Radioautographic localization of specific binding sites for blood-borne angiotensin II in the rat brain

Houten, Mark Van; Schiffrin, Ernesto L.; Mann, Johannes F.E.; Posner, Barry I.; Boucher, R.

doi:10.1016/0006-8993(80)90995-6

Cited by 184 publications

(62 citation statements)

References 11 publications

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“…Then 1 ml aliquots were incubated with 1M I-AII in polyethylene tubes for 25 minutes at 37°C. The Ile'-AII was iodinated as described 11 by the method of Freedlender and Goodfriend" to a specific activity of 1.5 Ci/mol. The 115 I-AII was stored at -20° and thawed only once.…”

Section: Iu I-aii Bindingmentioning

confidence: 99%

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Central actions and brain receptor binding of angiotensin II: Influence of sodium intake.

Mann¹,

Schiffrin²,

Schiller³

et al. 1980

Hypertension

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Section: Iu I-aii Bindingmentioning

confidence: 99%

“…Some parts of the brain, especially the circumventricular organs, may be reached by bloodborne All. 11 Angiotensin II may be produced by a renin angiotensin system within the brain, too. 29 The increase of circulating levels of All during sodium deficiency is well documented, 10 but the levels of brain All are not known under these conditions.…”

Section: Drinkingmentioning

confidence: 99%

Central actions and brain receptor binding of angiotensin II: Influence of sodium intake.

Mann¹,

Schiffrin²,

Schiller³

et al. 1980

Hypertension

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“…In calf brain, All binding was highest in the cerebellum (23), whereas in the rat it was found mainly in the thalamus, hypothalamus, midbrain, septum, and medulla (23,25), with highest concentrations in the lateral septum, superior colliculus, and area postrema (26,28). Binding sites for blood-borne All have been localized in the circumventricular organs, particularly the subfornical organ (29), and, after All injection into the cerebral ventricles, in the organum vasculosum of the lamina terminalis (30). In such studies, labeling of the respective sites depends on access of All to the brain after intravenous or intracerebroventricular injection as well as the presence of specific binding sites.…”

mentioning

confidence: 99%

Autoradiographic localization of angiotensin II receptors in rat brain.

Mendelsohn¹,

Quirion²,

Saavedra³

et al. 1984

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

443

209

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The 125I-labeled agonist analog [1-sarcosine]-angiotensin II ([Sar']AII) bound with high specificity and affinity (Ka = 2 x 109 M-1) to a single class of receptor sites in rat brain. This ligand was used to analyze the distribution of All receptors in rat brain by in vitro autoradiography followed by computerized densitometry and color coding. A very high density of All receptors was found in the subfornical organ, paraventricular and periventricular nuclei of the hypothalamus, nucleus of the tractus solitarius, and area postrema. A high concentration of receptors was found in the suprachiasmatic nucleus of the hypothalamus, lateral olfactory tracts, nuclei of the accessory and lateral olfactory tracts, triangular septal nucleus, subthalamic nucleus, locus coeruleus, and inferior olivary nuclei. Moderate receptor concentrations were found in the organum vasculosum of the lamina terminalis, median preoptic nucleus, medial habenular nucleus, lateral septum, ventroposterior thalamic nucleus, median eminence, medial geniculate nucleus, superior colliculus, subiculum, preand parasubiculum, and spinal trigeminal tract. Low concentrations of sites were seen in caudate-putamen, nucleus accumbens, amygdala, and gray matter of the spinal cord. These studies have demonstrated that All receptors are distributed in a highly characteristic anatomical pattern in the brain. The high concentrations of All receptors at numerous physiologically relevant sites are consistent with the emerging evidence for multiple roles of All as a neuropeptide in the central nervous system.

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“…Peripheral ANGII increases blood pressure but cannot surpass the blood-brain barrier, except via the circumventricular organs (area postrema, organum vasculosum laminae terminalis). 12,13 These structures express a magnitude of AT1 receptors and seem to serve as an interface gating effects of circulating ANGII to brain stem and hypothalamic nuclei (ie, nucleus tractus solitarius, supraoptic nucleus, and paraventricular nuclei). Such humoral ANGII input is known to increase tonic blood pressure levels by an upward resetting of the sympathetic baroreceptor reflex activity 2,[14][15][16][17] and may also activate intrinsic hypothalamic neurohypophysial fiber pathways, inducing the release of vasopressin.…”

mentioning

confidence: 99%

Intranasal Angiotensin II in Humans Reduces Blood Pressure When Angiotensin II Type 1 Receptors Are Blocked

et al. 2014

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T he peptide hormone angiotensin II (ANGII) displays a wide range of regulatory actions on blood pressure. Besides its systemic effects on the blood vessels and different organ systems, local ANGII is crucially involved in the central nervous regulation of blood pressure.1-6 ANGII receptors, mainly type 1 receptors (AT1) and also type 2 receptors (AT2), are expressed in several cerebral nuclei where they mediate effects of locally produced ANGII.7-10 Inhibition of central nervous ANGII synthesis reversed hypertension in spontaneously hypertensive rats. 11The differentiation of central nervous and peripheral actions of ANGII is important for understanding blood pressure homeostasis and the development of essential hypertension in humans. Peripheral ANGII increases blood pressure but cannot surpass the blood-brain barrier, except via the circumventricular organs (area postrema, organum vasculosum laminae terminalis).12,13 These structures express a magnitude of AT1 receptors and seem to serve as an interface gating effects of circulating ANGII to brain stem and hypothalamic nuclei (ie, nucleus tractus solitarius, supraoptic nucleus, and paraventricular nuclei). Such humoral ANGII input is known to increase tonic blood pressure levels by an upward resetting of the sympathetic baroreceptor reflex activity 2,14-17 and may also activate intrinsic hypothalamic neurohypophysial fiber pathways, inducing the release of vasopressin. 3,[18][19][20] When ANGII is directly injected into the nucleus tractus solitarius, the baroreceptor reflex is suppressed via activation of AT1 receptors. After intracerebral administration, however, pressor effects of ANGII were revealed to be variable and even contradictory depending on dose and location of the injection, therefore suggesting differential effects on blood pressure regulation. 3,4,9,10,19,[21][22][23][24] The intranasal administration of small peptide molecules represents an established approach to bypass the bloodbrain barrier in humans and to achieve direct central nervous effects. [25][26][27][28][29] These studies demonstrate that peptide molecules such as ANGII directly enter the cerebrospinal fluid after their intranasal administration without previous uptake to the blood but instead via diffusion along neuronal clefts in the nasal mucosa. Importantly, because of the relatively great amounts of substance administered to achieve central nervous effects of the peptide, it cannot be prevented that, rather than directly accessing the cerebrospinal fluid compartment, some portion of the substance spills over into the circulation. Peptide that enters the circulation might then mask direct central nervous effects after intranasal peptide administration. Thus, a viable approach to unravel direct brain effects of intranasal peptide administration is to combine this treatment with a peripherally acting receptor blocker of the peptide.Abstract-Intranasal administration of angiotensin II (ANGII) affects blood pressure in a mode different from intravenously administered ANGII via a d...

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Radioautographic localization of specific binding sites for blood-borne angiotensin II in the rat brain

Cited by 184 publications

References 11 publications

Central actions and brain receptor binding of angiotensin II: Influence of sodium intake.

Central actions and brain receptor binding of angiotensin II: Influence of sodium intake.

Autoradiographic localization of angiotensin II receptors in rat brain.

Intranasal Angiotensin II in Humans Reduces Blood Pressure When Angiotensin II Type 1 Receptors Are Blocked

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