Estrogen Replacement Increases &amp;beta;-Adrenoceptor-Mediated Relaxation of Rat Mesenteric Arteries

Ferrer, Mercedes; Meyer, Marjorie; Osol, George

doi:10.1159/000159140

Cited by 56 publications

(43 citation statements)

References 31 publications

(37 reference statements)

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“…Other studies, from two different vascular beds in Hx male rats, have demonstrated a decrease in NA sensitivity after GH supplementation (24,27). However, those results might reflect b-adrenergic effects of GH, since in the present study, propranolol was present during all NA experiments avoiding any influence of E 2 on b-adrenergic relaxation (28). Oestrogen treatment has been shown to increase both the a-adrenergic receptor affinity (29) and the a-1 adrenoceptor population (30) in different vascular beds.…”

Section: Discussioncontrasting

confidence: 54%

Interactive effects of growth hormone and oestrogen on vascular responses in hypophysectomised female rats

Gustafsson

Tordby²,

Brandin³

et al. 2002

European Journal of Endocrinology

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Objective: Growth hormone (GH) and oestrogen (E 2 ) are associated with beneficial effects on the cardiovascular system and it is therefore of great interest to study their interactive effects on haemodynamics and vascular function. Design and Methods: Female hypophysectomised (Hx) rats were treated for seven days with GH, E 2 or a combination of the hormones. Systolic blood pressure (SBP), heart rate (HR) and plasma insulin-like growth factor-I (IGF-I) were measured. Contractile properties and endothelial function were studied in isolated resistance arteries using the wire-myograph technique. Results: Hypophysectomy, per se, caused a fall in SBP and HR, while vascular adrenergic reactivity (sensitivity to applied noradrenaline) was enhanced. Impaired acetylcholine-induced relaxation and basal release of nitric oxide, suggests endothelial dysfunction after Hx. After supplementation with GH, SBP remained low while HR increased towards the control level. GH increased plasma IGF-I, but had no effect on vascular contractility or endothelial responses. E 2 replacement resulted in blunted plasma IGF-I, while the vascular adrenergic and serotonergic responses were reinforced. Endothelial function was not improved after E 2 treatment. When GH and E 2 were given in combination, the GH-induced increase in body weight, plasma IGF-I levels and HR were counteracted by E 2 . Moreover, the anticipated reinforcement of the vascular serotonergic response by E 2 was reduced. Neither E 2 nor GH+E 2 affected SBP. Conclusions:The results suggest that GH and E 2 might have interactive effects on haemodynamic and metabolic parameters, but not on the contractility or endothelial function of resistance arteries, in Hx female rats.

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Section: Discussioncontrasting

confidence: 54%

Interactive effects of growth hormone and oestrogen on vascular responses in hypophysectomised female rats

Gustafsson

Tordby²,

Brandin³

et al. 2002

European Journal of Endocrinology

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“…However, because these studies either studied women under low hormone conditions (15) or did not control for menstrual cycle phase (13,25), these sex differences cannot be attributed to estrogen and/or progesterone. In ovariectomized rats, estrogen supplementation has been documented to increase ␤-adrenergic sensitivity (12). However, this effect would produce the opposite results from what we observed (a blunting of the fall in FVC in response to neck pressure instead Values are F(p).…”

Section: Discussioncontrasting

confidence: 67%

Short-term administration of progesterone and estradiol independently alter carotid-vasomotor, but not carotid-cardiac, baroreflex function in young women

