Increased Number of Angiotensin II Binding Sites Determined by Autoradiography in Anterior Pituitary of Water-Deprived and Brattleboro Rats

Israel, A; Plunkett, Laura M.; Saavedra, Juan M.

doi:10.1159/000124249

Cited by 13 publications

(12 citation statements)

References 34 publications

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“…Angiotensin receptor density was unaffected in both magnocellular and parvocellular paraventricular nucleus of Brattleboro rats. As described earlier (27), angiotensin-receptor density was higher in the anterior pituitary gland of both homozygous and heterozygous Brattleboro rats compared with the Long-Evans strain (Fig. 2, Table 1).…”

Section: Resultssupporting

confidence: 79%

“…Although the evidence is indirect, these results do not lend support to the hypothesis that angiotensin II increases vasopressin secretion by acting directly through angiotensin receptors on vasopressin cells. Angiotensin receptors in the anterior pituitary gland seem to be sensitive to dehydration, because they are increased in chronically dehydrated Brattleboro rats but also in acutely dehydrated normal rats (27,36). It has been suggested that angiotensin II might contribute to the stimulation of ACTH secretion in the pituitary gland, either by itself of by potentiating the effects of CRH (8,37).…”

Section: Discussionmentioning

confidence: 99%

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Angiotensin II receptors in paraventricular nucleus, subfornical organ, and pituitary gland of hypophysectomized, adrenalectomized, and vasopressin-deficient rats.

Ċastrén

Saavedra²

1989

Proc. Natl. Acad. Sci. U.S.A.

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Angiotensin II has been implicated in the regulation of adrenocorticotropin and vasopressin secretion. Angiotensin II may influence the secretion of these hormones either directly at the pituitary gland or by increasing corticotropin-releasing hormone or vasopressin release from cells that are located in the paraventricular hypothalamic nucleus. Pituitary hormone release may also be influenced by circulating angiotensin H through receptors outside the blood-brain barrier in the subfornical organ. We have used alterations in angiotensin II receptors in hypophysectomized, adrenalectomized, and vasopressin-deficient Brattleboro rats as indicators of the activity of angiotensin II in the regulation of adrenocorticotropin and vasopressin secretion. Angiotensin receptor number in the paraventricular nucleus and the subfornical organ, but not in the anterior pituitary gland, was significantly decreased by adrenalectomy, and this effect was reversed by corticoids. Vasopressin deficiency decreased angiotensin receptors in the subfornical organ and increased them in the anterior pituitary gland but did not affect angiotensin II binding in either magnocellular or parvocellular subnucleus of the paraventricular nucleus. Our results suggest that angiotensin II may have a corticoid-dependent role in the regulation of corticotropin-releasing hormone secretion, which could be important in the adaptation to elevated corticosterone secretion in stress.Angiotensin II is a physiologically active product of the renin-angiotensin system and has an important role in hemodynamic regulation (1). All components of the reninangiotensin system have been found in the central nervous system (2). Brain angiotensin II seems to work in concert with the peripheral renin-angiotensin system to regulate blood pressure and fluid homeostasis (2). Both in the periphery and in the central nervous system angiotensin II acts through specific membrane receptors (3-5). In brain, angiotensin receptors show highly discrete localization in only few brain areas (4, 5). Angiotensin receptors in circumventricular organs, such as the subfornical organ, are accessible to circulating as well as central peptides, whereas those in other brain areas are inside the blood-brain barrier and can thus only be stimulated by endogenous brain angiotensin II (6).Angiotensin II also plays a role in the regulation of adrenocorticotropin (ACTH) and vasopressin secretion from the pituitary gland (7-10). Vasopressin release is increased by central (10) and perhaps also by peripheral (11) administration of angiotensin II. Peripheral angiotensin II administration stimulates ACTH release from the anterior pituitary gland (12), but this effect may be mediated through the brain angiotensin II system: circulating angiotensin II may bind to receptors in circumventricular organs and stimulate the brain angiotensin II system, which leads to increased ACTH release probably through the stimulation of corticotropinreleasing hormone (CRH) secretion from the hypothalamus (9, 12).The para...

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Section: Resultssupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Angiotensin II receptors in paraventricular nucleus, subfornical organ, and pituitary gland of hypophysectomized, adrenalectomized, and vasopressin-deficient rats.

Ċastrén

Saavedra²

1989

Proc. Natl. Acad. Sci. U.S.A.

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“…Thus, DEX did not initiate transcription of reporter genes regulated by the AT1B promoter [69, 70]or the AT2 promoter [70], which is consistent with the failure of DOCA or DEX treatment in this study to modulate AT2 binding in the locus ceruleus or inferior olive, which express predominantly AT2 receptors [35]or in the pituitary, which expresses few AT2 receptors [34]. Although mineralocorticoids and glucocorticoids do not modulate pituitary AngII receptor binding, other experimental conditions can do so [33, 71, 72, 73, 74, 75]. The general pattern that emerges is that adrenal steroids selectively regulate the AT1A receptor in these tissues.…”

Section: Discussionsupporting

confidence: 72%

“…Pituitaries were obtained from the same animals used in the behavioral and the brain receptor autoradiography studies. Membrane binding analysis was performed on the pituitary because it is an easily dissectable tissue with a uniformly high density of AngII receptors [31, 32, 33, 34]. The anterior pituitaries were separated from posterior and intermediate lobes.…”

