Fluctuations in arterial blood pressure (ABP), the pattern of their power spectrum and the frequency specificity of the various pressor mechanisms, may provide important information regarding the maintenance of normal ABP levels. The study of these parameters may contribute to the characterization of a cardiovascular system prone to hypertension, and to the understanding of its pathogenesis.

We investigated ABP fluctuations under steady state conditions and following acute perturbations, with and without blockade of various ABP control branches, in spontaneously hypertensive rats (SHR) and age-matched (1 to 6 mo) normotensive WKY. A continuous ABP signal was recorded from the caudal artery in conscious rats. Though heart-rate (HR) power spectra were similar in both strains, the low frequency ABP fluctuations (below 0.18Hz), reflecting vasomotor control, were markedly reduced in SHR at all ages, including the prehypertensive stage of 1 mo. This steady state abnormality was shown to be of neural origin, most probably α-sympathetic. Furthermore, SHR and WKY responded differently to a blood pressure perturbation, even at the age of 1 mo. In particular, a sudden drop in blood volume caused an exaggerated increase in low frequency ABP fluctuations in SHR: 8.7x before hemorrhage (bh) in SHR vs 1.5x in WKY, in the 0.004-0.04Hz range, and, 5.7x bh in SHR vs 1.4x in WKY, in the 0.04-0.07Hz range. Pharmacological blockade of either of the main pressor mechanisms, α or renin-angiotensin (R-A), clearly affected this abnormal response, displaying an interesting frequency specificity. Under α_l -blockade with prazosin, the difference in response to hemorrhage was eliminated: the response was reduced in SHR in the 0.04-0.07Hz range (1.5x bh in SHR and 2.1x bh in WKY) and enhanced in WKY in the 0.004-0.04Hz range (4.6x bh in WKY vs 4.3x bh in SHR). R-A-blockade with CEI reduced the response to hemorrhage in SHR to the level in WKY, in both frequency ranges. R-A-control is thus prominent mainly below 0.04Hz, enhancing its activity when α-control is impaired (under α-blockade or in SHR), its contribution between 0.04-0.07Hz being mainly via its effect on α-release. The α-control manifests itself between 0.04-0.1Hz and seems to contribute to the abnormality in blood pressure control in the spontaneously hypertensive system.