Autoradiographic localization of angiotensin II receptors in rat brain.

Mendelsohn, Frederick A.O.; Quirion, Rémi; Saavedra, Juan M.; Aguilera, Greti; Catt, Kevin J.

doi:10.1073/pnas.81.5.1575

Cited by 443 publications

(221 citation statements)

References 64 publications

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“…Therefore, the Ang II-induced effects are inhibited by a lower dose of [Sar1, Ile$]Ang II in the SON than in the PVN. Also, this is consistent with evidence from auto radiographic binding studies that the Ang II receptor concentration is higher in the PVN than in the SON (8,10). It is suggested that Ang II receptors exist on cell bodies of vasopressin-containing neurons in the nuclei and direct ly promotes vasopressin release (11)(12)(13)(14).…”

Section: Effects Of Antagonists On Ang Ii-induced Antidiuresessupporting

confidence: 77%

Microinjections of Angiotensin II into the Supraoptic and Paraventricular Nuclei Produce Potent Antidiureses by Vasopressin Release Mediated through Adrenergic and Angiotensin Receptors

Tsushima

Mori

Matsuda

1994

Japanese Journal of Pharmacology

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ABSTRACT-We investigated the effects of angiotensin II (Ang II), microinjected into the supraoptic (SON) and paraventricular (PVN) nuclei of rats, on the urine outflow rate and underlying mechanisms. Ang II produced antidiuretic effects in a dose-dependent manner with ED50 values of 0.1 and 0.05 nmol in the SON and PVN, respectively. [Sar', Ile8]Ang II at 0.1 nmol diminished the Ang II (0.5 nmol)-induced anti diureses in the SON more markedly than in the PVN. A high dose of [Sar', Ile8]Ang II, 1 nmol, completely inhibited the effects in both the nuclei. In addition, the Ang II (1 nmol)-induced antidiuretic effects were par tially inhibited by phenoxybenzamine (80 nmol) in the SON and by phenoxybenzamine, timolol (100 nmol) and propranolol (100 nmol) in the PVN. The microinjection of Ang II (1 nmol) into both the nuclei, after pretreatment with a vasopressin V1V2-antagonist, d(CH2)5-u-Tyr(Et)VAVP (i.v.), significantly increased the urine outflow rate. These findings suggest that 1) Two mechanisms account for the Ang II receptor mediated antidiureses resulting from an increase in vasopressin release: direct stimulation on vasopressin containing neurons and indirect stimulation on them through a-adrenoceptors in the SON and a and ã drenoceptors in the PVN; 2) The Ang II-induced antidiuretic effect in the SON is slightly less potent than that in the PVN; and 3) Ang II receptors in the nuclei may possibly produce the diureses through mecha nisms that are not presently understood.

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Section: Effects Of Antagonists On Ang Ii-induced Antidiuresessupporting

confidence: 77%

Microinjections of Angiotensin II into the Supraoptic and Paraventricular Nuclei Produce Potent Antidiureses by Vasopressin Release Mediated through Adrenergic and Angiotensin Receptors

Tsushima

Mori

Matsuda

1994

Japanese Journal of Pharmacology

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“…Neurons in the CVOs, notably the subfornical organ (SFO) and the organum vasculosum of the lamina terminalis (OVLT), not only sense circulating peptides like ANG II (3,14) but also send ANG II-immunoreactive efferent projections to the PVN where neurons express a high concentration of ANG II AT 1 receptors (23,29). Electrophysiological studies demonstrate that ANG II can increase PVN unit discharge when applied either directly within the SFO or when given systemically (1,15).…”

Section: Discussionmentioning

confidence: 99%

Chronic angiotensin II infusion attenuates the renal sympathoinhibitory response to acute volume expansion

