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Sex Differences in Vascular Function

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Cardiovascular Neuroendocrinology

Part of the book series: Masterclass in Neuroendocrinology ((MANEURO,volume 14))

Abstract

Sex is an important biological variable that impacts several organism functions at the genetic, molecular, and cellular levels. Sex differences are observed in all components of the vascular system—vascular smooth muscle, endothelial, and adventitia cells—as well as in the mechanisms that control vascular function, including the nervous, cardiac, renal, immune, and hormonal systems. Sex differences are observed not only in health conditions but also in the course, outcome, and complications of many diseases, including cardiovascular disease. Arterial hypertension, as an example, has a higher incidence in men than in age-matched women up to the menopause, but its incidence is higher in postmenopausal women than in men at the same age. Sex differences in the cardiovascular system are either present throughout life or are apparent only in specific life periods, e.g., after puberty or post menopause, suggesting that both genes and sex hormones are involved. Sex differences contribute not only to variations in the incidence of cardiovascular disease but also to differential responses to pharmacological treatment in males and females. In this chapter, a brief overview of the sex differences in physiological mechanisms that control vascular function is provided. Special attention is given to sex differences in the endothelial and the perivascular adipose tissue (PVAT) function, and whenever possible, the role of chromosomes and sex hormones to sex differences in vascular (dys)function is also discussed. The impact of sex hormones in the vascular system of the transgender population and how this may influence clinical perspectives on hormonal protocols are also considered.

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Abbreviations

ACh:

acetylcholine

ADRF:

adventitia-derived relaxing factors

ANG1–7:

angiotensin 1–7

ANGII:

angiotensin II

AT1R:

subtype 1 angiotensin receptor

Ca2+:

calcium

CAD:

coronary artery disease

COX:

cyclooxygenase

DAMPs:

damage-associated molecular patterns

DEGs:

differentially expressed genes

EDHF:

endothelium-derived hyperpolarizing factors

eNOS:

endothelial nitric oxide synthase

ER:

estrogen receptors

ET-1:

endothelin-1

H2O2:

hydrogen peroxide

H2S:

hydrogen sulfide

HAEC:

human aortic endothelial cells

HIF-1α:

hypoxia-induced factor-1

HUVECs:

human umbilical vein endothelial cells

ICAM-1:

intercellular adhesion molecule-1

IFNγ:

interferon gamma

IL:

interleukin

IL-6R:

IL-6 receptor

miRNAs:

microRNAs

NF-κB:

nuclear factor kappa B

NO:

nitric oxide

NOS:

nitric oxide synthase

O2•-:

superoxide anion

OVX:

ovariectomy

PAMPs:

pathogen-associated molecular patterns

PDRF:

PVAT-derived relaxing factors

PGF2α:

prostaglandin F2α

PGI2:

prostacyclin

PVAT:

perivascular adipose tissue

RAAS:

renin–angiotensin–aldosterone system

ROS:

reactive oxygen species

SERM:

selective estrogen receptor modulators

SHR:

spontaneously hypertensive rats

SHRSP:

stroke-prone spontaneously hypertensive rats

SMCs:

smooth muscle cells

SNP:

sodium nitroprusside

TBARS:

thiobarbituric acid reactive substances

Th1:

T helper type 1 cells

Th17:

T helper type 1 cells

TLRs:

Toll-like receptors

TNFα:

tumor necrosis factor alpha

Treg:

regulatory T cells

TXA2:

thromboxane A2

VCAM-1:

vascular cell adhesion molecule-1

VEGF:

vascular endothelium growth factor

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Costa, T.J., Tostes, R.C. (2023). Sex Differences in Vascular Function. In: Yosten, G.L.C., Cunningham, J.T. (eds) Cardiovascular Neuroendocrinology. Masterclass in Neuroendocrinology, vol 14. Springer, Cham. https://doi.org/10.1007/978-3-031-39995-4_4

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