Brunt

Miner

Kaplan

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Brunt VE, Miner JA, Kaplan PF, Halliwill JR, Strycker LA, Minson CT. Short-term administration of progesterone and estradiol independently alter carotid-vasomotor, but not carotid-cardiac, baroreflex function in young women. Am J Physiol Heart Circ Physiol 305: H1041-H1049, 2013. First published July 19, 2013 doi:10.1152/ajpheart.00194.2013.-The individual effects of estrogen and progesterone on baroreflex function remain poorly understood. We sought to determine how estradiol (E 2) and progesterone (P 4) independently alter the carotid-cardiac and carotid-vasomotor baroreflexes in young women by using a hormone suppression and exogenous add-back design. Thirty-two young women were divided into two groups and studied under three conditions: 1) after 4 days of endogenous hormone suppression with a gonadotropin releasing hormone antagonist (control condition), 2) after continued suppression and 3 to 4 days of supplementation with either 200 mg/day oral progesterone (N ϭ 16) or 0.1 to 0.2 mg/day transdermal 17␤-estradiol (N ϭ 16), and 3) after continued suppression and 3 to 4 days of supplementation with both hormones. Changes in heart rate (HR), mean arterial pressure (MAP), and femoral vascular conductance (FVC) were measured in response to 5 s of ϩ50 mmHg external neck pressure to unload the carotid baroreceptors. Significant hormone effects on the change in HR, MAP, and FVC from baseline at the onset of neck pressure were determined using mixed model covariate analyses accounting for P 4 and E2 plasma concentrations. Neither P4 (P ϭ 0.95) nor E2 (P ϭ 0.95) affected the HR response to neck pressure. Higher P 4 concentrations were associated with an attenuated fall in FVC (P ϭ 0.01), whereas higher E 2 concentrations were associated with an augmented fall in FVC (P ϭ 0.02). Higher E 2 was also associated with an augmented rise in MAP (P ϭ 0.01). We conclude that progesterone blunts whereas estradiol enhances carotidvasomotor baroreflex sensitivity, perhaps explaining why no differences in sympathetic baroreflex sensitivity are commonly reported between low and high combined hormone phases of the menstrual cycle. menstrual cycle; hormones; estrogen; arterial baroreceptors; blood pressure BOTH THE CARDIOVAGAL AND SYMPATHETIC branches of the baroreflex are important for the short-term control of blood pressure. Clear differences in cardiovagal and sympathetic baroreflex sensitivity have been documented between men and women (1,2,26,42,43), and women experience higher rates of orthostatic hypotension compared with men (7, 32, 39). Furthermore, the incidence of hypertension and cardiovascular disease is greatly increased in woman after menopause (23). These data provide evidence that the female sex hormones, estrogen and progesterone, influence the cardiovascular system; however, these influences are still poorly understood.In young women, the cardiovascular effects of the female sex hormones have predominantly been studied across the natural menstrual cycle. The majority of studies have found no differences in both ...

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“…In this context, Ferrer et al (1996) demonstrated that oestrogen supplementation in ovariectomised rats increased isoproterenol (isoprenaline)-mediated relaxation in the rat mesenteric arteries. This response was abolished when propranolol was infused.…”

Section: Resting Blood Pressure Regulation and The β-Adrenergic Recepmentioning

confidence: 99%

Sex and ageing differences in resting arterial pressure regulation: the role of the β‐adrenergic receptors

Hart¹,

Charkoudian

Wallin

et al. 2011

The Journal of Physiology

281

301

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Non-technical summary In young men, sympathetic nerve activity is directly related to the level of vasoconstrictor tone in the peripheral vasculature. However, in young women this relationship does not exist, suggesting that certain factors (potentially related to the female sex hormones) offset the transfer of sympathetic nerve activity into vasoconstrictor tone in this population. In the present study we show that, in young women, the β-adrenergic receptors (which cause vasodilatation in response to noradrenaline) blunt the vasoconstrictor effect of resting sympathetic nerve activity in young women. This mechanism does not occur in young men or postmenopausal women. It is possible that the β-adrenergic receptors may partially protect young women against the sometimes harmful effects of high sympathetic nerve activity. This may explain why the risk of developing hypertension is greater in young men and postmenopausal women (who have very high sympathetic nerve activity) compared to young women.Abstract In men, muscle sympathetic nerve activity (MSNA) is positively related to total peripheral resistance (TPR) and inversely related to cardiac output (CO). However, this relationship was not observed in young women. We aimed to investigate whether simultaneous β-adrenergic stimulation offsets this balance in young women. Furthermore, we aimed to examine whether the ability of the β-adrenergic receptors to offset the transduction of MSNA into vasoconstrictor tone was lost in postmenopausal women. We measured MSNA (peroneal microneurography), arterial pressure (brachial line), CO (Modelflow), TPR and changes in forearm vascular conductance (FVC) to increasing doses of noradrenaline (NA; 2, 4 and 8 ng (100 ml) −1 min −1 ) before and after systemic β-blockade with propranolol in 17 young men, 17 young women and 15 postmenopausal (PM) women. The percentage and absolute change in FVC to the last two doses of NA were greater during β-blockade in young women (P < 0.05), whereas the change in FVC was similar before and during β-blockade in young men and PM women (P > 0.05). Before β-blockade there was no relationship of MSNA to TPR or mean arterial pressure (MAP) in young women. Following β-blockade, MSNA became positively related to TPR (r = 0.59, P < 0.05) and MAP (r = 0.58, P < 0.05). In the PM women and young men, MSNA was positively associated with TPR. β-Blockade had no effect on this relationship. Our data suggest that the β-adrenergic receptors offset α-adrenergic vasoconstriction in young women but not young men or PM women. These findings may explain in part the tendency for blood pressure to rise after menopause in women.

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Estrogen Replacement Increases β-Adrenoceptor-Mediated Relaxation of Rat Mesenteric Arteries

Cited by 56 publications

References 31 publications

Interactive effects of growth hormone and oestrogen on vascular responses in hypophysectomised female rats

Interactive effects of growth hormone and oestrogen on vascular responses in hypophysectomised female rats

Short-term administration of progesterone and estradiol independently alter carotid-vasomotor, but not carotid-cardiac, baroreflex function in young women

Sex and ageing differences in resting arterial pressure regulation: the role of the β‐adrenergic receptors

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