LaGrange

Toney

Bishop

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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In this study the hypothesis was tested that chronic infusion of ANG II attenuates acute volume expansion (VE)-induced inhibition of renal sympathetic nerve activity (SNA). Rats received intravenous infusion of either vehicle or ANG II (12 ng·kg −1 ·min −1 ) for 7 days. ANG II-infused animals displayed an increased contribution of SNA to the maintenance of mean arterial pressure (MAP) as indicated by ganglionic blockade, which produced a significantly (P < 0.01) greater decrease in MAP (75 ± 3 mmHg) than was observed in vehicle-infused (47 ± 8 mmHg) controls. Rats were then anesthetized, and changes in MAP, mean right atrial pressure (MRAP), heart rate (HR), and renal SNA were recorded in response to right atrial infusion of isotonic saline (20% estimated blood volume in 5 min). Baseline MAP, HR, and hematocrit were not different between groups. Likewise, MAP was unchanged by acute VE in vehicle-infused animals, whereas VE induced a significant bradycardia (P < 0.05) and increase in MRAP (P < 0.05). MAP, MRAP, and HR responses to VE were not statistically different between animals infused with vehicle vs. ANG II. In contrast, VE significantly (P < 0.001) reduced renal SNA by 33.5 ± 8% in vehicle-infused animals but was without effect on renal SNA in those infused chronically with ANG II. Acutely administered losartan (3 mg/kg iv) restored VEinduced inhibition of renal SNA (P < 0.001) in rats chronically infused with ANG II. In contrast, this treatment had no effect in the vehicle-infused group. Therefore, it appears that chronic infusion of ANG II can attenuate VE-induced renal sympathoinhibition through a mechanism requiring AT 1 receptor activation. The attenuated sympathoinhibitory response to VE in ANG II-infused animals remained after arterial barodenervation and systemic vasopressin V 1 receptor antagonism and appeared to depend on ANG II being chronically increased because ANG II given acutely had no effect on VE-induced renal sympathoinhibition. Keywordssympathetic nerve activity; cardiopulmonary reflex; body fluid balance; arterial baroreceptor reflex Numerous studies have investigated interactions between circulating ANG II and the arterial baroreceptor reflex. Whereas recent studies indicate that an acute increase in circulating ANG II can attenuate the increase in sympathetic nerve activity (SNA) that follows arterial baroreceptor unloading (34), chronic increases of ANG II have been repeatedly demonstrated to reset arterial baroreflex control of SNA (4, 6). The latter effect may permit SNA to rise relative to the prevailing level of arterial pressure. In addition to the arterial Copyright © 2003 NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript baroreflex, the cardiopulmonary baroreflex is also an important determinant of sympathetic outflow as well as sodium and water balance. However, the extent to which chronic increases of ANG II might interact with this reflex to modify the SNA response to volume expansion (VE) is not known. This is surprising given that norma...

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“…It is therefore intriguing that radioligand binding studies have consistently demonstrated either relatively very low levels of AT receptors in the adult rat striatum (Sirett et al, 1977;Mendelsohn et al, 1984) or levels often below the limits of detection (e.g. see Gehlert et al, 1991).…”

Section: Stereotaxic Implantation Of Chronic Indwelling Guide Cannulaementioning

confidence: 99%

Ability of angiotensin II to modulate striatal dopamine release via the AT₁ receptor in vitro and in vivo

Brown

Steward

Jin

et al. 1996

British J Pharmacology

107

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1 The ability of angiotensin II to modulate dopamine release from rat striatal slices in vitro and in the intact rat striatum in vivo was assessed by the microdialysis technique.2 In slices of rat striatum, angiotensin II (0.1-1.0 gM) induced a concentration-related increase in endogenous dopamine release which was maximal (approximately 250% above basal levels) within the first 2-4 min of agonist application and subsequently declined to near

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Autoradiographic localization of angiotensin II receptors in rat brain.

Cited by 443 publications

References 64 publications

Microinjections of Angiotensin II into the Supraoptic and Paraventricular Nuclei Produce Potent Antidiureses by Vasopressin Release Mediated through Adrenergic and Angiotensin Receptors

Microinjections of Angiotensin II into the Supraoptic and Paraventricular Nuclei Produce Potent Antidiureses by Vasopressin Release Mediated through Adrenergic and Angiotensin Receptors

Chronic angiotensin II infusion attenuates the renal sympathoinhibitory response to acute volume expansion

Ability of angiotensin II to modulate striatal dopamine release via the AT₁ receptor in vitro and in vivo

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Autoradiographic localization of angiotensin II receptors in rat brain.

Cited by 443 publications

References 64 publications

Microinjections of Angiotensin II into the Supraoptic and Paraventricular Nuclei Produce Potent Antidiureses by Vasopressin Release Mediated through Adrenergic and Angiotensin Receptors

Microinjections of Angiotensin II into the Supraoptic and Paraventricular Nuclei Produce Potent Antidiureses by Vasopressin Release Mediated through Adrenergic and Angiotensin Receptors

Chronic angiotensin II infusion attenuates the renal sympathoinhibitory response to acute volume expansion

Ability of angiotensin II to modulate striatal dopamine release via the AT1 receptor in vitro and in vivo

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Ability of angiotensin II to modulate striatal dopamine release via the AT₁ receptor in vitro and in vivo