Central oxytocin modulates exercise-induced tachycardia.
We have shown that vasopressinergic projections to dorsal brain stem are activated during exercise and facilitate exercise tachycardia in both trained (T) and sedentary (S) rats (Dufloth DL, Morris M, and Michelini LC. Am J Physiol Regulatory Integrative Comp Physiol 273: R1271-R1282, 1997). In the present study, we investigated whether oxytocinergic projections to the nucleus of the solitary tract (NTS)-dorsal motor nucleus of the vagus (DMV) complex (NTS/DMV) are involved in the differential heart rate (HR) response to exercise in T and S rats. Arterial pressure (AP) and HR responses to dynamic exercise (0.4-1.4 km/h) were compared in S and T pretreated with vehicle (saline), oxytocin (OT; 20 pmol/200 nl) or OT-receptor antagonist (OT(ant); 20 pmol/200 nl) into the NTS/DMV. OT content in specific brain regions and plasma were measured in separate S and T groups at rest and immediately after exercise. Exercise increased OT content in dorsal (4.5-fold) and ventral brain stem (2.7-fold) and spinal cord (3.4-fold) only in T rats. No significant changes were observed in neurosecretory regions or medial eminence and posterior pituitary, but plasma levels of T rats were reduced immediately after exercise. Blockade of NTS/DMV OT receptors did not change basal mean AP (MAP) and HR or the MAP response to exercise. However, OT(ant) potentiated exercise-induced tachycardia (average increase of 26%) only in the T group. Pretreatment with exogenous OT in the NTS/DMV blunted the tachycardic response both in S and T rats without changing the MAP response. Administration of OT-receptor antagonist or OT into the fourth cerebral ventricle had no effect on the cardiovascular response to dynamic exercise. Taken together, the results suggest that oxytocinergic projections to the NTS/DMV are stimulated when T rats exercise and that OT released at this level acts on OT receptors to restrain exercise-induced tachycardia.
Braga
D C
DC
Department of Physiology and Biophysics, Biomedical Sciences Institute, University of Sao Paulo, 05508-900 Sao Paulo, Brazil.
Mori
E
E
Higa
K T
KT
Morris
M
M
Michelini
L C
LC
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D003213:Conditioning, Psychological / Q000502:physiology; D003243:Consciousness; D020546:Fourth Ventricle / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006727:Hormone Antagonists / Q000494:pharmacology; D007276:Injections, Intraventricular; D008124:Locomotion / Q000502:physiology; D008297:Male; D008845:Microinjections; D009046:Motor Neurons / Q000502:physiology; D010121:Oxytocin / Q000032:analysis / Q000097:blood*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D005082:Physical Exertion / Q000502:physiology*; D051381:Rats; D011921:Rats, Inbred WKY; D018045:Receptors, Oxytocin / Q000378:metabolism; D017552:Solitary Nucleus / Q000737:chemistry / Q000502:physiology*; D013610:Tachycardia / Q000378:metabolism*; D014630:Vagus Nerve / Q000737:chemistry / Q000166:cytology / Q000502:physiology; D014668:Vasotocin / Q000031:analogs & derivatives / Q000494:pharmacology
D006727:Hormone Antagonists; D018045:Receptors, Oxytocin; C047046:atosiban; D010121:Oxytocin; D014668:Vasotocin