Sex differences in central cholinergic and angiotensinergic control of vasopressin release

Stone, J. D.; Crofton, J. T.; Share, Leonard

doi:10.1152/ajpregu.1992.263.5.r1030

Cited by 18 publications

(15 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There is also evidence for cholinergic and angiotensinergic innervation of vasopressinergic cells in the PVN and SON, both of which are modulated by sex steroids. 40 Finally, in older women, estrogen effects on osmoregulation may be related to follicle-stimulating hormone through an adenylate cyclase mechanism, although in PM women gonadotropins are reduced after estrogen administration as reported by Studd et al 41 Ovarian hormone effects on the renin-angiotensin-aldosterone system in PM women. Both estrogens and progesterones play important roles in whole-body water and sodium regulation as well as in the brain.…”

Section: Menopause and Hydrationmentioning

confidence: 90%

Hormonal Changes During Menopause and the Impact on Fluid Regulation

Stachenfeld

2014

Reprod. Sci.

View full text Add to dashboard Cite

Reproductive surgeries leave women more susceptible to postoperative hypervolemic hyponatremia because during this period women can retain water at an accelerated pace and much faster than they do sodium. This review proposes that estrogen and progestogen exposure play an important role in the increased risk of hyponatremia in menopausal women. Estrogen and progesterone exposure have important effects on both body fluid regulation and cardiovascular function and both of these reproductive hormones impact blood pressure responses to sodium loads. This article provides information on the effects of female reproductive hormones and hormone therapy (HT) on fluid regulation and cardiovascular function during menopause. Thirst-and fluid-regulating hormones respond to both osmotic and volume stimuli. Aging women maintain thirst sensitivity to osmotic stimuli but lose some thirst sensitivity to changes in central body fluid volume. Thus, older adults are more at risk of dehydration because they may replenish fluids at a slower rate. Estrogen therapy increases osmotic sensitivity for mechanisms to retain body water so may help menopausal women control body fluids and avoid dehydration. Some progestogens can mitigate estradiol effects on water and sodium retention through competition with aldosterone for the mineralocorticoid receptor and attenuating aldosterone-mediated sodium retention in the distal tubule. However, some progestogens can increase cardiovascular risks. Appropriate balance of these hormones within HT is important to avoid the negative consequences of body fluid and sodium retention, including edema and hypertension.Keywords hormone therapy, estrogen, progesterone, body fluid regulation, arginine vasopressin Reproductive surgeries leave women more susceptible to postoperative hypervolemic hyponatremia because women retain water at a faster rate than sodium during this period, 1-5 especially after reproductive surgeries. 4,7 Indeed, women are at high risk of postoperative hyponatremia even after relatively low-risk surgeries such as operative hysteroscopy. In such surgeries, glycine solution (lacking electrolytes) is used as a distension medium and can cause intravascular volume retention, increasing the risk of hyponatremia, cerebral and/or pulmonary edema, psychological disturbances, and even death. 4,[8][9] A combination of anesthesia, nausea, and the postsurgical experience tends to increase arginine vasopressin (AVP). This hormone, the primary hormone involved in free water retention, is also associated with altered astroglia volume regulation in both pre-and postmenopausal (PM) women. 3,5,10,11 Studies in animals support an important role for estradiol in increasing astroglia volume in women with hyponatremia, suggesting a role for female reproductive hormones in the dire consequences that can be associated with postoperative hyponatremia in both young and PM women. 6,12 Hormones During MenopauseThe stages of the menopause transition are classified by changes in menstrual bleeding, concomitant...

show abstract

Section: Menopause and Hydrationmentioning

confidence: 90%

Hormonal Changes During Menopause and the Impact on Fluid Regulation

Stachenfeld

2014

Reprod. Sci.

View full text Add to dashboard Cite

show abstract

“…At the same point in the rat estrous cycle, when AVP levels are believed to increase, water intake behavior is attenuated [4]. Generally, plasma osmolality does not change over the estrous cycle [47]or following estrogen treatment [45, 46, 47, 48, 49]. Thus, the elevated AVP levels may help to conserve water in a period of decreased intake.…”

Section: Discussionmentioning

confidence: 99%

“…However, the consequences of estradiol action on AVP-induced pressor responses are less clear in the in vivo situation. In rats, AngII causes AVP release, but this release does not appear to be influenced by the stage of the estrous cycle [47]or by ovarian steroid hormone treatment [52]. Others report that OVX rats chronically treated with estradiol exhibit decreased pressor responsivity to AVP [53].…”

