Document Detail


Persistence of circadian variation in arterial blood pressure in beta1/beta2-adrenergic receptor-deficient mice.
MedLine Citation:
PMID:  18305025     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The beta-adrenergic pathway has been considered one important effector of circadian variation in arterial pressure. Experiments were performed in beta1/beta2-adrenergic receptor-deficient mice (beta1/beta2ADR-/-) to assess whether this pathway is required for circadian variation in mean arterial pressure (MAP) and to determine the impact of its loss on the response to changes in dietary salt. Twenty-four-hour recordings of MAP, heart rate (HR), and locomotor activity were made in conscious 16- to 17-wk-old mice [wild-type, (WT), n = 7; beta1/beta2ADR-/-, n = 10] by telemetry. Both WT and beta1/beta2ADR-/- mice demonstrated robust circadian variation in MAP and HR, although 24-h mean MAP was 10% lower (102.02 +/- 1.81 vs. 92.11 +/- 2.62 mmHg) in beta1/beta2ADR-/- than WT, HR was 16% lower and day-night differences reduced. Both WT and beta1/beta2ADR-/- mice adapted to changed salt intake without changed MAP. However, the beta1/beta2ADR-/- mice demonstrated a striking reduction in locomotor activity in light and dark phases of the day. In WT mice, MAP was markedly affected by locomotor activity, resulting in bimodal distributions in both light and dark. When MAP was analyzed using only intervals without locomotor activity, bimodality and circadian differences were reduced, and there was no significant difference between the two genotypes. The results indicate that there is no direct effect or role for the beta-adrenergic system in circadian variation of arterial pressure in mice, aside from the indirect consequences of altered locomotor activity. Our results also confirm that locomotor activity contributes strongly to circadian variation in blood pressure in mice.
Authors:
Soo Mi Kim; Yuning Huang; Yan Qin; Diane Mizel; Jurgen Schnermann; Josephine P Briggs
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural     Date:  2008-02-27
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  294     ISSN:  0363-6119     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2008 May 
Date Detail:
Created Date:  2008-05-02     Completed Date:  2008-06-18     Revised Date:  2013-06-05    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R1427-34     Citation Subset:  IM    
Affiliation:
National Institute of Digestive and Diabetes and Kidney Diseases, NIH, Bethesda, MD 20892, USA.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin-Converting Enzyme Inhibitors / pharmacology
Animals
Blood Pressure / physiology*
Circadian Rhythm / physiology*
DNA / genetics
Enalapril / pharmacology
Genotype
Heart Rate / drug effects,  physiology
Mice
Mice, Inbred C57BL
Mice, Knockout
Motor Activity / drug effects,  genetics,  physiology
Receptors, Adrenergic, beta-1 / deficiency,  genetics,  physiology*
Receptors, Adrenergic, beta-2 / deficiency,  genetics,  physiology*
Renin-Angiotensin System / drug effects,  physiology
Reverse Transcriptase Polymerase Chain Reaction
Sodium, Dietary / pharmacology
Telemetry
Grant Support
ID/Acronym/Agency:
Z01 DK043410-01/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 0/Receptors, Adrenergic, beta-1; 0/Receptors, Adrenergic, beta-2; 0/Sodium, Dietary; 75847-73-3/Enalapril; 9007-49-2/DNA
Comments/Corrections

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