These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Attenuation of haemodynamic, metabolic and energy expenditure responses to isoproterenol in patients with hypertension.
    Author: Valentini M, Julius S, Palatini P, Brook RD, Bard RL, Bisognano JD, Kaciroti N.
    Journal: J Hypertens; 2004 Oct; 22(10):1999-2006. PubMed ID: 15361773.
    Abstract:
    OBJECTIVE: Overweight and heightened sympathetic activity are more common in hypertensive than normotensive subjects. beta-adrenoceptor down-regulation has been described in hypertension. We tested the hypothesis that chronic sympathetic overactivity impairs beta-adrenergic-mediated thermogenesis and thereby favours gain of weight in hypertension. PARTICIPANTS: The study included 13 hypertensive subjects aged 35.3 +/- 7.9 years and 25 normotensive subjects of control of similar age. METHODS: To measure beta-adrenergically mediated haemodynamic, metabolic and thermogenic responsiveness, increasing doses of isoproterenol diluted in 2.5 ml saline were injected as intravenous boluses (0.1, 0.25, 0.5, 1.0 and 2.0 microg/m). On a separate day, isoproterenol was infused continuously intravenously in increasing doses (10, 20 and 40 ng/kg per min), each dose for 30 min. RESULTS: The sitting heart rate and body mass were greater in hypertensives (P = 0.000, and P = 0.005, respectively). The heart rate responses to 1 and 2 microg/m isoproterenol bolus (P = 0.01 and P = 0.03, respectively) were reduced in hypertensives. The energy expenditure (P = 0.002) and oxygen consumption (P = 0.0004) increase with 40 ng/kg per min isoproterenol infusion, and glucose and phosphate responses at both 20 (P = 0.01 and P = 0.05) and 40 (P = 0.001 and P = 0.02) ng/kg per min isoproterenol infusion were attenuated in hypertensives. The baseline heart rate negatively correlated with heart rate (P = 0.015) response to isoproterenol bolus and blood pressure (P = 0.02) response to isoproterenol infusion. The urinary noradrenaline negatively correlated with heart rate response to isoproterenol bolus (P = 0.001), and with systolic blood pressure (P = 0.02) and energy expenditure responsiveness to isoproterenol infusion (P = 0.04). Furthermore, plasma noradrenaline negatively correlated with heart rate responsiveness to isoproterenol bolus (P = 0.004). CONCLUSIONS: These results show a generalized decrease of beta-adrenergic responsiveness in stage 1 hypertension and support the concept that sympathetic overactivity, via down-regulation of beta-adrenoceptor-mediated thermogenic responses, may facilitate the development of obesity in hypertension.
    [Abstract] [Full Text] [Related] [New Search]