Role of chloride in angiotensin II-induced salt-sensitive hypertension.

Sato, Yuji; Ogata, Etsuro; Fujita, Toshiro

doi:10.1161/01.hyp.18.5.622

Cited by 31 publications

(26 citation statements)

References 26 publications

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“…In addition, these findings may provide a link between increased chloride reabsorption in the early distal tubule in salt-sensitive hypertension and blood pressure elevation (Kirchner, 1990;Roman & Kaldunski, 1991) and, conversely, between the defect in chloride reabsorption in the loop of Henle and the hypotension in Bartter's syndrome (Gill & Bartter, 1978). This effect of chloride on vasoactivity may explain the requirement for chloride as the anion accompanying sodium in salt-sensitive (Boegehold & Kotchen, 1989) and AII-dependent (Passmore & Jimenez, 1991;Sato et al, 1991) models of hypertension. Finally, the results of the present study support the hypothesis that the ability of high chloride to increase RVR and lower GFR is due, at least in part, to the ability of chloride to modify responsiveness of the kidney to pressor agents.…”

Section: Discussionmentioning

confidence: 96%

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Quilley

Lin

McGiff

1993

British J Pharmacology

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Section: Discussionmentioning

confidence: 96%

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Quilley

Lin

McGiff

1993

British J Pharmacology

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“…Therefore, when ANG II was clamped, the progressive increase in body fluid volume and renal interstitial pressure became excessive (or inappropriate) to the existing plasma or renal levels of ANG II. The word inappropriate may be more pertinent because the hypertensinogenic effect of ANG II was produced in the presence of volume expansion that was not different from animals that did not receive ANG II and remained normotensive, although many other investigators have shown that increased sodium intake causes a marked potentiation of ANG II pressor effect (6,35,74,108,142,154). DeClue et al (36) was the first to demonstrate that a dissociation between extracellular fluid volume and the plasma or perhaps tissue levels of ANG II may be an important alteration underlying the development of high blood pressure.…”

Section: The Effects Of Sodium Intake On the Pressor Response To Ang IImentioning

confidence: 99%

Role of oxidative stress in angiotensin-induced hypertension

Reckelhoff

Romero

2003

American Journal of Physiology-Regulatory, Integrative and Comp

166

133

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Reckelhoff, Jane F., and J. Carlos Romero. Role of oxidative stress in angiotensin-induced hypertension. Am J Physiol Regul Integr Comp Physiol 284: R893-R912, 2003; 10.1152/ajpregu.00491.2002.-Infusion of ANG II at a rate not sufficient to evoke an immediate vasoconstrictor response, produces a slow increase in blood pressure. Circulating levels of ANG II may be within ranges found in normotensive individuals, although inappropriately high with respect to sodium intake. When ANG II levels are dissociated from sodium levels, oxidative stress (OXST) occurs, which can increase blood pressure by several mechanisms. These include inadequate production or reduction of bioavailability of nitric oxide, alterations in metabolism of arachidonic acid, resulting in an increase in vasoconstrictors and decrease in vasodilators, and upregulation of endothelin. This cascade of events appears to be linked, because ANG II hypertension can be blocked by inhibition of any factor located distally, blockade of ANG II, OXST, or endothelin. Such characteristics are shared by other models of hypertension, such as essential hypertension, hypertension induced by reduction in renal mass, and renovascular hypertension. Thus these findings are clinically important because they reveal 1) uncoupling between ANG II and sodium, which can trigger pathological conditions; 2) the various OXST mechanisms that may be involved in hypertension; and 3) therapeutic interventions for hypertension developed with the knowledge of the cascade involving OXST.isoprostanes; endothelin; spontaneous hypertension; renovascular hypertension; sodium balance THREE DECADES AGO, the production of free radicals was thought to be the result of severe injuries or pathological insults such as those resulting from exposure to high-energy radiation or toxins such as carbon tetrachloride (127). However, in 1968, the discovery of superoxide dismutase (SOD) by McCord and Fridovich (96) strongly suggested that all aerobically metabolizing cells are capable of producing superoxide ions, which could play a role in normal metabolic processes. The concomitant discovery of the biology of nitric oxide (NO) strongly suggested that free radicals could constitute the basis of metabolic regulation (67,90,118). One of the first findings supporting such a notion was the demonstration that the inhibition of the synthesis of NO produced by the administration of an NO synthesis competitor, such as N -monomethyl-Larginine] or N G -nitro-L-arginine methyl ester (L-NAME), produced a marked vasoconstriction (13,136,173), sodium retention (82, 83), and thereby a sustained increase in mean arterial pressure (MAP) (13,82,83,136,173). The identification of a specific pathological situation in humans, where a decrease of NO may end up in an elevation of blood pressure was thought to be linked to endothelial dysfunction (105), such as those involved in aging, arteriosclerosis, etc., but the specific metabolic alterations involved in this process were poorly understood. However, the relationship betw...

