Central oxytocin modulates exercise-induced tachycardia

Abstract

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.

Hypertension and Exercise Training Differentially Affect Oxytocin and Oxytocin Receptor Expression in the Brain

“…2,3,5,12,14 In brief, a catheter was placed in the femoral artery and exteriorized on the back of the neck under anesthesia. After a 24-hour recovery period, the catheter was connected to the recording system, and the rat was allowed to rest for stabilization of cardiovascular parameters; basal values of arterial pressure (AP) and heart rate (HR) were then recorded in conscious, freely moving rats for Ϸ30 minutes.…”

“…For example, whereas vasopressin resets baroreceptor reflex control of the heart toward higher heart rate values and improves exercise tachycardia, 12,13 OT improves reflex bradycardia and blunts exercise tachycardia. 14,15 Furthermore, we showed that vasopressinergic and oxytocinergic modulation of cardiovascular control in normotensive rats is improved after training, resulting in occlusion of reflex bradycardia and thus facilitating tachycardic response and increased cardiac output during dynamic exercise. 13,16,17 There is no information, however, on the efficiency of vasopressin and OT modulation of cardiovascular control in hypertensive subjects.…”

Efeitos sequenciais do treinamento aeróbio sobre o sistema renina-angiotensina em núcleos autonômicos de ratos normotensos e hipertensos.

“…Para o treinamento, foi utilizado protocolo de treinamento anteriormente padronizado (DUFLOTH et al, 1997;BRAGA et al, 2000), realizado 5 vezes/semana, 1h/dia por 1, 2, 4, 8 ou 12 semanas, sempre com 0% de inclinação.…”

Expressão/funcionalidade de vias noradrenérgicas ascendentes ao hipotálamo: efeitos da desnervação sino-aórtica e do treinamento aeróbio.

“…• a administração de VP no NTS não alterou a sensibilidade do reflexo, mas diminuiu a resposta bradicárdica por reduzir a inibição simpática durante elevações transitórias da PA, deslocando o ponto de operação do reflexo para níveis mais elevados de FC (MICHELINI, 1994(MICHELINI, , 1998BONAGAMBA, 1988) • em ratos sedentários e treinados observou-se durante exercício dinâmico aumento do • pré-tratamento do NTS com antagonista de receptores de OT (OTR) não alterou a resposta pressora, mas potencializou a taquicardia do exercício apenas nos ratos treinados, sugerindo que o treinamento ativa mecanismos OTérgicos supra-bulbares de controle da FC os quais, determinam redução da taquicardia do exercício; nenhuma alteração de PA ou FC após bloqueio dos OTR foi observada em ratos sedentários submetidos ao exercício dinâmico (BRAGA et al, 2000;MICHELINI, 2001);…”

“…• tanto nos grupos treinados quanto sedentários, a administração exógena de OT no NTS determinou redução significativa e similar da taquicardia do exercício, sugerindo que o treinamento não alterava receptores, mas apenas a disponibilidade do neurotransmissor, aumentada após treinamento (BRAGA et al, 2000;MICHELINI, 2001);…”