Evidence of angiotensin II involvement in prolactin secretion in response to hemorrhage in adrenodemedullated and guanethidine-treated rats

Machado, Luciana A. C.; Reis, Adelina M.; Coimbra, Cândido Celso

doi:10.1530/eje.0.1460439

Cited by 8 publications

(6 citation statements)

References 46 publications

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“…Moreover, data that show a reduced prolactin secretion after thiopental-anesthesia also provide further evidence that prolactin secretion in normal rats is under the control of hypothalamic noradrenergic tonus. We recently showed that both plasma prolactin baselines and prolactin secretion stimulated by hemorrhage decrease in animals bearing sympathoadrenal blockade (12). These results are in agreement with the concept that anesthesia induction by barbiturates may produce both a decreased noradrenaline turnover in the hypothalamus (1) as well as peripheral sympathetic suppression (1,2,4).…”

supporting

confidence: 83%

“…It is also a therapeutic agent frequently used in clinical practice to inhibit prolactin secretion in both sexes of all mammalian species tested so far. Therefore, the effect of thiopental on prolactin secretion has also been evaluated since, in addition to its effects in insulin secretion and glucose metabolism (10,11), prolactin release from pituitary gland is a highly sensitive marker of stress situations such as trauma and hemorrhage (11,12). Furthermore, prolactin as an immunomodulating hormone has been shown to reverse immunodepression following severe blood loss, as well as decreasing mortality from subsequent sepsis (13).…”

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confidence: 99%

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Acute Metabolic Effects of Thiopental Anesthesia on Fed and Fasted Rats Chronically Treated With Bromocriptine

et al. 2003

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We investigated the acute effects of thiopental anesthesia (4 mg/100 g, i.v.) on plasma glucose, insulin, triacylglycerol, and prolactin levels in rats treated with bromocriptine (BR) (0.4 mg/100 g body wt, i.p., for two weeks). Thiopental anesthesia induced a rapid increase in plasma insulin that was more pronounced in the animals treated with BR (116%, P <0.05). Thiopental anesthesia also produced a 55% decreased in plasma prolactin levels (P <0.01) in control fed rats, and a 22% reduction in plasma triacylglycerol (P <0.05) in both controls and BR-treated rats. We conclude that BR may constitute and additional sympatholytic factor in animals submitted to thiopental anesthesia.

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confidence: 83%

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confidence: 99%

Acute Metabolic Effects of Thiopental Anesthesia on Fed and Fasted Rats Chronically Treated With Bromocriptine

et al. 2003

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“…Although these neurotoxins do eliminate sympathetic activity, there are, in parallel, major central consequences. In particular, both treatments reduce hypothalamic dopamine, which leads to an increase in serum prolactin levels (57,59). In light of the present data, the possibility of a prolactin involvement in chemical sympathectomy should certainly be considered.…”

Section: Discussionmentioning

confidence: 73%

Experimental estrogen-induced hyperprolactinemia results in bone-related hearing loss in the guinea pig

Horner¹,

Cazals²,

Guieu³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Our group (Horner KC, Guieu R, Magnan J, Chays A, Cazals Y. Neuropsychopharmacology 26: 135–138, 2002) has earlier described hyperprolactinemia in some patients presenting inner ear dysfunction. However, in that study, it was not possible to determine whether hyperprolactinemia was a cause or an effect of the symptoms. To investigate the effect of hyperprolactinemia on inner ear function, we first developed a model of hyperprolactinemia in estrogen-primed Fischer 344 rats and then performed functional studies on pigmented guinea pigs. Hyperprolactinemia induced, after 2 mo, a hearing loss of ∼30–40 dB across all frequencies, as indicated by the compound action potential audiogram. During the 3rd mo, the hearing loss continued to deteriorate. The threshold shifts were more substantial in males than in females. Observations under a dissection microscope revealed bone dysmorphology of the bulla and the cochlea. Light microscopy observations of cryostat sections confirmed bone-related pathology of the bony cochlear bulla and the cochlear wall and revealed morphopathology of the stria vascularis and spiral ligament. Scanning electron microscopy revealed loss of hair cells and stereocilia damage, in particular in the upper three cochlear turns and the two outermost hair cell rows. The data provide the first evidence of otic capsule and hair cell pathology associated with estrogen-induced prolonged hyperprolactinemia and suggest that conditions such as pregnancy, anti-psychotic drug treatment, aging, and/or stress might lead to similar ear dysfunctions.

