Literature DB >> 15498809

Augmented sympathetic vasoconstriction in exercising forearms of postmenopausal women is reversed by oestrogen therapy.

Paul J Fadel1, Zhongyun Wang, Hitoshi Watanabe, Debbie Arbique, Wanpen Vongpatanasin, Gail D Thomas.   

Abstract

Sympathetic vasoconstriction is normally attenuated in exercising muscles of young men and women. Recent evidence indicates that such modulation, termed functional sympatholysis, may be impaired in older men. Whether a similar impairment occurs in older women, and what role oestrogen deficiency might play in this impairment, are not known. Based on the strong positive correlation between circulating oestrogen levels and functional sympatholysis previously reported in female rats, we hypothesized that sympatholysis would be impaired in oestrogen-deficient postmenopausal women, and that this impairment would be reversed by oestrogen replacement. To test these hypotheses, we measured vasoconstrictor responses in the forearms of pre- and postmenopausal women using near infrared spectroscopy to detect decreases in muscle oxygenation in response to reflex activation of sympathetic nerves evoked by lower body negative pressure (LBNP). In eight premenopausal women, LBNP decreased muscle oxygenation by 20 +/- 1% in resting forearm, but only by 3 +/- 2% in exercising forearm (P < 0.05). In contrast, in eight postmenopausal women, LBNP decreased muscle oxygenation by 15 +/- 3% in resting forearm, and by 12 +/- 4% in exercising forearm (P > 0.05). After 1 month of transdermal oestradiol replacement in these women, the normal effect of exercise to blunt sympathetic vasoconstriction was restored (rest, -19 +/- 3%; exercise, -2 +/- 3%; P < 0.05). These data indicate that functional sympatholysis is impaired in oestrogen-deficient postmenopausal women. The effect of short-term unopposed oestrogen replacement to correct this impairment implicates a role for oestrogen in the sympathetic neural control of muscle haemodynamics during exercise.

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Year:  2004        PMID: 15498809      PMCID: PMC1665388          DOI: 10.1113/jphysiol.2004.073619

Source DB:  PubMed          Journal:  J Physiol        ISSN: 0022-3751            Impact factor:   5.182


  44 in total

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3.  Endothelial dysfunction and oxidative stress during estrogen deficiency in spontaneously hypertensive rats.

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4.  Postmenopausal estrogen administration suppresses muscle sympathetic nerve activity.

Authors:  G Weitz; M Elam; J Born; H L Fehm; C Dodt
Journal:  J Clin Endocrinol Metab       Date:  2001-01       Impact factor: 5.958

5.  Transdermal estrogen replacement therapy decreases sympathetic activity in postmenopausal women.

Authors:  W Vongpatanasin; M Tuncel; Y Mansour; D Arbique; R G Victor
Journal:  Circulation       Date:  2001-06-19       Impact factor: 29.690

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Journal:  J Physiol       Date:  2002-04-01       Impact factor: 5.182

9.  Functional muscle ischemia in neuronal nitric oxide synthase-deficient skeletal muscle of children with Duchenne muscular dystrophy.

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  37 in total

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Review 3.  Regulation of skeletal muscle blood flow during exercise in ageing humans.

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Review 4.  Regulation of increased blood flow (hyperemia) to muscles during exercise: a hierarchy of competing physiological needs.

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Review 5.  Impact of sex hormone metabolism on the vascular effects of menopausal hormone therapy in cardiovascular disease.

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6.  Impaired modulation of postjunctional α1 - but not α2 -adrenergic vasoconstriction in contracting forearm muscle of postmenopausal women.

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Journal:  J Physiol       Date:  2018-05-30       Impact factor: 5.182

7.  Respiratory muscle blood flow during exercise: Effects of sex and ovarian cycle.

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8.  Modulation of postjunctional α-adrenergic vasoconstriction during exercise and exogenous ATP infusions in ageing humans.

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9.  Exercise training modulates functional sympatholysis and α-adrenergic vasoconstrictor responsiveness in hypertensive and normotensive individuals.

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Review 10.  New insights into the effects of age and sex on arterial baroreflex function at rest and during dynamic exercise in humans.

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