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The analysis of heart rate variability (HRV) by nonlinear methods has been gaining increasing interest due to their ability to quantify the complexity of cardiovascular regulation. In this study, multiscale entropy (MSE) and refined MSE (RMSE) were applied to track the complexity of HRV as a function of time scale in three pathological conscious animal models: rats with heart failure (HF), spontaneously hypertensive rats (SHR), and rats with sinoaortic denervation (SAD). Results showed that HF did not change HRV complexity, although there was a tendency to decrease the entropy in HF animals. On the other hand, SHR group was characterized by reduced complexity at long time scales, whereas SAD animals exhibited a smaller short- and long-term irregularity. We propose that short time scales (1 to 4), accounting for fast oscillations, are more related to vagal and respiratory control, whereas long time scales (5 to 20), accounting for slow oscillations, are more related to sympathetic control. The increased sympathetic modulation is probably the main reason for the lower entropy observed at high scales for both SHR and SAD groups, acting as a negative factor for the cardiovascular complexity. This study highlights the contribution of the multiscale complexity analysis of HRV for understanding the physiological mechanisms involved in cardiovascular regulation., (Copyright © 2016 the American Physiological Society.)

The crosstalk between the immune and the autonomic nervous system may impact the cardiovascular function. Toll-like receptors are components of the innate immune system and play developmental and physiological roles. Toll-like receptor 9 (TLR9) is involved in the pathogenesis of cardiovascular diseases, such as hypertension and heart failure. Since such diseases are commonly accompanied by autonomic imbalance and lower baroreflex sensitivity, we hypothesized that TLR9 modulates cardiac autonomic and baroreflex control of arterial pressure (AP). Toll-like receptor 9 knockout (TLR9 KO) and wild-type (WT) mice were implanted with catheters into carotid artery and jugular vein and allowed to recover for 3 days. After basal recording of AP, mice received methyl-atropine or propranolol. AP and pulse interval (PI) variability were evaluated in the time and frequency domain (spectral analysis), as well as by multiscale entropy. Spontaneous baroreflex was studied by sequence technique. Behavioral and cardiovascular responses to fear-conditioning stress were also evaluated. AP was similar between groups, but TLR9 KO mice exhibited lower basal heart rate (HR). AP variability was not different, but PI variability was increased in TLR9 KO mice. The total entropy was higher in TLR9 KO mice. Moreover, baroreflex function was found higher in TLR9 KO mice. Atropine-induced tachycardia was increased in TLR9 KO mice, whereas the propranolol-induced bradycardia was similar to WT mice. TLR9 KO mice exhibit increased behavioral and decreased tachycardia responses to fear-conditioning stress. In conclusion, our findings suggest that TLR9 may negatively modulate cardiac vagal tone and baroreflex in mice., (Copyright © 2015 the American Physiological Society.)

The role played by the sympathetic drive in the development of N(G)-nitro-l-arginine methyl ester (l-NAME)-induced hypertension is not firmly established. Therefore, the present study was undertaken in conscious rats in which hypertension was induced by treatment with l-NAME over the course of either 2 or 14 days. Mean arterial pressure (MAP) was measured via a catheter placed in the femoral artery, drugs were administered via a cannula placed in the femoral vein, and renal sympathetic nerve activity (RSNA) was monitored using an implanted electrode. Despite the remarkable increase in arterial pressure, heart rate did not change after treatment with l-NAME. RSNA was similar in l-NAME-induced hypertensive rats treated over the course of 2 or 14 days, as well as in normotensive rats. It was also demonstrated that l-NAME-induced hypertensive rats displayed a resetting of the baroreflex control of RSNA to hypertensive levels, with decreased sensitivity over the course of 2 or 14 days. Furthermore, the sympathetic-vagal balance examined in the time and frequency domain and the renal and plasma norepinephrine content did not differ between groups. In conclusion, the evaluation of the sympathetic drive in conscious rats demonstrated that the arterial hypertension induced by l-NAME treatment over the course of 2 and 14 days does not show sympathetic overactivity.