β-Adrenergic-mediated vasodilation in young men and women: cyclooxygenase restrains nitric oxide synthase

Limberg, Jacqueline K.; Johansson, Rebecca; Peltonen, Garrett L.; Harrell, John W.; Kellawan, J. Mikhail; Eldridge, Marlowe W.; Sebranek, Joshua J.; Schrage, William G.

doi:10.1152/ajpheart.00886.2015

Cited by 22 publications

(28 citation statements)

References 40 publications

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“…This is supported by a similar pattern of response observed in human conduit artery in vivo (Limberg et al . ). Furthermore, although not β‐adrenergic cutaneous vasodilatation, the COX‐dependent limiting effect on cutaneous perfusion has also been observed during (1) the reactive hyperaemia observed following a period of arterial occlusion of the forearm in young adults (Medow et al .…”

Section: Discussionmentioning

confidence: 97%

“…Secondly, NOS‐ and COX‐dependent mechanisms involved in β‐adrenergic forearm vasodilatation have been shown to differ between males and females (Limberg et al . ). Thus, there may be sex‐related differences in the underlying mechanism(s) associated with β‐adrenergic cutaneous vasodilatation and possibly sweating.…”

Section: Discussionmentioning

confidence: 97%

“…Furthermore, a recent study by Limberg et al . () demonstrated that COX activation has an opposing effect by restraining β‐adrenergic vasodilatation in the human forearm conduit artery. These responses may remain intact in cutaneous vasculature.…”

Section: Introductionmentioning

confidence: 99%

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Nitric oxide synthase and cyclooxygenase modulate β‐adrenergic cutaneous vasodilatation and sweating in young men

Fujii

McNeely

Kenny

2016

The Journal of Physiology

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Key pointsr β-Adrenergic receptor agonists such as isoproterenol induce cutaneous vasodilatation and sweating in humans, but the mechanisms underpinning this response remain unresolved.r Using intradermal microdialysis, we evaluated the roles of nitric oxide synthase (NOS) and cyclooxygenase (COX) in β-adrenergic cutaneous vasodilatation and sweating elicited by administration of isoproterenol.r We show that while NOS contributes to β-adrenergic cutaneous vasodilatation, COX restricts cutaneous vasodilatation.r We also show that combined inhibition of NOS and COX augments β-adrenergic sweating r These new findings advance our basic knowledge regarding the physiological control of cutaneous blood flow and sweating, and provide important and new information to better understand the physiological significance of β-adrenergic receptors in the skin.Abstract β-Adrenergic receptor agonists such as isoproterenol can induce cutaneous vasodilatation and sweating in humans, but the mechanisms underpinning this response remain unresolved. We evaluated the hypotheses that (1) nitric oxide synthase (NOS) contributes to β-adrenergic cutaneous vasodilatation, whereas cyclooxygenase (COX) limits the vasodilatation, and (2) COX contributes to β-adrenergic sweating. In 10 young males (25 ± 5 years), cutaneous vascular conductance (CVC) and sweat rate were evaluated at four intradermal forearm skin sites infused with (1) lactated Ringer solution (control), (2) 10 mM N ω -nitro-L-arginine (L-NNA), a non-specific NOS inhibitor, (3) 10 mM ketorolac, a non-specific COX inhibitor, or (4) a combination of L-NNA and ketorolac. All sites were co-administered with a high dose of isoproterenol (100 μM) for 3 min to maximally induce β-adrenergic sweating (β-adrenergic sweating is significantly blunted by subsequent activations). Approximately 60 min after the washout period, three incremental doses of isoproterenol were co-administered (1, 10 and 100 μM each for 25 min). Increases in CVC induced by the first and second 100 μM isoproterenol were attenuated by L-NNA alone, and those in response to all doses of isoproterenol were reduced by L-NNA with co-infusion of ketorolac (all P ࣘ 0.05). Ketorolac alone augmented increases in CVC induced by 10 μM and by the second 100 μM isoproterenol (both P ࣘ 0.05). While isoproterenol-induced sweating was not affected by the separate administration of L-NNA or ketorolac (all P > 0.05), their combined administration augmented sweating elicited by the first 3 min of 100 μM isoproterenol (P = 0.05). We show that while NOS contributes to β-adrenergic cutaneous vasodilatation, COX restrains the vasodilatation. Finally, combined inhibition of NOS and COX augments β-adrenergic sweating.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 97%

See 1 more Smart Citation

Nitric oxide synthase and cyclooxygenase modulate β‐adrenergic cutaneous vasodilatation and sweating in young men

