Adrenergic origin of very low-frequency blood pressure oscillations in the unanesthetized rat

Abstract

Spectral analysis of cardiovascular signals has been extensively used to investigate circulatory homeostatic mechanisms. However, the nature of very low-frequency (VLF) fluctuations remains unclear. Because we previously observed enhanced VLF fluctuations in blood pressure (BP) in the sympathectomized rat (a model characterized by markedly increased plasma epinephrine levels), the aims of our study were to assess whether the genesis of VLF fluctuations in BP depends on circulating catecholamines and to determine which adrenergic receptor(s) and which membrane ion channel(s) are involved. We used continuous intra-arterial BP recordings from unanesthetized unrestrained rats to compute the power of VLF fluctuations in BP in the intact condition, during acute ganglionic blockade with hexamethonium, and after restoration of BP levels by infusion (in addition to hexamethonium) of adrenergic agonists (epinephrine, norepinephrine, and clonidine) or nonadrenergic vasoconstrictors (vasopressin). Effects of infusion of specific adrenergic receptor blockers (propranolol, prazosin, and yohimbine) with hexamethonium and catecholamines and infusion of various membrane ion channel blockers on VLF fluctuations in BP were also evaluated. Our results are as follows. 1) Ganglionic blockade drastically reduced BP levels and VLF fluctuations. 2) All vasoconstrictors restored BP levels, but only adrenergic vasoconstrictors generated striking VLF fluctuations in BP. 3) Catecholamine-induced fluctuations were abolished by alpha2-, but not alpha1- or beta-, adrenergic receptor blockade and by Ba2+-sensitive K+ channel or L-type Ca2+ channel, but not by other ion channel, blockers. We conclude that, in the conscious, unrestrained ganglion-blocked rat, catecholamine infusion generates VLF fluctuations in BP through stimulation of alpha2-receptors and activation of Ba2+-sensitive K+ channels. These fluctuations may have (patho)physiological relevance under conditions of disrupted circulatory homeostasis.

Blood pressure-renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats

“…The BP power at the heartbeat frequency was then calculated within a frequency range centered at the peak between 4 and 8 Hz with its edges defined by the points where the spectral density drops to 1% of the maximum power (27). These frequency bins were selected on the basis of our previous study (27) and their inclusion of various cardiovascular regulatory components (e.g., respiratory, Meyer waves, and myogenic activity) that have been suggested to contribute to BP oscillations (53,72).…”

“…Interestingly, whereas ANG II increased LF BP power, PE administration led to reduced BP power in this range. Fluctuations in the Meyer waves (ϳ0.1 Hz) and that due to the myogenic mechanism of RBF autoregulation (ϳ0.25 Hz) are thought to operate within this frequency band (53,72). Thus, despite the relatively modest effects of PE on MAP (DC BP power), it had a more potent effect on AC BP power compared with ANG II.…”

Components of arterial systolic pressure and RR-interval oscillation spectra in a case of baroreflex failure, a human open-loop model of vascular control

“…31 VLF in blood pressure was related to increased plasma epinephrine levels in sympathectomized rats and catecholamine infusion generated VLF fluctuations in blood pressure, suggesting an adrenergic origin of VLF. 32 Possibly, the unrestrained central rhythms observed in our case in presence of damage of the baroreflex arc may be linked to the central sympathetic outflow. This interpretation of our data is in agreement with the anatomical finding of destruction of sympathetic inhibitory centers (nucleus tractus solitarii) with sparing of centers that exert a positive modulation on the sympathetic tone described in a patient with baroreflex failure due to central nervous system lesions.…”

Role of Beta-Adrenoceptors in Cooling-Evoked Hemodynamic Perturbations of Rats: Investigation by Spectral Analysis

“…Therefore, the efferent sympathetic discharges (oscillations) were activated as LF BPV power was enhanced (Figure 3-right lower panel: PreCS) by reducing the afferent input of arterial and cardiopulmonary baroreceptors. Consequently, the secretion of epinephrine from adrenal medulla might be upraised and further increased the VLF BPV power (Figure 3-right upper panel: PreCS) [21]. Second, we assumed that skin and muscle vessels their α-ADRs were activated because of β2-ADRblocking effects and/or sympathetic activation due to the inotropicblocking effect of PRO.…”

“…Nevertheless, our data here demonstrated an attenuation of PRO effects on the spectral power of VLF BPV . Since VLF BPV is known to represent vasculomyogenic oscillations and sympathetic activation is important for generating this power [11,[13][14][15]21], in addition, the cooling-induced vasculomyogenic activation is noted depending on peripheral α2-ADR tone [15], we consider in this study, therefore, a weak attenuation of PRO on VLF BPV indicates an example of how VLF BPV is governed by activations of ADRs [21], in which β-ADR is not the key factor.…”