Section: Discussionmentioning

confidence: 99%

Estrogen Increases Angiotensin II-Induced c-Fos Expression in the Vasopressinergic Neurons of the Paraventricular Nucleus in the Female Rat

Kisley¹,

Sakai

Flanagan‐Cato

et al. 2000

Neuroendocrinology

View full text Add to dashboard Cite

Previous studies in female rats have shown that estrogen treatment attenuates angiotensin II (AngII)-induced water intake. The mechanism underlying this attenuation may be decreased responsiveness to AngII, as revealed by a reduction in AngII binding to the angiotensin type 1 (AT₁) receptor in the subfornical organ (SFO). It has not been determined whether these changes in receptor binding translate into changes in neuronal activity that, in turn, may influence behavior. Therefore, an estrogen-modulated change in neuronal pathways relevant to AngII-induced water intake was tested in ovariectomized (OVX) female rats using immunohistochemistry for the immediate early gene c-Fos as a marker for neuronal activation. Third cerebroventricular injection of AngII (6 ng) induced intense c-Fos immunoreactivity in forebrain regions associated with fluid intake, including the organum vasculosum of the lamina terminalis, the median preoptic nucleus, the SFO, the supraoptic nucleus and the paraventricular nucleus (PVN). Forty-eight-hour estradiol (10 µg) administration to OVX female rats increased AngII-induced c-Fos labeling in the lateral magnocellular neurons of the PVN by 30% as compared to vehicle-treated controls. Double labeling neurons in the PVN with c-Fos and either vasopressin or oxytocin antisera revealed that estrogen increased AngII-induced c-Fos expression by 28%, specifically in vasopressinergic neurons. Such changes in neuronal activation may explain the estrogen modulation of AngII-induced water intake that has been previously reported; it may be due to increased water retention to maintain plasma osmolality or to induction of a pressor response.

show abstract

“…Central cholinergic mechanisms play important roles in the control of cardiovascular responses (Fitzsimons, 1972;Hoffman et al, 1977;Grossman, 1960;Stone et al, 1992). Central application of carbachol, a nonselective cholinergic agonist, produces an increase of blood pressure (BP), vasopressin release, and drinking (Barbosa et al, 1995;Iitake et al, 1986;Mahon et al, 1995;Poole, 1983).…”

Section: Introductionmentioning

confidence: 99%

The Association of Cardiovascular Responses with Brain c-fos Expression after Central Carbachol in the Near-Term Ovine Fetus

Shi

Morrissey

Yao

et al. 2005

Neuropsychopharmacol

View full text Add to dashboard Cite

Central cholinergic mechanisms play important roles in the control of cardiovascular responses. However, in utero development of brain cholinergic mechanism in regulation of arterial pressure before birth is largely unknown. This study investigated cardiovascular responses to central application of carbachol in fetuses and determined functional development of the central cholinergic systems controlling fetal pressor responses in utero. Chronically prepared near-term ovine fetuses (90% gestation) received an injection of carbachol intracerebroventricularly (i.c.v.). Fetal cardiovascular responses were measured, and the brains were used for c-fos mapping studies. In response to carbachol injection i.c.v., fetal systolic, diastolic, and mean arterial pressure (MAP) immediately increased, accompanied by a bradycardia. The maximum increase of MAP was at 30 min after the i.c.v. injection of carbachol and lasted 90 min. Associated with the pressor response, the neuronal activity marked with c-fos was enhanced significantly in the fetal anterior third ventricle (AV3V) region (including the median preoptic nucleus and organum vasculosum of the lamina terminalis) in the forebrain, and in the area postrema, lateral parabrachial nucleus, nucleus tractus solitary, and rostral ventrolateral medulla in the hindbrain. These results indicate that the central cholinergic mechanism is functional in the control of fetal blood pressure at the last third of gestation, and the central AV3V region and hindbrain have been intact relatively during in utero development in sheep at 90% gestational stage.

show abstract

Sex differences in central cholinergic and angiotensinergic control of vasopressin release

Cited by 18 publications

References 0 publications

Hormonal Changes During Menopause and the Impact on Fluid Regulation

Hormonal Changes During Menopause and the Impact on Fluid Regulation

Estrogen Increases Angiotensin II-Induced c-Fos Expression in the Vasopressinergic Neurons of the Paraventricular Nucleus in the Female Rat

The Association of Cardiovascular Responses with Brain c-fos Expression after Central Carbachol in the Near-Term Ovine Fetus

Contact Info

Product

Resources

About