Section: Methodsmentioning

confidence: 99%

Mineralocorticoids and Glucocorticoids Cooperatively Increase Salt Intake and Angiotensin II Receptor Binding in Rat Brain

Shelat

King²,

Flanagan‐Cato³

et al. 1999

Neuroendocrinology

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Mineralocorticoids, such as deoxycorticosterone acetate (DOCA), and angiotensin II (AngII) act synergistically in the brain to elicit salt appetite. Glucocorticoids, such as dexamethasone (DEX), also may enhance the behavioral effects of DOCA and AngII. However, the brain regions involved in these behavioral interactions have not been elucidated. This study tested the hypothesis that DEX potentiates the effects of DOCA on AngII binding, especially at the AT1 receptor. We confirmed that DEX potentiated the effects of DOCA on salt appetite. Concomitantly, steroid-specific and region-specific changes in AT1 binding were noted. Specifically, in the hypothalamic paraventricular nucleus, treatment with DEX or DOCA + DEX increased AT1 binding. In the subfornical organ (SFO) and area postrema, there was an increase in AT1 binding when both steroids were combined, but not when given individually. However, there was no change in AT2 binding in any brain region studied and no change in AT1 or AT2 binding to either receptor subtype in the pituitary. The results indicate that DOCA and DEX may increase the sensitivity of the brain to the behavioral and physiological actions of AngII by upregulating AT1 receptors in the SFO and area postrema.

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“…relationship between the natural logarithm of the optical densities of each standard concentration and the natural logarithm of the radioactivity contained in that section at any exposure of Ultrofilm 3H (13). This plot of In OD vs.…”

mentioning

confidence: 99%

Increased angiotensin II binding affinity in the nucleus tractus solitarius of spontaneously hypertensive rats.

Plunkett¹,

Saavedra²

1985

Proc. Natl. Acad. Sci. U.S.A.

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Angiotensin II (Ang) binding kinetics were determined in discrete brainstem nuclei of 14-week-old spontaneously hypertensive rats (SHR) and normotensive WistarKyoto rats (WKY) by a quantitative autoradiographic technique. Tissue sections were incubated with 125I-labeled [sarcosine-l]Ang, and results were analyzed by computerized densitometry and comparison to '25I-labeled standards. A single class of high-affinity binding sites was identified in the nucleus tractus solitarius, the area postrema, and the inferior olivary nuclei of both SHR and WKY rats. Ang binding affinity was significantly greater in the nucleus tractus solitarius of SHR compared to normotensive WKY rats (0.27 ± 0.06 x 109 M-1 in WKY rats vs. 0.59 ± 0.15 x 109 M-1 in SHR), with no apparent changes in the maximum binding capacity of this area. There were no changes in the Ang binding kinetics of the area postrema or the inferior olivary nuclei. Our results suggest that central Ang activity is altered in established hypertension in a brainstem area of SHR associated with peripheral cardiovascular control.After the identification of components ofa central renin-angiotensin system, angiotensin II (Ang) was linked with centrally mediated cardiovascular effects (1, 2). Specific receptors for Ang have been localized to brain areas involved in cardiovascular regulation, including the nucleus tractus solitarius, area postrema, locus coeruleus, and dorsal motor nucleus of the vagus (3, 4). Additionally, Ang immunoreactive cells and fibers have been identified in the rat central nervous system, also in areas associated with peripheral cardiovascular control (5). Microinjections of Ang into the nucleus tractus solitarius have been shown to produce dose-dependent increases in blood pressure that are similar to increases seen after intraventricular injection of Ang (6). These studies link central Ang activity with cardiovascular control.Evidence has also shown that alterations in central Ang activity occur during the pathogenesis of spontaneous hypertension. Angiotensin-converting enzyme antagonists, such as captopril, lower blood pressure in spontaneously hypertensive rats (SHR), with a greater reduction occurring after intraventricular administration (7). Ang levels have been shown to be increased in the brain of SHR, including brain areas known to affect cardiovascular function (8). These results suggest that Ang hyperactivity may contribute to the maintenance of hypertension in SHR. The purpose of this study was to determine ifbrainstem Ang receptor binding kinetics are altered in spontaneous hypertension, a change that could contribute to the hyperactivity of the central Ang system in these animals. (9,10). METHODSTo allow for quantitation of ligand binding, sets of 1251I labeled standards were prepared as described for 3H-labeled standards (11). Known amounts of 1251 in increasing concentrations were thoroughly mixed with a brain paste, mounted as blocks on specimen holders, and frozen. Sections (16 ,um) were cut on a cryostat at -14°C and t...

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Increased Number of Angiotensin II Binding Sites Determined by Autoradiography in Anterior Pituitary of Water-Deprived and Brattleboro Rats

Cited by 13 publications

References 34 publications

Angiotensin II receptors in paraventricular nucleus, subfornical organ, and pituitary gland of hypophysectomized, adrenalectomized, and vasopressin-deficient rats.

Angiotensin II receptors in paraventricular nucleus, subfornical organ, and pituitary gland of hypophysectomized, adrenalectomized, and vasopressin-deficient rats.

Mineralocorticoids and Glucocorticoids Cooperatively Increase Salt Intake and Angiotensin II Receptor Binding in Rat Brain

Increased angiotensin II binding affinity in the nucleus tractus solitarius of spontaneously hypertensive rats.

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