Sodium-dependent hypertension produced by chronic central angiotensin II infusion

Bruner, C. A.; Weaver, Justin; Fink, Gershon

doi:10.1152/ajpheart.1985.249.2.h321

Cited by 19 publications

(22 citation statements)

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“…It must be considered that at least part of the effect of central ANG II administration to influence splenic cytokine gene expression may have resulted from ANG II leaking from the cerebrospinal fluid into the peripheral circulation and causing norepineprine release from adrenergic nerve ending sites. Although the present data do not exclude this possibility, it seems unlikely on the basis of the results of Bruner et al (7), who reported that plasma ANG II levels were not increased during the 5th day of a chronic intracerebroventricular infusion of ANG II administered in the microgram dose range. In contrast, the present study used a single 10-min central infusion of a dose of ANG II in the nanogram range.…”

Section: Discussioncontrasting

confidence: 75%

Central angiotensin II-enhanced splenic cytokine gene expression is mediated by the sympathetic nervous system

Ganta

Lü

Helwig

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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We tested the hypothesis that central angiotensin II (ANG II) administration would activate splenic sympathetic nerve discharge (SND), which in turn would alter splenic cytokine gene expression. Experiments were completed in sinoaortic nerve-lesioned, urethane-chloralose-anesthetized, splenic nerve-intact (splenic-intact) and splenic nerve-lesioned (splenic-denervated) Sprague-Dawley rats. Splenic cytokine gene expression was determined using gene-array and real-time RT-PCR analyses. Splenic SND was significantly increased after intracerebroventricular administration of ANG II (150 ng/kg, 10 microl), but not artificial cerebrospinal fluid (aCSF). Splenic mRNA expression of IL-1beta, IL-6, IL-2, and IL-16 genes was increased in ANG II-treated splenic-intact rats compared with aCSF-treated splenic-intact rats. Splenic IL-1beta, IL-2, and IL-6 gene expression responses to ANG II were significantly reduced in splenic-denervated compared with splenic-intact rats. Splenic gene expression responses did not differ significantly in ANG II-treated splenic-denervated and aCSF-treated splenic-intact rats. Splenic blood flow responses to intracerebroventricular ANG II administration did not differ between splenic-intact and splenic-denervated rats. These results provide experimental support for the hypothesis that ANG II modulates the immune system through activation of splenic SND, suggesting a novel relation between ANG II, efferent sympathetic nerve outflow, and splenic cytokine gene expression.

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Section: Discussioncontrasting

confidence: 75%

Central angiotensin II-enhanced splenic cytokine gene expression is mediated by the sympathetic nervous system

Ganta

Lü

Helwig

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…In a previous study, the continuous ICV infusion of angiotensin II caused salt-sensitive hypertension in rats. 21 Together, these findings indicate that the genesis of hypertension in saltinduced hypertensive models such as DOCA-salt hypertension through the upregulation of the brain renin-angiotensin system genes involves not epithelial sodium channels, as previously reported, 22 but rather newly cloned amiloridesensitive sodium channels in the brain that are activated by FMRFamide. 6 FMRFamide-activated brain sodium channel may participate in the upregulation of the brain renin-angiotensin system genes.…”

Section: Discussionsupporting

confidence: 74%

Role of FMRFamide-Activated Brain Sodium Channel in Salt-Sensitive Hypertension

et al. 2000

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Abstract-FMRFamide, a cardioexcitatory neuropeptide, directly activates a newly cloned amiloride-sensitive sodium channel that is expressed specifically in the brain and blocked by benzamil hydrochloride. In the present study, we investigated the effects of short-and long-term intracerebroventricular infusion of FMRFamide on arterial pressure, sympathetic activity, vasopressin release, and brain renin-angiotensin system genes in rats and studied the role of FMRFamide-activated brain sodium channels in salt-sensitive hypertension. The intracerebroventricular preinjection of FMRFamide and subsequent intracerebroventricular infusion of 0.15 mol/L NaCl increased mean arterial pressure (FMRFamide: 30 nmol/kg ϩ13Ϯ2.6 mm Hg, PϽ0.01; 100 nmol/kg ϩ21Ϯ1.8 mm Hg, PϽ0.01), heart rate, abdominal sympathetic activity, and plasma vasopressin concentration compared with vehicle. The intracerebroventricular copreinjection with either benzamil or CV-11974 abolished these increases. In rats administered a high-salt diet (8% NaCl), the continuous intracerebroventricular infusion of FMRFamide (50 and 200 nmol ⅐ kg Ϫ1 ⅐ d Ϫ1 ) for 5 days increased mean arterial pressure, heart rate, urinary excretion of vasopressin and norepinephrine, and mRNAs of renin, angiotensin I-converting enzyme, and angiotensin II type 1 receptor in hypothalamus and brain stem compared with vehicle. These increases were abolished by intracerebroventricular coinfusion of benzamil. In rats administered a low-salt diet (0.3% NaCl), however, increases in these variables were smaller than those in rats receiving a high-salt diet. Together, these findings suggest that brain FMRFamide-activated sodium channels may be involved in the mechanism of salt-sensitive hypertension through regulation of the brain renin-angiotensin system.