Fujii

McNeely

Kenny

2016

The Journal of Physiology

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“…57 As such, infusion of the selective a 1 agonist, phenylephrine elicits, greater vasoconstriction during the luteal phase than during menstruation, 58 but b-mediated vasodilation is also higher in this phase. 32,59 These changes in adrenergic sensitivity could be seen as a regulatory mechanism counterbalancing the cyclic variations in endothelin-1 and NO production. Interestingly, infusion of the selective a 2 agonist, clonidine, elicits a greater vasoconstrictive response during the early follicular phase, 58 suggesting that a 1 sensitivity and a 2 sensitivity are regulated in opposite directions during the cycle.…”

Section: The Effect Of Cyclic Variation In Plasma Estrogen On Vascumentioning

confidence: 99%

“…However, the vascular transduction (vasoconstriction for a given MSNA level) and total systemic resistance remain lower when estrogen is high which is likely the effect of variations at the adrenergic receptor level that result in a balanced vascular transduction . As such, infusion of the selective α 1 agonist, phenylephrine elicits, greater vasoconstriction during the luteal phase than during menstruation, but β‐mediated vasodilation is also higher in this phase . These changes in adrenergic sensitivity could be seen as a regulatory mechanism counterbalancing the cyclic variations in endothelin‐1 and NO production.…”

Section: Introductionmentioning

confidence: 99%

Limb vascular function in women-Effects of female sex hormones and physical activity

Hellsten

Gliemann

2018

Transl Sports Med

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Throughout life, women are subjected to both acute fluctuations in sex hormones, associated with the menstrual cycle, and chronic changes following the onset of menopause. Female sex hormones, and in particular estrogen, strongly influence cardiovascular function such as the regulation of vascular tone and oxidative stress and thereby functions such as oxygen delivery and blood pressure. The acute hormonal fluctuations do not substantially impact health, but their influence should be considered with regard to measurements of vascular function. The chronic hormonal change with menopause strongly impacts the vasculature and markedly increases the risk of cardiovascular events. Physical activity activates signaling pathways also triggered by estrogen; therefore, exercise training could be an effective means of reducing the deleterious effects of estrogen loss at menopause. However, findings are divergent with some reporting marked improvements in vascular health with physical activity and others showing lower gains compared to age-matched males. Potential explanations for this discrepancy in findings are timing after menopause and training mode, aspects that should be further addressed in future studies. Physical activity should be recommended for women of all ages, but the most essential timing for maintenance of vascular health may be from menopause and onwards. K E Y W O R D Sblood vessel, estrogen, exercise, nitric oxide, prostacyclin | INTRODUCTIONFemale sex hormones, and in particular estrogen, are known to have numerous protective and functional roles in the vasculature including regulation of vasodilator systems, vascular growth, reduction in platelet reactivity, and vascular inflammation. 1,2 Alterations in the levels of sex hormones occur short term during the menstrual cycle and chronically at menopause with an almost complete loss of progesterone and estrogen. The chronic alterations in sex hormones at menopause greatly influence a number of aspects in women's health and substantially impact on the cardiovascular system resulting in impairment in vascular function 3,4 and a markedly increased prevalence of cardiovascular disease. 5 In this overview, we focus on how the short-term changes in sex hormones during the menstrual cycle and the chronic changes with menopause affect the vascular system in women. Focus lies primarily on basal regulation of vascular tone and the role of physical activity on the blood vessels supplying skeletal muscle tissue. After a brief overview of the physiology and molecular mechanisms underlying regulation of vascular tone, the influence of sex hormones is briefly addressed. We then discuss the effect of exercise and exercise training on vascular function during acute and chronic changes in female sex hormones, with an emphasis on estrogen. The main focus of this review was on humans but includes data from studies on laboratory animals and cell culture where relevant.

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Sex-differences in cholinergic, nicotinic, and β-adrenergic cutaneous vasodilation: Roles of nitric oxide synthase, cyclooxygenase, and K+ channels

Fujii

McGarr

Ghassa

et al. 2020

Microvascular Research

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β-Adrenergic-mediated vasodilation in young men and women: cyclooxygenase restrains nitric oxide synthase

Cited by 22 publications

References 40 publications

Nitric oxide synthase and cyclooxygenase modulate β‐adrenergic cutaneous vasodilatation and sweating in young men

Nitric oxide synthase and cyclooxygenase modulate β‐adrenergic cutaneous vasodilatation and sweating in young men

Limb vascular function in women-Effects of female sex hormones and physical activity

Sex-differences in cholinergic, nicotinic, and β-adrenergic cutaneous vasodilation: Roles of nitric oxide synthase, cyclooxygenase, and K+ channels

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