Physical exercise attenuates the cardiac autonomic deficit induced by nitric oxide synthesis blockade.
BACKGROUND
The nitric oxide (NO) synthesis blockade is characterized by an increase in the cardiac sympathetic activity and the physical training promotes the decrease in the sympathetic activity.


OBJECTIVE
We investigated the effect of the NO synthesis blockade on the autonomic cardiovascular control in rats submitted to aerobic exercises during a 10-week period.


METHODS
Male Wistar rats were divided in four groups: control rats, treated with chow food and water ad libitum for 10 weeks (CR); control rats, treated with N G-nitro-L-arginine methyl ester (L-NAME) during the last week (CRL); rats trained during 10 weeks on an electrical treadmill (TR); rats trained for 10 weeks and treated with L-NAME during the last week (TRL). The autonomic cardiovascular control was investigated in all groups with the use of a double blockade with methylatropine and propranolol and analysis of variability.


RESULTS
The CRL and TRL groups presented hypertension. The CRL group presented tachycardia and predominance of the sympathetic tonus in heat rate (HR) measurement after the pharmacological autonomic blockade. The TR group presented bradycardia and lower intrinsic HR when compared to the others. The evaluation of the HR variability showed lower absolute and normalized values in the low frequency (LF) band in the CRL group. On the other hand, the TRL presented an increase in the LF band in absolute values. The analysis of variability of the systemic arterial pressure (SAP) showed that the CRL and TRL groups presented higher values in the LF band.


CONCLUSIONS
The previous physical exercise prevented the deficit in the autonomic cardiac control induced by the treatment with L-NAME, but did not prevent the increase in the SAP variability.
Rossi
Bruno Rafael Orsini
BR
Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Rua Luís Basso 130, Jardim Recreio, Ribeirão Preto, SP, Brazil.
Mazer
Denise
D
Silveira
Larissa Christina Rossit
LC
Jacinto
Cynthia Pelegrino
CP
Di Sacco
Thaísa Helena Roseli
TH
Blanco
João Henrique Dutra
JH
Cesarino
Evandro José
EJ
Souza
Hugo Celso Dutra de
HC
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D001286:Atropine Derivatives / Q000494:pharmacology; D001341:Autonomic Nervous System / Q000187:drug effects / Q000503:physiopathology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar
D000319:Adrenergic beta-Antagonists; D001286:Atropine Derivatives; D004791:Enzyme Inhibitors; C006649:methylatropine; D011433:Propranolol; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester