Gender differences in the regulation of vascular tone
Identifieur interne : 000B75 ( Main/Exploration ); précédent : 000B74; suivant : 000B76Gender differences in the regulation of vascular tone
Auteurs : Janell Thompson [États-Unis] ; Raouf A. Khalil [États-Unis]Source :
- Clinical and Experimental Pharmacology and Physiology [ 0305-1870 ] ; 2003-01.
English descriptors
- KwdEn :
- Teeft :
- Androgen, Angiotensin, Aorta, Aortic, Aortic rings, Aortic strips, Arterial pressure, Basal, Blood pressure, Blood vessels, Bovine aortic, Canine, Cardiovasc, Cardiovascular, Cardiovascular disease, Cardiovascular diseases, Castrated, Cell contraction, Cell length, Cell physiol, Circ, Clin, Coronary, Coronary arteries, Coronary artery, Coronary artery disease, Coronary heart disease, Cytosolic, Doca rats, Endothelial, Endothelial cells, Endothelial dysfunction, Endothelial function, Endothelium, Enos, Entry mechanisms, Estradiol, Estrogen, Estrogen receptor, Estrogen replacement therapy, Extracellular, Female rats, Gender, Gender difference, Gender differences, Genomic, Genomic effects, Gonadal, Gonadal hormones, Greater incidence, Heart circ, Hormone, Hormone receptors, Hormone replacement therapy, Human umbilical vein, Hyperpolarization, Hypertens, Hypertension, Hypertensive, Hypertensive rats, Implant, Inhibitory effects, Intact females, Intact males, Intracellular, Intracoronary administration, Khalil, Kinase, Mesenteric, Mesenteric arteries, Mrna, Muscle cells, Muscle contraction, Myocardial ischaemia, Nitric, Nitric oxide, Nongenomic, Oestradiol, Oestrogen, Oestrogen implants, Oestrogen receptor, Oestrogen receptors, Oestrogen replacement, Other protein kinases, Other studies, Ovariectomized, Oxidative stress, Pathway, Pharmacol, Phorbol, Physiol, Physiological levels, Physiological nanomolar concentrations, Porcine, Possible role, Postmenopausal, Postmenopausal women, Premenopausal, Premenopausal women, Progesterone, Progestin, Protective effects, Protein kinase, Rat, Receptor, Relaxation, Replacement study, Risk factors, Sarrel, Signal transduction, Smooth muscle, Smooth muscle cells, Smooth muscle contraction, Steroid, Synthase, Testosterone, Testosterone receptors, Thromboxane, Uterine, Vascular, Vascular cells, Vascular contraction, Vascular effects, Vascular functions, Vascular reactivity, Vascular relaxation, Vascular strips, Vascular tone, Vasoconstriction, Vasodilation, Vasodilator.
Abstract
1. The greater incidence of hypertension and coronary artery disease in men and post‐menopausal women compared with premenopausal women has suggested vascular protective effects of the female sex hormone oestrogen. However, vascular effects of the female sex hormone progesterone and the male sex hormone testosterone have also been suggested. 2. Oestrogen, progesterone and testosterone receptors have been identified in the plasmalemma, cytosol and nuclear compartments of vascular cells. The interaction of sex hormones with their specific receptors triggers not only long‐term genomic vascular effects, but also acute non‐genomic vascular responses. 3. Sex hormones may activate endothelium‐dependent vascular relaxation pathways, including the nitric oxide–cGMP and prostacyclin–cAMP pathways and a hyperpolarizing factor pathway. 4. Sex hormones may also inhibit the mechanisms of vascular smooth muscle contraction, such as [Ca2+]i, protein kinase C and other protein kinases. 5. The sex hormone‐induced stimulation of endothelium‐dependent vascular relaxation and inhibition of vascular smooth muscle contraction may contribute to the gender differences in vascular tone and may represent potential beneficial vascular effects of hormone‐replacement therapy during natural and surgically induced deficiencies of gonadal hormones.
