AT1 receptors mediate chronic central nervous system AII hypertension in rats fed high sodium chloride diet from weaning

Amadou K.S. Camara; Jeffrey L. Osborn

doi:10.1016/S0165-1838(98)00080-0

AT₁ receptors mediate chronic central nervous system AII hypertension in rats fed high sodium chloride diet from weaning

Amadou K.S. Camara, Jeffrey L. Osborn

Biology

Research output: Contribution to journal › Article › peer-review

13 Scopus citations

Abstract

CNS angiotensin II (AII) hypertension is induced by chronic, low dose intracerebroventricular (ICV) AII infusion only in rats raised on a relatively high sodium chloride diet (250 meq kg^-1 food) from weaning. This experimental model of hypertension is dependent upon renal sympathetic innervation and associated with neurogenic sodium retention. This study determined whether AT₁ and/or AT₂ receptor subtypes in the CNS mediate this neurogenic ICV AII hypertension. Rats were weaned at 21 days of age and fed a 1.5% sodium chloride diet for 10-12 weeks. At adulthood, animals were instrumented with CNS lateral ventricular cannulas, femoral arterial and vein catheters and housed in metabolic pens for chronic study. Low dose ICV AII infusion (20 ng min^-1) increased mean arterial pressure by 12±2 mm Hg and decreased urinary sodium excretion for three consecutive days. Subsequent ICV AT₁ blockade with losartan abolished both the pressor and antinatriuretic responses to low dose ICV AII. In contrast, ICV AT₂ receptor blockade with PD 123319 did not affect either angiotensin induced pressor or antinatriuretic responses. Following cessation of ICV AII infusion, arterial pressure and sodium excretion returned to values not significantly different from control in both groups of rats. These data confirm that low dose ICV AII causes hypertension and sodium retention in rats raised from early age on moderately elevated sodium intakes. This AII mediated neurogenic hypertension and antinatriuresis is transduced by activation of CNS AT₁ receptors and not by activation of central AT₂ receptors. Copyright (C) 1998 Elsevier Science B.V.

Original language	English
Pages (from-to)	16-23
Number of pages	8
Journal	Journal of the Autonomic Nervous System
Volume	72
Issue number	1
DOIs	https://doi.org/10.1016/S0165-1838(98)00080-0
State	Published - Aug 6 1998

Bibliographical note

Funding Information:
We gratefully acknowledge the generous gifts of losartan by the Merck Dupont and that of PD 123319 by Parke-Davis. The authors wish to thank Mr Erez Gordin for his technical and computer assistance. We would also like to extend our appreciation to the following individuals for their technical assistance: Ms Terry Kurth, Mr Harold Eick and Mr David Eick. This work was supported in part by an NIH Minority Graduate Assistant Supplement and by NHLBI PO1-29587 and NHLBI RO1-40137. Address reprint requests to Dr Jeffrey L. Osborn, Department of Physiology, Medical College of Wisconsin, Milwaukee, WI.

Funding

We gratefully acknowledge the generous gifts of losartan by the Merck Dupont and that of PD 123319 by Parke-Davis. The authors wish to thank Mr Erez Gordin for his technical and computer assistance. We would also like to extend our appreciation to the following individuals for their technical assistance: Ms Terry Kurth, Mr Harold Eick and Mr David Eick. This work was supported in part by an NIH Minority Graduate Assistant Supplement and by NHLBI PO1-29587 and NHLBI RO1-40137. Address reprint requests to Dr Jeffrey L. Osborn, Department of Physiology, Medical College of Wisconsin, Milwaukee, WI.

Funders	Funder number
National Institutes of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)	PO1-29587, RO1-40137

Keywords

Angiotensin receptors
Central nervous system
Hypertension
Kidney function
Sodium chloride intake
Sympathetic nerves

ASJC Scopus subject areas

General Neuroscience
Physiology
Clinical Neurology

Access to Document

10.1016/S0165-1838(98)00080-0

Cite this

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title = "AT1 receptors mediate chronic central nervous system AII hypertension in rats fed high sodium chloride diet from weaning",

abstract = "CNS angiotensin II (AII) hypertension is induced by chronic, low dose intracerebroventricular (ICV) AII infusion only in rats raised on a relatively high sodium chloride diet (250 meq kg-1 food) from weaning. This experimental model of hypertension is dependent upon renal sympathetic innervation and associated with neurogenic sodium retention. This study determined whether AT1 and/or AT2 receptor subtypes in the CNS mediate this neurogenic ICV AII hypertension. Rats were weaned at 21 days of age and fed a 1.5% sodium chloride diet for 10-12 weeks. At adulthood, animals were instrumented with CNS lateral ventricular cannulas, femoral arterial and vein catheters and housed in metabolic pens for chronic study. Low dose ICV AII infusion (20 ng min-1) increased mean arterial pressure by 12±2 mm Hg and decreased urinary sodium excretion for three consecutive days. Subsequent ICV AT1 blockade with losartan abolished both the pressor and antinatriuretic responses to low dose ICV AII. In contrast, ICV AT2 receptor blockade with PD 123319 did not affect either angiotensin induced pressor or antinatriuretic responses. Following cessation of ICV AII infusion, arterial pressure and sodium excretion returned to values not significantly different from control in both groups of rats. These data confirm that low dose ICV AII causes hypertension and sodium retention in rats raised from early age on moderately elevated sodium intakes. This AII mediated neurogenic hypertension and antinatriuresis is transduced by activation of CNS AT1 receptors and not by activation of central AT2 receptors. Copyright (C) 1998 Elsevier Science B.V.",

