[Sar1, Ala8] angiotensin II in cerebrospinal fluid blocks the binding of blood-borne [125I]angiotensin II to the circumventricular organs

Houten, Mark Van; Mangiapane, Michael L.; Reid, Ian A.; Ganong, William F.

doi:10.1016/0306-4522(83)90123-9

Cited by 80 publications

(39 citation statements)

References 4 publications

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“…On the other hand, since P has been shown to facilitate the positive feedback effect of high lev els of E: on LH secretion [ 17], we cannot completely rule out that the presence of elevated levels of P during MLP may con tribute to the LH-stimulating activity of A ll in women, differ ently from what has been observed in rats [6,10], Our data do not allow us to comment on either the mechanism or the main site of action of AIL Since plasma All crosses the blood-brain barrier to a very limited degree, its action would be largely restricted to anterior pituitary an d /o r to circumventricular organs containing specific A ll receptors, which can be reached and activated by peripheral A ll [18][19][20], Although All-like immunorcactivity has been localized within gonadotrophs [7,21 ], a direct stimulatory action of AI I on LH secretion from the anterior pituitary is unlikely since it has been shown that it does not affect LH release when added to pituitary cells in vitro [5,9,22], Otherwise, the increase of LH after A ll infusion might depend on an action of the peptide at the circumventricular organs, such as the median eminence, resulting in a stimulating of LH-releasing hormone (LH-RH) thereby eliciting LH release [23][24][25].…”

Section: Discussioncontrasting

confidence: 79%

Stimulatory Effect of Angiotensin II upon Luteinizing Hormone Release Normal Women

Uberti

Trasforini²,

Margutti³

et al. 1991

Neuroendocrinology

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In this study we investigated the effect of intravenous infusion of angiotensin II (AII) on plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels in fertile healthy women examined both in the middle follicular phase (MFP) and in the middle luteal phase (MLP). As expected, AII induced a significant increase in blood pressure and plasma aldosterone concentration. In MFP, plasma FSH and LH levels did not show any significant change after AII infusion, if compared to both saline and preinfusion basal values. In MLP, AII significantly increased plasma LH (p < 0.02 vs. baseline values and p < 0.01 vs. placebo values), but not plasma FSH. The area under the curve during AII infusion resulted significantly higher than during placebo infusion (p < 0.001). Therefore, these data demonstrate that peripherally injected AII at pressive dose produces an increase in plasma LH levels in normal women on luteal phase when the circulating concentrations of both estradiol and progesterone are high. The study suggests that AII may have a stimulatory role in the regulation of LH secretion, but this role is closely related to the gonadal steroid plasma levels.

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Section: Discussioncontrasting

confidence: 79%

Stimulatory Effect of Angiotensin II upon Luteinizing Hormone Release Normal Women

Uberti

Trasforini²,

Margutti³

et al. 1991

Neuroendocrinology

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“…46,47 Only when the antagonist was administered directly into the AP was a lowering of the BP observed, suggesting that chronic intravenous AII-hypertension does not involve activation of AT-1 receptors in intrinsic brain sites or in CVOs that are known to be penetrated by antagonists administered ICV (eg, SFO). 47,48 In addition to evidence that ICV administered AT-1 receptor blockers may not reach AP neurons, 47,49 a role for the AP in the hypertension of RAϩ mice in the present study is not supported, because the mechanism of chronic intravenous AII/AP-mediated hypertension involves increased sympathetic nerve activity rather than enhanced AVP secretion. 44 This does not, however, rule out a possible role for the AP in the maintenance of normal BP in the control mice in this study.…”

Section: Discussionmentioning

confidence: 55%

The Brain Renin-Angiotensin System Contributes to the Hypertension in Mice Containing Both the Human Renin and Human Angiotensinogen Transgenes

