Contribution of the renin-angiotensin system to the short-term blood pressure variability in the conscious rat.

This study was designed to assay, using spectral analysis, the influence of the renin-angiotensin system activation on the blood pressure variability. Rats were surgically prepared with a supra-renal catheter inserted via the left carotid artery to perform local infusions and with a femoral artery ca theter to measure blood pressure (BP) and heart rate (HR). The beta-adrenoc eptors stimulation by isoprenaline was used to increase the plasma renin ac tivity (PRA). A first group (n=8) was infused with isoprenaline (0, 0.003, 10, 100, 300 ng/kg/min) at a rate of 20 mu L/min. A second group (n=8) rece ived a bolus of the angiotensin II (AII) AT1 receptor-antagonist valsartan (2 mg/kg/mL, i.a.) prior to isoprenaline infusions. Five groups were used f or blood sampling tone group infused with one concentration of isoprenaline ) to assay PRA and catecholamines (CA). BP recordings were analysed using t he fast Fourier transforms (FFT) on 2048 points time series (204.8 s). Isoprenaline from the concentration of 10 ng/kg/min increased PRA with a ma ximum effect of 8.5 fold with the highest concentation (300 ng/kg/min, p<0. 05); CA were not modified. Isoprenaline amplified the low-frequency (LF: 0. 02-0.20 Hz) component of the systolic BP (SBP) variability (10 ng/kg/min : 4.16+/-0.62 mmHg(2) versus : 2.90+/-0.44 mmHg(2) for control value, p<0.05) even if It did not modify BP and HR levels, Isoprenaline lowered BP and ha d a tachycardic effect at concentrations greater than or equal to 100 ng/kg /mL (at 100 ng/kg/mL : SEP = 115+/-3 mmHg, HR = 464+/-5 bpm, versus control : SEP = 128+/-3 mmHg, HR = 351+/7 bpm, p<0.05). Valsartan modified neither BP levels nor BP variability but exerted a tachycardic effect (+25 bpm, p< 0.001). Valsartan prevented the amplification of the LF oscillations of SEP induced by isoprenaline (10 ng/kg/min : 2.53+/-0.38 mmHg(2) versus : 2.20/-0.25 mmHg(2) for control value (valsartan, ns). We conclude that a moderate endogenous production of renin increases SEP va riability in the LF range in the conscious rat. This effect which does not affect BP and HR levels is mediated by All AT1 receptors and does not invol ve the sympathetic nervous system.