Document Detail

Negative inotropic and chronotropic effects of oxytocin.
MedLine Citation:
PMID:  11509492     Owner:  NLM     Status:  MEDLINE    
We have previously shown that oxytocin receptors are present in the heart and that perfusion of isolated rat hearts with oxytocin results in decreased cardiac flow rate and bradycardia. The mechanisms involved in the negative inotropic and chronotropic effects of oxytocin were investigated in isolated dog right atria in the absence of central mechanisms. Perfusion of atria through the sinus node artery with 10(-6) mol/L oxytocin over 5 minutes (8 mL/min) significantly decreased both beating rate (-14.7+/-4.9% of basal levels, n=5, P<0.004) and force of contraction (-52.4+/-9.1% of basal levels, n=5, P<0.001). Co-perfusion with 10(-6) mol/L oxytocin receptor antagonist (n=3) completely inhibited the effects of oxytocin on frequency (P<0.04) and force of contraction (P<0.004), indicating receptor specificity. The effects of oxytocin were also totally inhibited by co-perfusion with 5x10(-8) mol/L tetrodotoxin (P<0.02) or 10(-6) mol/L atropine (P<0.03) but not by 10(-6) mol/L hexamethonium, which implies that these effects are neurally mediated, primarily by intrinsic parasympathetic postganglionic neurons. Co-perfusion with 10(-6) mol/L NO synthase inhibitor (L-NAME) significantly inhibited oxytocin effects on both beating rate (-1.85+/-1.27% versus -14.7+/-4.9% in oxytocin alone, P<0.05) and force of contraction (-24.9+/-4.4% versus -52.4+/-9.1% in oxytocin alone, n=4, P<0.04). The effect of oxytocin on contractility was further inhibited by L-NAME at 10(-4) mol/L (-8.1+/-1.8%, P<0.01). These studies imply that the negative inotropic and chronotropic effects of oxytocin are mediated by cardiac oxytocin receptors and that intrinsic cardiac cholinergic neurons and NO are involved in these actions.
S Mukaddam-Daher; Y L Yin; J Roy; J Gutkowska; R Cardinal
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Hypertension     Volume:  38     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2001 Aug 
Date Detail:
Created Date:  2001-08-17     Completed Date:  2001-08-30     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  292-6     Citation Subset:  IM    
Laboratory of Cardiovascular Biochemistry, Centre Hospitalier de L'Université de Montréal Research Center, Pavilion Hotel-Dieu, Montreal, Canada.
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MeSH Terms
Atropine / pharmacology
Culture Techniques
Depression, Chemical
Enzyme Inhibitors / pharmacology
Heart Atria / drug effects
Heart Rate / drug effects*
Hormone Antagonists / pharmacology
Myocardial Contraction / drug effects*
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide Synthase / antagonists & inhibitors
Oxytocin / analogs & derivatives*,  pharmacology*
Parasympatholytics / pharmacology
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Hormone Antagonists; 0/KB 5-21; 0/Parasympatholytics; 50-56-6/Oxytocin; 50903-99-6/NG-Nitroarginine Methyl Ester; 51-55-8/Atropine; EC Oxide Synthase

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