Url:
DOI: 10.1046/j.1440-1681.2003.03790.x
Affiliations:
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Le document en format XML
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<term>hypertension</term>
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<term>signal transduction</term>
<term>vascular smooth muscle</term>
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<keywords scheme="Teeft" xml:lang="en"><term>Androgen</term>
<term>Angiotensin</term>
<term>Aorta</term>
<term>Aortic</term>
<term>Aortic rings</term>
<term>Aortic strips</term>
<term>Arterial pressure</term>
<term>Basal</term>
<term>Blood pressure</term>
<term>Blood vessels</term>
<term>Bovine aortic</term>
<term>Canine</term>
<term>Cardiovasc</term>
<term>Cardiovascular</term>
<term>Cardiovascular disease</term>
<term>Cardiovascular diseases</term>
<term>Castrated</term>
<term>Cell contraction</term>
<term>Cell length</term>
<term>Cell physiol</term>
<term>Circ</term>
<term>Clin</term>
<term>Coronary</term>
<term>Coronary arteries</term>
<term>Coronary artery</term>
<term>Coronary artery disease</term>
<term>Coronary heart disease</term>
<term>Cytosolic</term>
<term>Doca rats</term>
<term>Endothelial</term>
<term>Endothelial cells</term>
<term>Endothelial dysfunction</term>
<term>Endothelial function</term>
<term>Endothelium</term>
<term>Enos</term>
<term>Entry mechanisms</term>
<term>Estradiol</term>
<term>Estrogen</term>
<term>Estrogen receptor</term>
<term>Estrogen replacement therapy</term>
<term>Extracellular</term>
<term>Female rats</term>
<term>Gender</term>
<term>Gender difference</term>
<term>Gender differences</term>
<term>Genomic</term>
<term>Genomic effects</term>
<term>Gonadal</term>
<term>Gonadal hormones</term>
<term>Greater incidence</term>
<term>Heart circ</term>
<term>Hormone</term>
<term>Hormone receptors</term>
<term>Hormone replacement therapy</term>
<term>Human umbilical vein</term>
<term>Hyperpolarization</term>
<term>Hypertens</term>
<term>Hypertension</term>
<term>Hypertensive</term>
<term>Hypertensive rats</term>
<term>Implant</term>
<term>Inhibitory effects</term>
<term>Intact females</term>
<term>Intact males</term>
<term>Intracellular</term>
<term>Intracoronary administration</term>
<term>Khalil</term>
<term>Kinase</term>
<term>Mesenteric</term>
<term>Mesenteric arteries</term>
<term>Mrna</term>
<term>Muscle cells</term>
<term>Muscle contraction</term>
<term>Myocardial ischaemia</term>
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<term>Nongenomic</term>
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<term>Oestrogen implants</term>
<term>Oestrogen receptor</term>
<term>Oestrogen receptors</term>
<term>Oestrogen replacement</term>
<term>Other protein kinases</term>
<term>Other studies</term>
<term>Ovariectomized</term>
<term>Oxidative stress</term>
<term>Pathway</term>
<term>Pharmacol</term>
<term>Phorbol</term>
<term>Physiol</term>
<term>Physiological levels</term>
<term>Physiological nanomolar concentrations</term>
<term>Porcine</term>
<term>Possible role</term>
<term>Postmenopausal</term>
<term>Postmenopausal women</term>
<term>Premenopausal</term>
<term>Premenopausal women</term>
<term>Progesterone</term>
<term>Progestin</term>
<term>Protective effects</term>
<term>Protein kinase</term>
<term>Rat</term>
<term>Receptor</term>
<term>Relaxation</term>
<term>Replacement study</term>
<term>Risk factors</term>
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<term>Signal transduction</term>
<term>Smooth muscle</term>
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<term>Smooth muscle contraction</term>
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<term>Synthase</term>
<term>Testosterone</term>
<term>Testosterone receptors</term>
<term>Thromboxane</term>
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<term>Vascular</term>
<term>Vascular cells</term>
<term>Vascular contraction</term>
<term>Vascular effects</term>
<term>Vascular functions</term>
<term>Vascular reactivity</term>
<term>Vascular relaxation</term>
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<term>Vascular tone</term>
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<front><div type="abstract" xml:lang="en">1. The greater incidence of hypertension and coronary artery disease in men and post‐menopausal women compared with premenopausal women has suggested vascular protective effects of the female sex hormone oestrogen. However, vascular effects of the female sex hormone progesterone and the male sex hormone testosterone have also been suggested. 2. Oestrogen, progesterone and testosterone receptors have been identified in the plasmalemma, cytosol and nuclear compartments of vascular cells. The interaction of sex hormones with their specific receptors triggers not only long‐term genomic vascular effects, but also acute non‐genomic vascular responses. 3. Sex hormones may activate endothelium‐dependent vascular relaxation pathways, including the nitric oxide–cGMP and prostacyclin–cAMP pathways and a hyperpolarizing factor pathway. 4. Sex hormones may also inhibit the mechanisms of vascular smooth muscle contraction, such as [Ca2+]i, protein kinase C and other protein kinases. 5. The sex hormone‐induced stimulation of endothelium‐dependent vascular relaxation and inhibition of vascular smooth muscle contraction may contribute to the gender differences in vascular tone and may represent potential beneficial vascular effects of hormone‐replacement therapy during natural and surgically induced deficiencies of gonadal hormones.</div>
</front>
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