ABSTRACT
BACKGROUND: Excess visceral fat is a major risk factor for hypertension. Enhanced blood pressure (BP) reactivity and delayed BP recovery from physical and mental challenges predict future hypertension. OBJECTIVES: Determine whether visceral fat is associated with higher BP reactivity and delayed BP recovery from physical and mental challenges during adolescence. METHODS: In a community-based sample of 283 male and 308 female adolescents, we measured visceral fat with magnetic resonance imaging, total body fat with bioimpedance, and beat-by-beat BP with a Finometer at rest and during physical (10-min standing) and mental (2-min math stress) challenges. RESULTS: Males vs. females showed greater BP reactivity and no differences in BP recovery from either type of challenges. Visceral fat was positively associated with BP reactivity to standing up only and in males only (+8.4 ± 3.6 mmHg per 1 log cm(3) of visceral fat, P = 0.008), and this association was independent of total body fat. No association was seen between visceral fat and BP recovery from either type of challenge in either sex. All these associations were independent of age, puberty stage, height and initial BP. CONCLUSIONS: Adolescent males vs. females demonstrate greater BP reactivity but similar BP recovery from physical and mental challenges. Excess visceral fat enhances BP reactivity to physical but not mental challenges in males only.
Subject(s)
Blood Pressure , Hypertension/physiopathology , Intra-Abdominal Fat/physiopathology , Adolescent , Body Fat Distribution , Female , Humans , Intra-Abdominal Fat/metabolism , Male , Quebec/epidemiology , Risk Factors , Sex Factors , Surveys and Questionnaires , Task Performance and AnalysisABSTRACT
To determine the role of neuronal potassium conductance in rapid-eye-movement (REM)-sleep homeostasis, we have administered small doses of apamin (2-5 ng), a selective blocker of the calcium-dependent SK potassium channel, injected into the lateral ventricle in rats, and characterized the resultant effects on REM-sleep expression. Apamin produces a dose-dependent reduction in REM-sleep expression without an increase in the frequency of attempts to enter REM sleep, suggesting that accumulation of REM-sleep propensity is suppressed. The vast majority (84-95%) of lost REM sleep is not recovered 40 h after apamin administration. These findings suggest that accumulation of REM-sleep propensity is linked to the increased neuronal potassium conductance in nonREM sleep.
Subject(s)
Apamin/pharmacology , Potassium Channels/metabolism , Sleep, REM/drug effects , Animals , Behavior, Animal/drug effects , Dose-Response Relationship, Drug , Electrodes , Electroencephalography/drug effects , Injections, Intraventricular , Male , Polysomnography , Potassium Channels/drug effects , Rats , Rats, WistarABSTRACT
Two-hour, highly-selective, rest-period, rapid-eye-movement (REM)-sleep deprivation (RD) was performed on rats to characterize the time-course of the homeostatic response to REM-sleep loss. RD caused a dramatic and progressive increase in the frequency of attempts to enter REM sleep, suppressed non-REM sleep EEG delta power, and (in late rest period trials) was followed by a rebound increase in REM-sleep expression.
Subject(s)
Rest/physiology , Sleep Deprivation/physiology , Sleep, REM/physiology , Animals , Arousal/physiology , Electric Stimulation , Electroencephalography , Fourier Analysis , Male , Raphe Nuclei/physiology , Rats , Rats, WistarABSTRACT
The synthesis and labelling of a new bis-amide-oxime ligand E,E-2,9-bis(hydroxyimino)-4,7-diaza 5,6-dioxodecane (AdO) with 99mTc has been achieved. Protein binding, partition coefficient and tissue distribution of this complex and two related bis-amine-oxime ligands is reported. The biodistribution of the complexes are disappointing with only limited brain and myocardial uptake. Structures for the complex are postulated.
Subject(s)
Isotope Labeling/methods , Organotechnetium Compounds/chemical synthesis , Oximes/chemical synthesis , Technetium/chemistry , Animals , Electrophoresis, Paper , Male , Mice , Mice, Inbred BALB C , Organotechnetium Compounds/pharmacokinetics , Oximes/pharmacokinetics , Protein Binding , Serum Albumin, Bovine/metabolism , Tissue DistributionABSTRACT
A computer model of blood plasma which has allowed the effect of Gd(III) contrast agents to be simulated has been developed. Initial binding of Gd(III) is to transferrin. At high concentration the metal ion binds to citrate and salicylate. At a concentrate of 10(-3) M, GdCl3 is predicted to effect a redistribution of the in vivo Zn(II), Ca(II), and Fe(II) complexes present in blood plasma. There is little effect on the Cu(II) distribution. At a concentration below 10(-5) M EDTA and DTPA have little effect on the free Gd(III) metal ion concentration. Above this concentration though, the metal ion is bound almost exclusively to the EDTA or DTPA. An attempt is made to relate the toxicity of GdCl3, [Gd(EDTA)]-, and [Gd(DTPA)]2- to the thermodynamic stability of these complexes. The effect of substitution kinetics is also discussed.
