Document Detail


Very low-frequency blood pressure variability depends on voltage-gated L-type Ca2+ channels in conscious rats.
MedLine Citation:
PMID:  17056668     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The mechanisms generating high- frequency (HF) and low-frequency (LF) blood pressure variability (BPV) are reasonably well understood. However, little is known about the origin of very low-frequency (VLF) BPV. We tested the hypothesis that VLF BPV is generated by L-type Ca(2+) channel-dependent mechanisms. In conscious rats, arterial blood pressure was recorded during control conditions (n = 8) and ganglionic blockade (n = 7) while increasing doses (0.01-5.0 mg.100 micro l(-1).h(-1)) of the L-type Ca(2+) channel blocker nifedipine were infused intravenously. VLF (0.02-0.2 Hz), LF (0.2-0.6 Hz), and HF (0.6-3.0 Hz) BPV were assessed by spectral analysis of systolic blood pressure. During control conditions, nifedipine caused dose-dependent declines in VLF and LF BPV, whereas HF BPV was not affected. At the highest dose of nifedipine, VLF BPV was reduced by 86% compared with baseline, indicating that VLF BPV is largely mediated by L-type Ca(2+) channel-dependent mechanisms. VLF BPV appeared to be relatively more dependent on L-type Ca(2+) channels than LF BPV because lower doses of nifedipine were required to significantly reduce VLF BPV than to reduce LF BPV. Ganglionic blockade markedly reduced VLF and LF BPV and abolished the nifedipine-induced dose-dependent declines in VLF and LF BPV, suggesting that VLF and LF BPV require sympathetic activity to be evident. In conclusion, VLF BPV is largely mediated by L-type Ca(2+) channel-dependent mechanisms. We speculate that VLF BPV is generated by myogenic vascular responses to spontaneously occurring perturbations of blood pressure. Other factors, such as sympathetic nervous system activity, may elicit a permissive effect on VLF BPV by increasing vascular myogenic responsiveness.
Authors:
Amanda M Langager; Bailey E Hammerberg; Diane L Rotella; Harald M Stauss
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-10-20
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  292     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2007 Mar 
Date Detail:
Created Date:  2007-03-06     Completed Date:  2007-04-26     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1321-7     Citation Subset:  IM    
Affiliation:
Dept of Integrative Physiology, The Univ of Iowa, Iowa City, IA 52242, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Pressure / physiology*
Calcium Channels, L-Type / physiology*
Consciousness
Heart / physiology,  physiopathology
Hypotension / physiopathology*
Male
Rats
Rats, Inbred WKY
Chemical
Reg. No./Substance:
0/Calcium Channels, L-Type

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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