Davisson

Yang

Beltz

et al. 1998

Circulation Research

137

155

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Abstract-We have previously shown that mice transgenic for both the human renin and human angiotensinogen genes (RAϩ) exhibit appropriate tissue-and cell-specific expression of both transgenes, have 4-fold higher plasma angiotensin II (AII) levels, and are chronically hypertensive. However, the relative contribution of circulating and tissue-derived AII in causing hypertension in these animals is not known. We hypothesized that the brain renin-angiotensin system contributes to the elevated blood pressure in this model. To address this hypothesis, mean arterial pressure (MAP) and heart rate were measured in conscious, unrestrained mice after they were instrumented with intracerebroventricular cannulae and carotid arterial and jugular vein catheters. Intracerebroventricular administration of the selective AII type 1 (AT-1) receptor antagonist losartan (10 g, 1 L) caused a significantly greater peak fall in MAP in RAϩ mice than in nontransgenic RAϪ controls (Ϫ29Ϯ4 versus Ϫ4Ϯ2 mm Hg, PϽ0.01). To explore the mechanism of a central renin-angiotensin system-dependent hypertension in RAϩ mice, we determined the relative depressor responses to intravenous administration of the ganglionic blocking agent hexamethonium (5 mg/kg) or an arginine vasopressin (AVP) V 1 receptor antagonist (AVPX, 10 g/kg). Hexamethonium caused equal lowering of MAP in RAϩ mice and controls (Ϫ46Ϯ3 versus Ϫ52Ϯ3, PϾ0.05), whereas AVPX caused a significantly greater fall in MAP in RAϩ compared with RAϪ mice (Ϫ24Ϯ2 versus Ϫ6Ϯ1, PϽ0.01). Consistent with this was the observation that circulating AVP was 3-fold higher in RAϩ mice than in control mice. These results suggest that increased activation of central AT-1 receptors, perhaps those located at sites involved in AVP release from the posterior pituitary gland, plays a role in the hypertension in RAϩ mice. Furthermore, our finding that both human transgenes are expressed in brain regions of RAϩ mice known to be involved in cardiovascular regulation raises the possibility that augmented local production of AII and increased activation of AT-1 receptors at these sites is involved. (Circ Res. 1998;83:1047-1058.)Key Words: transgenic mice Ⅲ angiotensin Ⅲ blood pressure Ⅲ genetics Ⅲ pharmacology I t is well established that blood-borne angiotensin II (AII), the effector peptide of the renin-angiotensin system (RAS), plays a major role in the regulation of arterial blood pressure (BP) and volume homeostasis through its interaction with specific AII receptors present in vascular smooth muscle, kidney, and adrenal gland. Stimulation of these peripheral AII receptors leads to elevations in BP through increased vascular resistance, cardiac output, sodium reabsorption, and blood volume.1 However, in addition to these well-known actions at peripheral sites, AII also contributes to BP and volume regulation through its receptor-mediated effects on neurons located within the central nervous system (CNS). Indeed, central administration of AII causes increases in BP, antidiuresis, drinking, and salt appetite.2 This, ...

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“…infusions of ANG n . Despite this apparent drawback to the use of a rat model for studies on ANG II interactions with the AP, three additional considerations nevertheless encouraged our use of this species in the experiments reported here: 1) receptors for ANG II are found in high concentration in the rat AP, 20 and intravenously infused 123 I-ANGII readily penetrates the structure 8 ; 2) stimulation of the AP either electrically 21 or with direct microinjections of ANG I P causes an acute pressor response in the rat; and 3) recent work on chronic ANG H-induced hypertension in rats 7 pointed to the AP as a likely critical site for hormone interaction with the central nervous system (see Introduction).…”

Section: Resultsmentioning

confidence: 99%

Area postrema is critical for angiotensin-induced hypertension in rats.

Fink¹,

Bruner²,

Mangiapane³

1987

Hypertension

163

111

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SUMMARYThe effect of surgical ablation of the area postrema on acute (5-10 minutes) and chronic (5-10 days) increases in mean arterial pressure produced by intravenous infusion of angiotensin II hi conscious, instrumented rats was studied. In agreement with previous studies, pressor responses of area postrema-ablated rats (a = 11) to acute angiotensin II infusion were identical to those of control sham-lesioned rats (n = 13). In these same rats, however, a 5-day infusion of angiotensin II produced a sustained hypertension hi the sham-lesioned group whereas mean arterial pressure was increased only transiently (1-3 days) hi the area postrema-ablated rats. No differences before infusion of arterial pressure, heart rate, water intake, urinary sodium excretion, and urinary potassium excretion were observed between sham-lesioned and area postrema-ablated rats; only arterial pressure was changed significantly during angiotensin II infusion hi either group. Twenty-four hours after terminating angiotensin II infusion, mean arterial pressure was within the normotensive range hi both shamlesioned and area postrema-ablated rats. In a separate group of sham-lesioned (n = 13) and area postrema-ablated (n = 12) rats, angiotensin n was infused intravenously for a 10-day period; mean arterial pressure was increased significantly over the entire 10-day infusion hi sham-lesioned rats, but for only 1 day hi area postrema-ablated rats. An intact area postrema appears necessary for the development of chronic, but not acute, hypertension during intravenous infusion of angiotensin II hi the rat. Supported by National Heart, Lung, and Blood Institute Grants HL24111 andHL32981.Address for reprints: Dr. Gregory D. Fink, Dept. of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824.Received January 27, 1986; accepted October 20, 1986. perimental hypertension. A detailed analysis 1 of many of these studies led to the conclusion that ANG II does not cause chronic hypertension by direct vascular constriction, but rather by an ability to stimulate a more slowly developing (hours to days) pressor mechanism: a mechanism whose sensitivity to ANG II increases with prolonged exposure to the hormone. Actions of ANG II on aldosterone secretion, 2 renal handling of salt and water,

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[Sar1, Ala8] angiotensin II in cerebrospinal fluid blocks the binding of blood-borne [125I]angiotensin II to the circumventricular organs

Cited by 80 publications

References 4 publications

Stimulatory Effect of Angiotensin II upon Luteinizing Hormone Release Normal Women

Stimulatory Effect of Angiotensin II upon Luteinizing Hormone Release Normal Women

The Brain Renin-Angiotensin System Contributes to the Hypertension in Mice Containing Both the Human Renin and Human Angiotensinogen Transgenes

Area postrema is critical for angiotensin-induced hypertension in rats.

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