Effect of Angiotensin II on in Vivo and in Vitro Release of Anterior Pituitary Hormones in the Female Rat*

Steele, Marianne K.; Negro‐Vilar, A.; McCann, Samuel M.

doi:10.1210/endo-109-3-893

Cited by 153 publications

(63 citation statements)

References 17 publications

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“…In the anterior pituitary, Ang II is synthesized locally and stimulates prolactin release (Steele et al, 1981;Aguilera et al, 1982;Schramme and Denef, 1983;Ganong et al, 1989;Jones et al, 1990;Steele and Myers, 1990;Thomas and Sernia, 1990). Ang II also participates in brain mechanisms controlling pituitary prolactin release, but here its role is inhibitory rather than stimulatory Steele, 1989, 1991).…”

Section: Abstract: Angiotensin II Receptors; Catecholamines; Tyrosinmentioning

confidence: 99%

Angiotensin II AT_1AReceptor mRNA Expression Is Induced by Estrogen–Progesterone in Dopaminergic Neurons of the Female Rat Arcuate Nucleus

Jöhren¹,

Sanvitto²,

Egidy³

et al. 1997

J. Neurosci.

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Section: Abstract: Angiotensin II Receptors; Catecholamines; Tyrosinmentioning

confidence: 99%

Angiotensin II AT_1AReceptor mRNA Expression Is Induced by Estrogen–Progesterone in Dopaminergic Neurons of the Female Rat Arcuate Nucleus

Jöhren¹,

Sanvitto²,

Egidy³

et al. 1997

J. Neurosci.

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“…Their appearance in this situation is identical to that for established releasing factors huch as luteinizing hormone-releasing hormone and corticotrophin-releasing factor. In this regard, the regulation of both prolactin (20) and ACTH (21,22) from the anterior pituitary may be mediated, at least in part, by ANG I1 released into the portal circulation. This role of ANG I1 is not universally supported for several reasons including the fact that ANG I1 in portal blood is not elevated with respect to peripheral blood in rats (23), and that there is a local production and presumably secretion of ANG I1 by gonadotrophs in the pituitary (24).…”

Section: Discussionmentioning

confidence: 99%

An Ultrastructural Analysis of the Distribution of Angiotensin II in the Rat Brain

Oldfield

Ganten

1989

J Neuroendocrinology

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Abstractlmmunopositive angiotensin I1 nerve fibres and terminals are widely distributed throughout the rat brain, including areas of the brain with and without a blood-brain barrier. Ultrastructural examination indicates that in the circumventricular organs (areas which lack a blood-brain barrier), many angiotensin Il-positive nerve terminals are closely aligned with fenestrated blood vessels and do not have synaptic specializations. This appearance is in contrast to that of angiotensin II terminals in regions with a blood-brain barrier where there exists a more typical synaptic configuration. In both cases, angiotensin II is contained within large (100 to 125 nm) vesicles which coexist with smaller, lucent, non-immunoreactive vesicles. These observations suggest a possible duality of function such that angiotensin II in circumventricular organs may be secreted into the circulation, whereas angiotensin I I in the remainder of the brain is more likely to be acting as a neurotransmitter or neuromodulator.The octapeptide, angiotensin 11 (ANG II), when administered into the CNS, causes a number of well-defined physiological and behavioural responses including thirst, vasopressin secretion, natriuresis, increased blood pressure and salt appetite (1-3).One of the major questions central to understanding the actions of ANG I1 in the brain has been the source of its production. Ganten et al. (4) isolated angiotensin I and A N G II from the rat brain and demonstrated the central nature of ANG I1 production by the intracerebroventricular administration of an inhibitor of angiotensin-converting enzyme which caused a reduction in local ANG 11. Furthermore, the presence of each of the components of the renin angiotensin system (RAS) has been demonstrated immunocytochemically (5-8) and the likelihood of local production supported by the identification of mRNA for renin and angiotensinogen (9, 10). However, the cellular disposition of each of the components of the RAS still remains unclear, as does the nature of their interaction and the degree of their anatomical overlap. Immunocytochemically-identified A N G I1 is contained in a network of neural pathways connecting areas of the forebrain and brainstem which are largely concerned with autonomic or homeostatic functions (11). It is on the basis of these studies and the good correlation of A N G 11-positive terminal fields with A N G II receptors (12-15) that ANG I1 is suggested to act as a neurotransmitter/neuromodulator in the CNS.The present study has sought to further elucidate the action of ANG 11 in the CNS by examining its ultrastructural distribution. In particular, we have focused on the nature of morphological interactions between A N G 11-positive elements and other neural and non-neural structures in a range of brain areas.Previous studies at the light microscopic (LM) level have shown ANG 11-positive structures, presumed to be terminals, to be aggregated both in circumventricular organs (CVOs) and in regions behind the blood-brain barrier. Because the function of ...

