Chronic stress results in physiological and somatic changes. It has been recognized as a risk factor for several cardiovascular dysfunctions and changes in autonomic mechanisms, such as baroreflex and chemoreflex activity. However, the effects of different types of chronic stress on these mechanisms are still poorly understood. Therefore, in the present study we investigated, in adult male rats, the effect of repeated restraint stress (RRS) or chronic variable stress (CVS) on baroreflex, chemoreflex and heart rate variability in a protocol of 14 days of stress sessions. Exposure to RRS and CVS indicated no changes in basal level of neither pressure arterial nor heart rate. However, RRS and CVS were able to attenuate sympathovagal modulation and spontaneous baroreflex gain. Additionally, only RRS was able to increase the power of the low frequency band (LF) of the systolic blood pressure (SBP) spectrum, as well as the slope of linear regression of baroreflex bradycardic and tachycardic responses induced by vasoactive compounds. Additionally, our work is one of the first to show that exposure to RRS and CVS decreased the magnitude of the pressor response and potentiates respiratory responses to chemoreflex activation, which can trigger cardiovascular and respiratory pathologies. Furthermore, the basal respiratory parameters, such as minute ventilation (V_E) and tidal volume (V_T) was significantly decreased by both protocols of chronic stress. However, only CVS increased the basal respiratory frequency. In this way, the findings of the present study demonstrate the impact of chronic stress not only in depressive-like behavior, but also in alterations of the autonomic baroreflex responses and cardiocirculatory variability (systolic blood pressure and pulse interval).Our results have provided evidence that chronic stress promotes autonomic dysregulation, and impairment of baroreflex, chemoreflex and heart rate variability.

An implanted telemetry device transmitted ECG from the South American rattlesnake, Crotalus durissus, held under stable conditions without restraining cables or interaction with researchers. Mean heart rate (f_H) recovered rapidly (<24h) from anaesthesia and operative procedures. This anticipated a more gradual development of heart rate variability (HRV), with instantaneous f_H increasing during each lung ventilation cycle. Atropine injection increased mean f_H and abolished HRV. Complete autonomic blockade revealed a parasympathetic tonus on the heart of 55% and an adrenergic tonus of 37%. Power spectral analysis of HRV identified a peak at the same frequency as ventilation. Such correlation is sustained after temperature change and that is clear when ventilation is less episodic. This HRV peak is homologous to that observed in mammals and termed respiratory sinus arrhythmia - RSA. Evidence for instantaneous control of f_H implied rapid conduction of activity in the cardiac efferent nervous supply, supported by the description of myelinated fibres in the cardiac vagus. Establishment of HRV 10 days after surgical intervention seems a reliable indicator of the re-establishment of control of integrative functions by the autonomic nervous system. We suggest that this criterion could be applied to other animals exposed to natural or imposed trauma, thus improving protocols involving animal handling, including veterinarian procedures.

The objective of the present study was to evaluate cardiac tissue adaptations in rats submitted to aerobic training after nitric oxide (NO) synthesis blockade. The animals (n=48) were divided into four groups: sedentary (CONTROL group); hypertensive after administration of NG-nitro-L-arginine methyl ester for 7 days (L-NAME Group); trained for 8 weeks through swimming exercises (TRAINED Group);trained and treated with L-NAME during the last week (L-NAME TRAINED Group). All the animals were submitted to the experiment procedures for blood pressure (BP) readings and cardiac morphometric evaluation. In comparison to the other groups, the L-NAME and L-NAME TRAINED groups were hypertensive (p<0.05); however, BP elevation in the L-NAME TRAINED group was significantly lower than the L-NAME group (p<0.05). The heart weight indexes for the TRAINED and L-NAME TRAINED groups were higher than the CONTROL and L-NAME groups (p<0.05). Also they had presented higher rates of macroscopic cardiac area and cardiac fibrosis in relation to the rest (p<0.05); comparisons revealed that the values for the L-NAME TRAINED group were significantly higher (p<0.05) than the others. Short term NO synthesis blockade in sedentary animals induced hypertension but did not cause cardiac hypertrophy. In the trained animals, the inhibition of NO synthesis attenuated hypertension, induced cardiac hypertrophy and significantly increased myocardial fibrosis, indicating that NO plays an important role in cardiac tissue adaptations caused by aerobic exercise.