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“…24,26 It is well established that chronic low-dose Ang II infusion is a salt-sensitive model of hypertension, and there is evidence to suggest that the additional hypertensive effect of salt is mediated by sympathetic nervous system activation. 13,[27][28][29][30] Although the most compelling evidence for sympathetic nervous system activation in response to salt is described in rats, 13,[27][28][29][30] it has also been demonstrated recently in rabbits 31 using repeated assessment of response to ganglionic blockade. More importantly, there is considerable evidence that neurogenic mechanisms may play a role in the pathophysiology of salt sensitivity in human essential hypertension.…”

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confidence: 99%

Chronic Low-Dose Angiotensin II Infusion Increases Venomotor Tone by Neurogenic Mechanisms

King

Fink

2006

Hypertension

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Abstract-The purpose of this study was to identify changes in venomotor tone in the chronic low-dose angiotensin II (Ang II) model of hypertension and to establish the contribution of sympathetic nerve activation to these venomotor tone changes. Male Sprague-Dawley rats were acclimatized to a 0.4% or 2.0% NaCl diet for 7 days and then catheterized to allow chronic and repeated measures of arterial pressure, central venous pressure, and mean circulatory filling pressure (MCFP), an index of venous smooth muscle tone, in conscious undisturbed rats. After 4 days of recovery and a 3-day control period, an Ang II or physiological saline-filled osmotic minipump was implanted subcutaneously to deliver Ang II (150 ng/kg per minute) or vehicle control for 14 days. MCFP was measured in duplicate before and after acute ganglionic blockade with hexamethonium (30 mg/kg IV) on control day 2 and Ang II infusion on days 1, 3, 7, and 14. Blood volume was also measured on these days and was unchanged for the duration of the study in all of the groups. Arterial pressure was increased for the duration of Ang II infusion in rats on both 0.4% and 2% NaCl diets, but the increase was significantly greater in the 2% NaCl group and completely abolished by hexamethonium. MCFP was significantly increased for the entire Ang II infusion period only in rats fed 2% NaCl, and this increase was completely abolished by hexamethonium. We conclude that the combination of chronic low-dose Ang II infusion and high dietary salt intake engages the sympathetic nervous system to increase venomotor tone. Key Words: angiotensin II Ⅲ venomotor tone Ⅲ mean circulatory filling pressure Ⅲ sympathetic nervous system Ⅲ salt E merging evidence suggests that sympathetic nervous system activation may represent a common neurogenic mechanism of hypertension in both human essential hypertension 1-6 and many experimental animal models. 7-10 Angiotensin II (Ang II) has been identified as a humoral factor implicated in activating the sympathetic nervous system in human hypertension 11,12 ; and the pressor response to infusion of chronic low-dose Ang II in animals has been shown, at least in part, to be sympathetically driven. [13][14][15] Advances have been made in the elucidation of the central pathways involved in mediating this sympathoexcitatory effect, suggesting that systemically delivered Ang II likely activates critical circumventricular organs 16 -19 with efferent projections to brain centers known to influence sympathetic nervous system activity. 18 Oxidative stress may mediate this central sympathoexcitatory effect. 20 However, there is still substantial uncertainty as to the critical peripheral target and the hemodynamic response to this increased sympathetic activity.In this study, we investigated the possibility that the venous circulation may be an important target for Ang II-induced sympathetic nervous system activation. The venous system contains Ϸ70% of the blood volume, 21 mostly in the small veins and venules, and has been shown to be more sensitive t...

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Role of chloride in angiotensin II-induced salt-sensitive hypertension.

Cited by 31 publications

References 26 publications

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Role of oxidative stress in angiotensin-induced hypertension

Chronic Low-Dose Angiotensin II Infusion Increases Venomotor Tone by Neurogenic Mechanisms

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