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“…When ovarian steroids were absent none of the above protocols resulted in an increase in plasma prolactin levels, compared to values from rats treated with aCSF. Previous data had shown that a bolus injection of saralasin transiently increased prolactin levels in 4-to 6-week ovariectomized untreated animals, raising the possibility that brain A11 did tonically inhibit prolactin secretion in these animals (8). However, saline alone was not given as a control, rather the prolactin values following saralasin were compared t o pre-injection values.…”

Section: Discussionmentioning

confidence: 99%

“…To investigate the effects of ovarian hormones on the functioning of endogenous A11 in prolactin regulation, we examined the effects of disrupting the brain A11 system at the receptor level (by two A11 receptor blockers, saralasin or sarthran) and at the synthesis level (by the converting enzyme inhibitor, enalaprilat). Previous data had shown that, in the non-steroid treated, long-term ovariectomized rat, a bolus injection of saralasin transiently elevated prolactin levels, compared to pre-injection values (8). In the present study, we investigated this effect in the one-week ovariectomized animal, with and without estrogen and progesterone replacement.…”

mentioning

confidence: 82%

“…While there i s considerable evidence that brain-derived A11 participates in the physiological regulation o f LH secretion from the anterior pituitary gland (6), less information i s available concerning the regulation o f prolactin release by AII. I t i s known that central administration of the A11 generating enzyme, renin, or a high dose o f A11 suppresses the release o f prolactin (7)(8)(9), presumably through the release o f dopamine (7,9). However, a role for endogenous brain A11 in the physiological control o f prolactin secretion remains to be defined.…”

mentioning

confidence: 99%

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The Brain Renin‐Angiotensin System and the Regulation of Prolactin Secretion in Female Rats: Influence of Ovarian Hormones

Myers

Steele

1989

J Neuroendocrinology

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This study was designed to investigate the effects of exogenous and endogenous angiotensin II (All) on prolactin release in ovariectomized rats, with and without estrogen and progesterone pretreatment. In the first series of experiments, All or vehicle was injected into the third cerebral ventricle of conscious, freely-moving rats. In both treated and untreated rats, administration of 50 ng All suppressed prolactin levels within 15 min of injection, compared to vehicle-injected rats. In untreated rats, prolactin levels returned to baseline values by 30 min, while in treated rats, prolactin levels remained suppressed for an hour.In the second series of experiments, the involvement of endogenous brain All in tonically suppressing prolactin release was assessed by administering either All receptor blockers (saralasin or sarthran) or an All synthesis inhibitor (enalaprilat, an inhibitor of the conversion of angiotensin I to All). Neither All receptor blockade nor converting enzyme inhibition resulted in any change in prolactin levels in untreated levels in untreated rats. However, following treatment with ovarian steroids, infusion of saralasin or injection of enalaprilat resulted in a significant increase in plasma prolactin titers. During saralasin infusion, prolactin levels were significantly increased by 15 min and continued to be higher than controls at 60 min. After enalaprilat administration, prolactin levels did not rise significantly until 90 min and then remained elevated up to 120 min post-injection. These latter results suggest that at least one h is required for maximal inhibition of angiotensin synthesis in the brain.These data demonstrate that low doses of All suppressed basal prolactin secretion in both untreated and ovarian steroid-treated, ovariectomized rats. However, treated rats appeared to be more sensitive than untreated animals to the prolactin-lowering effects of centrally administered All. The lack of prolactin response in untreated rats when brain All synthesis was inhibited or All receptors were blocked suggests that, in the absence of ovarian steroids, endogenous All was not acting tonically to suppress prolactin secretion. Following exposure to ovarian steroids, however, the endogenous brain All system appeared to be activated and involved in controlling prolactin release.The anterior pituitary gland hormone, prolactin, i s involved in lactation, ovarian and mammillary gland function, pseudopregnancy in female rats, and i s released in response to stress (1). In human males and females, hyperprolactinemia i s associated with impaired sexual behavior and functioning, as well as infertility (2).Prolactin secretion is mainly under tonic inhibitory control by dopamine, derived from the brain tuberoinfundibular system (3). On the other hand, a variety o f peptides (e.g. vasoactive intestinal peptide, thyrotropin-releasing hormone) including angiotensin I1 (AII), have been identified as putative prolactin-releasing factors when applied directly to the anterior pituitary gland (4). Und...

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Effect of Angiotensin II on in Vivo and in Vitro Release of Anterior Pituitary Hormones in the Female Rat*

Cited by 153 publications

References 17 publications

Angiotensin II AT_1AReceptor mRNA Expression Is Induced by Estrogen–Progesterone in Dopaminergic Neurons of the Female Rat Arcuate Nucleus

Angiotensin II AT_1AReceptor mRNA Expression Is Induced by Estrogen–Progesterone in Dopaminergic Neurons of the Female Rat Arcuate Nucleus

An Ultrastructural Analysis of the Distribution of Angiotensin II in the Rat Brain

The Brain Renin‐Angiotensin System and the Regulation of Prolactin Secretion in Female Rats: Influence of Ovarian Hormones

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Effect of Angiotensin II on in Vivo and in Vitro Release of Anterior Pituitary Hormones in the Female Rat*

Cited by 153 publications

References 17 publications

Angiotensin II AT1AReceptor mRNA Expression Is Induced by Estrogen–Progesterone in Dopaminergic Neurons of the Female Rat Arcuate Nucleus

Angiotensin II AT1AReceptor mRNA Expression Is Induced by Estrogen–Progesterone in Dopaminergic Neurons of the Female Rat Arcuate Nucleus

An Ultrastructural Analysis of the Distribution of Angiotensin II in the Rat Brain

The Brain Renin‐Angiotensin System and the Regulation of Prolactin Secretion in Female Rats: Influence of Ovarian Hormones

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Angiotensin II AT_1AReceptor mRNA Expression Is Induced by Estrogen–Progesterone in Dopaminergic Neurons of the Female Rat Arcuate Nucleus

Angiotensin II AT_1AReceptor mRNA Expression Is Induced by Estrogen–Progesterone in Dopaminergic Neurons of the Female Rat Arcuate Nucleus