Different acquisition systems for heart rate variability analysis may lead to diverse outcomes.

Heart rate variability (HRV) is a relevant physiological variable for the estimation of cardiac autonomic function. Although the gold standard for HRV registration is the electrocardiogram (ECG), several applications (APPs) have been increasingly developed. The evaluation carried out by these devices must be compatible with ECG standards. The aim of this study was to compare the data obtained simultaneously with ECG and APP with chest heart rate transmitters. Fifty-six healthy individuals (28 men and 28 women) were evaluated at rest through a short simultaneous HRV measurement with both devices. Data from both acquisition systems were analyzed separately using their own analysis software and exported and analyzed using a validated software. Signal recordings were compatible between the two acquisition systems (Pearson r=0.99; P<0.0001). Although a high correlation was found for the HRV variables obtained in the time domain (Spearman r=0.99; P<0.0001), the correlation decreased in the frequency domain (Pearson r=0.85; P<0.0001) when two software programs were used. Comparison of the averages of spectral analysis parameters also showed differences when HRV data were analyzed separately in each device for low-frequency (LF) and high-frequency (HF) bands. Although the portability of these mobile devices allows for optimal HRV evaluation, the direct analysis obtained from these devices must be carefully evaluated with respect to frequency domain parameters.

Different acquisition systems for heart rate variability analysis may lead to diverse outcomes

Heart rate variability (HRV) is a relevant physiological variable for the estimation of cardiac autonomic function. Although the gold standard for HRV registration is the electrocardiogram (ECG), several applications (APPs) have been increasingly developed. The evaluation carried out by these devices must be compatible with ECG standards. The aim of this study was to compare the data obtained simultaneously with ECG and APP with chest heart rate transmitters. Fifty-six healthy individuals (28 men and 28 women) were evaluated at rest through a short simultaneous HRV measurement with both devices. Data from both acquisition systems were analyzed separately using their own analysis software and exported and analyzed using a validated software. Signal recordings were compatible between the two acquisition systems (Pearson r=0.99; P<0.0001). Although a high correlation was found for the HRV variables obtained in the time domain (Spearman r=0.99; P<0.0001), the correlation decreased in the frequency domain (Pearson r=0.85; P<0.0001) when two software programs were used. Comparison of the averages of spectral analysis parameters also showed differences when HRV data were analyzed separately in each device for low-frequency (LF) and high-frequency (HF) bands. Although the portability of these mobile devices allows for optimal HRV evaluation, the direct analysis obtained from these devices must be carefully evaluated with respect to frequency domain parameters.

Endogenous angiotensin II modulates nNOS expression in renovascular hypertension.

Nitric oxide (NO) influences renal blood flow mainly as a result of neuronal nitric oxide synthase (nNOS). Nevertheless, it is unclear how nNOS expression is modulated by endogenous angiotensin II, an inhibitor of NO function. We tested the hypothesis that the angiotensin II AT1 receptor and oxidative stress mediated by NADPH oxidase contribute to the modulation of renal nNOS expression in two-kidney, one-clip (2K1C) hypertensive rats. Experiments were performed on male Wistar rats (150 to 170 g body weight) divided into 2K1C (N = 19) and sham-operated (N = 19) groups. nNOS expression in kidneys of 2K1C hypertensive rats (N = 9) was compared by Western blotting to that of 2K1C rats treated with low doses of the AT1 antagonist losartan [10 mg x kg(-1) x day(-1); N = 5] or the superoxide scavenger tempol [0.2 mmol x kg(-1) x day(-1); N = 5], which still remain hypertensive. After 28 days, nNOS expression was significantly increased by 1.7-fold in the clipped kidneys of 2K1C rats and by 3-fold in the non-clipped kidneys of 2K1C rats compared with sham rats, but was normalized by losartan. With tempol treatment, nNOS expression increased 2-fold in the clipped kidneys and 1.4-fold in the non-clipped kidneys compared with sham rats. The changes in nNOS expression were not followed by changes in the enzyme activity, as measured indirectly by the cGMP method. In conclusion, AT1 receptors and oxidative stress seem to be primary stimuli for increased nNOS expression, but this up-regulation does not result in higher enzyme activity.

Endogenous angiotensin II modulates nNOS expression in renovascular hypertension

Nitric oxide (NO) influences renal blood flow mainly as a result of neuronal nitric oxide synthase (nNOS). Nevertheless, it is unclear how nNOS expression is modulated by endogenous angiotensin II, an inhibitor of NO function. We tested the hypothesis that the angiotensin II AT1 receptor and oxidative stress mediated by NADPH oxidase contribute to the modulation of renal nNOS expression in two-kidney, one-clip (2K1C) hypertensive rats. Experiments were performed on male Wistar rats (150 to 170 g body weight) divided into 2K1C (N = 19) and sham-operated (N = 19) groups. nNOS expression in kidneys of 2K1C hypertensive rats (N = 9) was compared by Western blotting to that of 2K1C rats treated with low doses of the AT1 antagonist losartan (10 mg·kg-1·day-1; N = 5) or the superoxide scavenger tempol (0.2 mmol·kg-1·day-1; N = 5), which still remain hypertensive. After 28 days, nNOS expression was significantly increased by 1.7-fold in the clipped kidneys of 2K1C rats and by 3-fold in the non-clipped kidneys of 2K1C rats compared with sham rats, but was normalized by losartan. With tempol treatment, nNOS expression increased 2-fold in the clipped kidneys and 1.4-fold in the non-clipped kidneys compared with sham rats. The changes in nNOS expression were not followed by changes in the enzyme activity, as measured indirectly by the cGMP method. In conclusion, AT1 receptors and oxidative stress seem to be primary stimuli for increased nNOS expression, but this up-regulation does not result in higher enzyme activity.