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“…Previous reports have also demonstrated the increased secretion of PRL after hemorrhage in male rats (35).…”

Section: Table 1 Number Of Total Fos In Sfo and Total Fos And Percenmentioning

confidence: 65%

Estradiol potentiates hypothalamic vasopressin and oxytocin neuron activation and hormonal secretion induced by hypovolemic shock

Mecawi

Vilhena‐Franco

Araujo

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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-Estrogen receptors are located in important brain areas that integrate cardiovascular and hydroelectrolytic responses, including the subfornical organ (SFO) and supraoptic (SON) and paraventricular (PVN) nuclei. The aim of this study was to evaluate the influence of estradiol on cardiovascular and neuroendocrine changes induced by hemorrhagic shock in ovariectomized rats. Female Wistar rats (220 -280 g) were ovariectomized and treated for 7 days with vehicle or estradiol cypionate (EC, 10 or 40 g/kg, sc). On the 8th day, animals were subjected to hemorrhage (1.5 ml/100 g for 1 min). Hemorrhage induced acute hypotension and bradycardia in the ovariectomized-oil group, but EC treatment inhibited these responses. We observed increases in plasma angiotensin II concentrations and decreases in plasma atrial natriuretic peptide levels after hemorrhage; EC treatment produced no effects on these responses. There were also increases in plasma vasopressin (AVP), oxytocin (OT), and prolactin levels after the induction of hemorrhage in all groups, and these responses were potentiated by EC administration. SFO neurons and parvocellular and magnocellular AVP and OT neurons in the PVN and SON were activated by hemorrhagic shock. EC treatment enhanced the activation of SFO neurons and AVP and OT magnocellular neurons in the PVN and SON and AVP neurons in the medial parvocellular region of the PVN. These results suggest that estradiol modulates the cardiovascular responses induced by hemorrhage, and this effect is likely mediated by an enhancement of AVP and OT neuron activity in the SON and PVN.hemorrhage; female rats; supraoptic nuclei; paraventricular nuclei; arterial pressure; heart rate THE PRECISE REGULATION OF body fluids is essential for the metabolic function of virtually all cells in the body. A variety of mechanisms are activated to maintain plasma osmolality and blood volume within a very narrow range of values (3). For example, hypovolemia and/or hypotension induce vasopressin (AVP) and oxytocin (OT) release from the magnocellular neurons of the supraoptic (SON) and paraventricular (PVN) nuclei in the hypothalamus (3, 56). It is estimated that a decrease of 10 -20% in total blood volume induces the release of AVP in several species. This neurosecretory response is modulated by peripheral baroreceptors in the aortic arch and carotid sinus, cardiopulmonary volume receptors, and angiotensin II (ANG II) (50, 65).The precise role of estrogen in maintaining body fluid homeostasis is not yet fully understood (16). Our group has previously reported that ANG II type 1 (AT 1 ) receptors are involved in the regulation of water and hypertonic saline intake in ovariectomized (OVX) rats during the nocturnal period (37, 38). In addition, several reports have suggested that estrogen has modulatory effects on cardiovascular function, as evidenced by the cardiovascular changes observed in postmenopausal women, OVX rats, and, possibly, females of other species during senescence (12, 46). These effects occur by estrogen's action on the...

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Evidence of angiotensin II involvement in prolactin secretion in response to hemorrhage in adrenodemedullated and guanethidine-treated rats

Cited by 8 publications

References 46 publications

Acute Metabolic Effects of Thiopental Anesthesia on Fed and Fasted Rats Chronically Treated With Bromocriptine

Acute Metabolic Effects of Thiopental Anesthesia on Fed and Fasted Rats Chronically Treated With Bromocriptine

Experimental estrogen-induced hyperprolactinemia results in bone-related hearing loss in the guinea pig

Estradiol potentiates hypothalamic vasopressin and oxytocin neuron activation and hormonal secretion induced by hypovolemic shock

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