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“…8,10 Physiological interactions are also observed, such as Ang-mediated drinking and vasopressin responses, sodium-induced potentiation of the pressor action of Ang, and angiotensinergic modulation of the response to dehydration. [11][12][13][14] The question that has arisen is the role of the specific AT1 subtypes in the responses. Autoradiographic techniques used to measure receptor density do not distinguish between AT1a and AT1b subtypes because of the structural similarity of the receptors.…”

mentioning

confidence: 99%

Neuroendocrine Effects of Dehydration in Mice Lacking the Angiotensin AT1a Receptor

Morris

Callahan

et al. 1999

Hypertension

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Abstract-Angiotensin (Ang) type 1a (AT1a) receptors are critical in the control of blood pressure and water balance.Experiments were performed to determine the influence of dehydration on brain Ang receptors and plasma vasopressin (VP) in mice lacking this receptor. Control or AT1a knockout (AT1aKO) male mice were give water ad libitum or deprived of water for 48 hours. Animals were anesthetized with halothane, blood samples were collected by heart puncture, and brains were processed for Ang-receptor autoradiography with 125 I-sarthran (0.4 nmol/L). Dehydration produced an increase in AT1 receptors in the paraventricular nucleus (PVN) and anterior pituitary (AP) in control mice (PVN: 70Ϯ16 versus 146Ϯ10 fmol/mg protein; AP: 41Ϯ7 versus 86Ϯ15 fmol/mg protein). No changes were noted in the median preoptic nucleus. The majority of the brain receptors were of the AT1 subtype. There was little or no specific Ang binding in AT1aKO mice and no effect of dehydration. Plasma VP levels were elevated in the halothane-anesthetized animals (Ͼ200 pg/mL) with no significant effect of dehydration. A separate experiment was performed with decapitated mice anesthetized with pentobarbital. Dehydration increased plasma VP in control mice, from 3.3Ϯ0.6 to 13.3Ϯ4.7 pg/mL, whereas no change was noted in the AT1aKO mice, 5.1Ϯ0.3 versus 6.1Ϯ0.7 pg/mL (water versus dehydration). These results demonstrate a differential response to dehydration in mice lacking AT1a receptors. There was no evidence for AT1 receptors of any subtype in the brain regions examined and no effect of dehydration on VP secretion or brain Ang receptors. Key Words: central nervous system Ⅲ hypothalamus Ⅲ vasopressin Ⅲ water balance Ⅲ blood pressure T here are strong links between the renin angiotensin system (RAS) and fluid/electrolyte balance. 1-3 Alterations in volume status produced by dehydration, salt loading, or deprivation result in changes in brain and peripheral angiotensin (Ang) receptors. 4 -8 Dehydration in rats produced an increase in Ang type 1 (AT1) receptors in anterior pituitary (AP) and subfornical organ (SFO), with no change noted in the paraventricular nucleus (PVN). 4,5,9 Salt loading caused an increase in SFO and PVN Ang receptors. 8,10 Physiological interactions are also observed, such as Ang-mediated drinking and vasopressin responses, sodium-induced potentiation of the pressor action of Ang, and angiotensinergic modulation of the response to dehydration. [11][12][13][14] The question that has arisen is the role of the specific AT1 subtypes in the responses. Autoradiographic techniques used to measure receptor density do not distinguish between AT1a and AT1b subtypes because of the structural similarity of the receptors. [15][16][17][18] Likewise, specific pharmacological antagonists are not available. Gene deletion or knockout (KO) methods provide a new way of separating the receptor subtypes in an in vivo model. A comparison of the AT1a and AT1b receptor KO strains supports the idea that AT1a receptors are critical in blood pressure and flu...

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Sodium-dependent hypertension produced by chronic central angiotensin II infusion

Cited by 19 publications

References 0 publications

Central angiotensin II-enhanced splenic cytokine gene expression is mediated by the sympathetic nervous system

Central angiotensin II-enhanced splenic cytokine gene expression is mediated by the sympathetic nervous system

Role of FMRFamide-Activated Brain Sodium Channel in Salt-Sensitive Hypertension

Neuroendocrine Effects of Dehydration in Mice Lacking the Angiotensin AT1a Receptor

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