Adrenergic Origin of Very Low-frequency Blood Pressure Oscillations in the Unanesthetized Rat.
From: Divisione de Riabilitazione Cardiologica, Ospedale San Gerardo, Monza, Italy.
American journal of physiology. Heart and circulatory physiology
- Publish Date: Jan 2006
- ISSN: 0363-6135
- Volume: 290
- Issue: 1
- Pages: H357-64
- Medium: Print
- Language: English
- Citation (JAMA): Radaelli Alberto, Castiglioni Paolo, Centola Marco, et al. Adrenergic Origin of Very Low-frequency Blood Pressure Oscillations in the Unanesthetized Rat.. Am. J. Physiol. Heart Circ. Physiol. Jan 2006;290:H357-64
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.
Mesh Headings (Keywords): Adrenergic Agonists, Adrenergic Antagonists, Animals, Arginine Vasopressin, Barium Sulfate, Blood Pressure, Calcium Channel Blockers, Consciousness, Epinephrine, Ganglionic Blockers, Hemodynamics, Hexamethonium, Losartan, Nifedipine, Norepinephrine, Potassium Channel Blockers, Prazosin, Propranolol, Rats, Rats, Inbred WKY, Receptors, Adrenergic, Vasoconstrictor Agents, Yohimbine
Check for Full Text / PubMed Unique Identifier (PMID): 16143647
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