Vagal-induced tachycardia: release of vasoactive intestinal peptide and peptide HI.
The relationship between vagal-induced tachycardia (VT) and release of vasoactive intestinal peptide (VIP) and peptide HI (PHI) into cardiac lymph and coronary sinus blood was studied in 23 alpha-chloralose-anesthetized open-chest dogs that were autonomically decentralized and pretreated with atropine and propranolol. After simultaneous right and left cervical vagal stimulation at 5 V, 20 Hz for 3 min mean +/- SE, increase in heart rate was 38 +/- 6 beats/min, and increase in lymph VIP output from control was 0.308 +/- 0.093 pg/min (P = 0.004). The decrease in VIP arterial minus coronary sinus concentration was not significant. The increase in heart rate did not significantly correlate with increase in lymph VIP output (R2 = 0.141) or decrease in VIP arterial minus coronary sinus concentration (R2 = 0.059). The increases in heart rate and lymph VIP output were blocked by hexamethonium. Increase in lymph PHI output from control during VT (5 dogs) was 0.797 +/- 0.658 pg/min. Arterial-coronary sinus PHI concentration difference did not change in these dogs. These data indicate that VT is associated but not significantly correlated with VIP and PHI release into cardiac lymph. Cholinoceptive nicotinic receptors may mediate VIP release and VT in anesthetized dogs.
Department of Internal Medicine (Cardiology), University of Utah School of Medicine, Salt Lake City.
F L
FL
Anderson
A C
AC
Kralios
N
N
Cluff
G R
GR
Hanson
D000818:Animals; D001794:Blood Pressure; D004285:Dogs; D004558:Electric Stimulation; D004562:Electrocardiography; D006339:Heart Rate / Q000502:physiology*; D008208:Lymphatic System / Q000502:physiology / Q000503:physiopathology; D010451:Peptide PHI / Q000097:blood / Q000378:metabolism*; D013610:Tachycardia / Q000503:physiopathology*; D014630:Vagus Nerve / Q000502:physiology*; D014660:Vasoactive Intestinal Peptide / Q000097:blood / Q000378:metabolism*
D010451:Peptide PHI; D014660:Vasoactive Intestinal Peptide