Effect of nitric oxide on prolactin secretion and hypothalamic biogenic amine contents

Lafuente, A.; González-Carracedo, A.; Romero, Alejandro; Cano, Pilar; Esquifino, Ana I.

doi:10.1016/j.lfs.2003.09.041

Cited by 17 publications

(12 citation statements)

References 31 publications

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“…A decrease in renin would in turn reduce activation of the angiotensin conversion pathways with potential reductions in angiotensin II (AII) related decreases in endothelial NO bioavailability [79, 87, 96]. Prolactin secretion from the pituitary is enhanced in the presence of estrogen [28, 42, 64]. However, once in the circulation, the prolactin metabolite, 16K-prolactin, inhibits eNOS [30, 63].…”

Section: Introductionmentioning

confidence: 99%

Hormonal modulation of endothelial NO production

Duckles

Miller

2010

Pflugers Arch - Eur J Physiol

138

106

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Since the discovery of endothelium-derived relaxing factor and the subsequent identification of nitric oxide (NO) as the primary mediator of endothelium-dependent relaxations, research has focused on chemical and physical stimuli that modulate NO levels. Hormones represent a class of soluble, widely circulating chemical factors that impact production of NO both by rapid effects on the activity of endothelial nitric oxide synthase (eNOS) through phosphorylation of the enzyme and longer term modulation through changes in amount of eNOS protein. Hormones that increase NO production including estrogen, progesterone, insulin, and growth hormone do so through both of these common mechanisms. In contrast, some hormones, including glucocorticoids, progesterone, and prolactin, decrease NO bioavailability. Mechanisms involved include binding to repressor response elements on the eNOS gene, competing for co-regulators common to hormones with positive genomic actions, regulating eNOS co-factors, decreasing substrate for eNOS, and increasing production of oxygenderived free radicals. Feedback regulation by the hormones themselves as well as the ability of NO to regulate hormonal release provides a second level of complexity that can also contribute to changes in NO levels. These effects on eNOS and changes in NO production may contribute to variability in risk factors, presentation of and treatment for cardiovascular disease associated with aging, pregnancy, stress, and metabolic disorders in men and women.

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Section: Introductionmentioning

confidence: 99%

Hormonal modulation of endothelial NO production

Duckles

Miller

2010

Pflugers Arch - Eur J Physiol

138

106

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“…В настоящее время накоплены убедительные дан-ные о том, что ингибитором выработки пролактина, кроме дофамина, γ-аминомасляной кислоты, сомато-статина, является оксид азота [25], -эндотелий-зави-симый расслабляющий фактор. Оксид азота блокирует периодическую секрецию пролактина у ненаркоти-зированных взрослых свободно содержащихся крыс.…”

Section: пролактин и эндотелиальная дисфункцияunclassified

“…Оксид азота блокирует периодическую секрецию пролактина у ненаркоти-зированных взрослых свободно содержащихся крыс. Блокатор синтазы оксида азота N(омега)-нитро-L-аргинин-метилэфир увеличил средний уровень про-лактина в плазме по сравнению с контролем, повысил содержание дофамина и серотонина в переднем ги-поталамусе; в срединном возвышении введение этого вещества снизило содержание дофамина и серотонина по сравнению с контролем [25].…”

Section: пролактин и эндотелиальная дисфункцияunclassified

The role of prolactin in the development of hypertension and metabolic syndrome in children

Каладзе¹,

Lychkova²,

Ревенко³

et al. 2016

Ross. vestn. perinatol. pediatr.

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Каладзе Н.Н. и соавт. Роль пролактина в формировании артериальной гипертензии и метаболического синдрома у детей РОССИЙСКИЙ ВЕСТНИК ПЕРИНАТОЛОГИИ И ПЕДИАТРИИ, 3, 2016 ROSSIYSKIY VESTNIK PERINATOLOGII I PEDIATRII, 3, 2016 © Коллектив авторов, 2016 Ros Vestn Perinatol Pediat 2016 3:31-39 DOI: 10.21508/1027 3:31-39 DOI: 10.21508/ -4065-2016 Адрес для корреспонденции: Каладзе Николай Николаевич -д. м. н., проф., зав. кафедрой педиатрии, физиотерапии и курортологии Меди-цинской академии имени С.И. Георгиевского Ревенко Наталья Анатольевна -к. м. н., асс. той же кафедры Юрьева Алла Викторовна -к. м. н., асс. той же кафедры 95006 Симферополь, бул. Ленина, д. 5/7 Лычкова Алла Эдуардовна -д.м.н., зав. лабораторией клинической фи-зиологии Центрального НИИ гастроэнтерологии 777123 Москва, шоссе Энтузиастов, д. 86 The review of literature analyzes the results of the current scientific works highlighting the role of prolactin in the body's metabolic processes and its effect on the cardiovascular system.

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“…The toxic effects of cadmium in the testis include necrosis, hemorrhage, and sterility in rats (Cameron and Foster 1963;Gunn and Gould 1970a;Nordberg 1971;Parizek and Zahor 1956) and humans (see Table 2). Its possible mechanisms of action include disruption of (1) Leydig cell function (Gunnarsson et al 2003;Laskey and Phelps 1991), (2) the hypothalamic-pituitary-testicular hormonal axis (Lafuente and Esquifino 1999;Lafuente et al 1997Lafuente et al , 2001Lafuente et al , 2004, (3) spermiation (Hew et al 1993a), (4) the BTB, and (5) the endothelial tight junctions (TJs) of blood vessels in the testis (Aoki and Hoffer 1978;Gouveia 1988;Setchell and Waites 1970), as well as (6) induction of germ cell apoptosis (Xu et al 1996;Zhou et al 1999).…”

Section: Introductionmentioning

confidence: 99%