycardia and the acceleration in heart rate before surfacing were abolished by
atropine and unaffected by
nadolol, demonstrating the importance of vagal efferent activity during diving. The results after blockade with
nadolol suggest that there is an accentuated antagonism between the two branches of the autonomic nervous system during diving, so that parasympathetic influences on the heart predominate.
Propranolol-treated muskrats had a higher diving heart rate than saline- and
nadolol-treated animals, which may be due to a
sedative effect caused by
propranolol crossing the blood-brain barrier, a blockade of central catecholaminergic pathways or a peripheral neural effect, due to the anaesthetic properties of
propranolol.
Phentolamine did not affect diving
bradycardia, indicating that diving
bradycardia occurs independently of peripheral vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)