Vagal control of the cranial venae cavae of the rat heart.
The cranial venae cavae of the rat heart are composed of cardiac muscle. We tested whether the vagus nerve has an inotropic action on these blood vessels. Stimulation of right or left vagal fibres (n = 7 animals) produced a negative chronotropic and inotropic effect. Before stimulation the basal cardiac interval was 319 +/- 25 ms and the vena caval diastolic force was 1.82 +/- 0.29 mN and the systolic force was 3.28 +/- 0.39 mN. Ten second stimulation increased the cardiac interval to a maximum of 484 +/- 77 ms and reduced the systolic force significantly to 2.83 +/- 0.39 mN (two-tailed paired t test). The diastolic or baseline force was unaffected by vagal stimulation (1.85 +/- 0.29 mN). The vagal negative inotropic action took significantly longer to reach peak effect (9.5 +/- 1.0 s versus 3.2 +/- 0.9 s) and lasted longer than the chronotropic effect (20.4 +/- 2.1 s versus 10.25 +/- 1.2 s). The negative inotropic action was still observed in paced preparations and preparations with transient constant-rate tachyarrhythmias. Both the chronotropic and inotropic effects were abolished by atropine (10(-6) M) and mimicked by acetylcholine chloride (10 nM). In order to minimize an atrial contribution to the force production a more reduced preparation was used and ganglion clusters at the cavo-atrial junction were stimulated electrically (n = 4 animals). Similar negative inotropic and chronotropic effects sensitive to hexamethonium were seen. After hexamethonium administration, positive inotopic and chronotropic effects were uncovered and these were abolished by atenolol (0.1 mg %). Methylene Blue staining of the preparation at the end of the experiment showed the presence of ganglion cells at the sites of stimulation. Ganglion clusters were never seen on the venae cavae per se. The results of this investigation show that the vagus has a powerful action on the venae cavae resembling that on the atria and mediated by acetylcholine.
Department of Human Anatomy and Physiology, University College Dublin, Earlsfort Terrace, Ireland. james.jones@ucd.ie
James F X
JF
Jones
Deirdre M
DM
O'Leary
Mark
M
Pickering
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D004558:Electric Stimulation; D006321:Heart / Q000294:innervation* / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013350:Subclavian Vein / Q000294:innervation / Q000502:physiology; D013610:Tachycardia / Q000503:physiopathology; D014630:Vagus Nerve / Q000187:drug effects / Q000502:physiology*; D014683:Vena Cava, Superior / Q000294:innervation* / Q000502:physiology*
D000889:Anti-Arrhythmia Agents; D001285:Atropine; D000109:Acetylcholine