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Am J Physiol Heart Circ Physiol 290: H357-H364, 2006. First published September 2, 2005; doi:10.1152/ajpheart.00773.2005
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Adrenergic origin of very low-frequency blood pressure oscillations in the unanesthetized rat

Alberto Radaelli,3 Paolo Castiglioni,4 Marco Centola,1,2 Francesca Cesana,1,2 Giulia Balestri,1,2 Alberto U. Ferrari,1,2,3 and Marco Di Rienzo4

1Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, and 3Divisione di Riabilitazione Cardiologica, Ospedale San Gerardo, Monza; and 2Centro Interuniversitario di Fisiologia Clinica e Ipertensione, Università di Milano-Bicocca, and 4Centro di Bioingegneria, Fondazione Don Gnocchi, Milan, Italy

Submitted 21 July 2005 ; accepted in final form 15 August 2005

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 {alpha}2-, but not {alpha}1- 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 {alpha}2-receptors and activation of Ba2+-sensitive K+ channels. These fluctuations may have (patho)physiological relevance under conditions of disrupted circulatory homeostasis.

catecholamines; spectral analysis; ganglionic blockade; adrenergic receptors


Address for reprint requests and other correspondence: A. U. Ferrari, Centro Fisiologia Clinica e Ipertensione, Via F. Sforza, 35, 20122 Milan, Italy (e-mail: alberto.ferrari{at}unimib.it)




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