Beat-to-beat fluctuations in the BP related signals in rats: can it contribute to the understanding of the development of hypertension?
The goal of this study was to investigate the alterations in blood pressure control in young spontaneously hypertensive rats (SHR), as reflected in the power distribution of blood pressure fluctuations. We studied six SHR preceding the onset of overt hypertension, compared to six age matched control rats, the normotensive Wistar-Kyoto rats (WKY), and analyzed the power density distribution of several blood pressure related signals, namely: arterial blood pressure (ABP), systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP) and heart rate (HR). ABP fluctuations exhibited a basic difference in the power distribution pattern between the strains: at low frequencies (< 0.15 Hz) more power was observed in WKY than in SHR, while in the (0.35-1.00 Hz) range, more power was observed in SHR. These significant differences in patterns which existed at baseline, were abolished by prazosin (2.5 mg/kg). Observing the power distribution in the BP related signals, the patterns were different from that found in the ABP itself. At baseline, in SBP and DBP, the most dominant power was located at low frequencies < 0.04 Hz, like in ABP. However, unlike ABP, the remainder of the power was located in the high frequency region (HF: 1.5-3.0 Hz), mainly in SHR. Prazosin had a marked effect on PP power spectra; it shifted the power to the HF region in both strains. In PP, power spectra differences observed between the strains at baseline in HF were eliminated by prazosin. This seems to indicate that, in SHR compared to WKY, respiratory fluctuations which are low at baseline in PP, are a mechanical reflection of the higher sympathetic tone in SHR before alpha1 sympathetic blockade. This study supports previous findings in which differences in cardiovascular control occur in SHR already at the prehypertensive stage. The above results suggest that alpha1 sympathetic control is altered in the SHR strain, and therefore, when this limb is blocked, some of the differences between the strains disappear. Furthermore, the analysis of the BP related signals enable us to identify alterations existing in the control mechanisms in SHR, which involve adjunct control mechanisms enhanced under alpha1 sympathetic blockade. Finally, an important result is, that for all BP related signals under study, excluding HR, the response to alpha1-blockade reduces the power density in the 0.07-0.15 Hz region indicating that this region is directly associated with the activity of alpha control.
Almog
Y
Y
School of Physics and Astronomy, Raymond and Beverly Sackler Faculty of Exact Sciences, Tel Aviv University, Israel.
Eldor
S
S
Oz
O
O
Akselrod
S
S
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D003971:Diastole; D006339:Heart Rate / Q000502:physiology; D006973:Hypertension / Q000209:etiology*; D008297:Male; D011224:Prazosin / Q000494:pharmacology; D011674:Pulse; D051381:Rats; D011918:Rats, Inbred SHR / Q000502:physiology; D011921:Rats, Inbred WKY / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology*; D013599:Systole
D000317:Adrenergic alpha-Antagonists; D011224:Prazosin