title: Persistence of circadian variation in arterial blood pressure in beta1/beta2-adrenergic receptor-deficient mice.
abstract: 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.affiliation: National Institute of Digestive and Diabetes and Kidney Diseases, NIH, Bethesda, MD 20892, USA.
authors.forename: Soo Mi
authors.initials: SM
authors.lastname: Kim
authors.forename: Yuning
authors.initials: Y
authors.lastname: Huang
authors.forename: Yan
authors.initials: Y
authors.lastname: Qin
authors.forename: Diane
authors.initials: D
authors.lastname: Mizel
authors.forename: Jurgen
authors.initials: J
authors.lastname: Schnermann
authors.forename: Josephine P
authors.initials: JP
authors.lastname: Briggs
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D002940:Circadian Rhythm / Q000502:physiology*; D004247:DNA / Q000235:genetics; D004656:Enalapril / Q000494:pharmacology; D005838:Genotype; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009043:Motor Activity / Q000187:drug effects / Q000235:genetics / Q000502:physiology; D018342:Receptors, Adrenergic, beta-1 / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D018343:Receptors, Adrenergic, beta-2 / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012982:Sodium, Dietary / Q000494:pharmacology; D013686:Telemetry
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D018342:Receptors, Adrenergic, beta-1; D018343:Receptors, Adrenergic, beta-2; D012982:Sodium, Dietary; D004656:Enalapril; D004247:DNA