keywords = "Angiotensin receptors, Central nervous system, Hypertension, Kidney function, Sodium chloride intake, Sympathetic nerves",

author = "Camara, {Amadou K.S.} and Osborn, {Jeffrey L.}",

note = "Funding Information: We gratefully acknowledge the generous gifts of losartan by the Merck Dupont and that of PD 123319 by Parke-Davis. The authors wish to thank Mr Erez Gordin for his technical and computer assistance. We would also like to extend our appreciation to the following individuals for their technical assistance: Ms Terry Kurth, Mr Harold Eick and Mr David Eick. This work was supported in part by an NIH Minority Graduate Assistant Supplement and by NHLBI PO1-29587 and NHLBI RO1-40137. Address reprint requests to Dr Jeffrey L. Osborn, Department of Physiology, Medical College of Wisconsin, Milwaukee, WI. ",

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T1 - AT1 receptors mediate chronic central nervous system AII hypertension in rats fed high sodium chloride diet from weaning

AU - Camara, Amadou K.S.

AU - Osborn, Jeffrey L.

N1 - Funding Information: We gratefully acknowledge the generous gifts of losartan by the Merck Dupont and that of PD 123319 by Parke-Davis. The authors wish to thank Mr Erez Gordin for his technical and computer assistance. We would also like to extend our appreciation to the following individuals for their technical assistance: Ms Terry Kurth, Mr Harold Eick and Mr David Eick. This work was supported in part by an NIH Minority Graduate Assistant Supplement and by NHLBI PO1-29587 and NHLBI RO1-40137. Address reprint requests to Dr Jeffrey L. Osborn, Department of Physiology, Medical College of Wisconsin, Milwaukee, WI.

PY - 1998/8/6

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N2 - CNS angiotensin II (AII) hypertension is induced by chronic, low dose intracerebroventricular (ICV) AII infusion only in rats raised on a relatively high sodium chloride diet (250 meq kg-1 food) from weaning. This experimental model of hypertension is dependent upon renal sympathetic innervation and associated with neurogenic sodium retention. This study determined whether AT1 and/or AT2 receptor subtypes in the CNS mediate this neurogenic ICV AII hypertension. Rats were weaned at 21 days of age and fed a 1.5% sodium chloride diet for 10-12 weeks. At adulthood, animals were instrumented with CNS lateral ventricular cannulas, femoral arterial and vein catheters and housed in metabolic pens for chronic study. Low dose ICV AII infusion (20 ng min-1) increased mean arterial pressure by 12±2 mm Hg and decreased urinary sodium excretion for three consecutive days. Subsequent ICV AT1 blockade with losartan abolished both the pressor and antinatriuretic responses to low dose ICV AII. In contrast, ICV AT2 receptor blockade with PD 123319 did not affect either angiotensin induced pressor or antinatriuretic responses. Following cessation of ICV AII infusion, arterial pressure and sodium excretion returned to values not significantly different from control in both groups of rats. These data confirm that low dose ICV AII causes hypertension and sodium retention in rats raised from early age on moderately elevated sodium intakes. This AII mediated neurogenic hypertension and antinatriuresis is transduced by activation of CNS AT1 receptors and not by activation of central AT2 receptors. Copyright (C) 1998 Elsevier Science B.V.

AB - CNS angiotensin II (AII) hypertension is induced by chronic, low dose intracerebroventricular (ICV) AII infusion only in rats raised on a relatively high sodium chloride diet (250 meq kg-1 food) from weaning. This experimental model of hypertension is dependent upon renal sympathetic innervation and associated with neurogenic sodium retention. This study determined whether AT1 and/or AT2 receptor subtypes in the CNS mediate this neurogenic ICV AII hypertension. Rats were weaned at 21 days of age and fed a 1.5% sodium chloride diet for 10-12 weeks. At adulthood, animals were instrumented with CNS lateral ventricular cannulas, femoral arterial and vein catheters and housed in metabolic pens for chronic study. Low dose ICV AII infusion (20 ng min-1) increased mean arterial pressure by 12±2 mm Hg and decreased urinary sodium excretion for three consecutive days. Subsequent ICV AT1 blockade with losartan abolished both the pressor and antinatriuretic responses to low dose ICV AII. In contrast, ICV AT2 receptor blockade with PD 123319 did not affect either angiotensin induced pressor or antinatriuretic responses. Following cessation of ICV AII infusion, arterial pressure and sodium excretion returned to values not significantly different from control in both groups of rats. These data confirm that low dose ICV AII causes hypertension and sodium retention in rats raised from early age on moderately elevated sodium intakes. This AII mediated neurogenic hypertension and antinatriuresis is transduced by activation of CNS AT1 receptors and not by activation of central AT2 receptors. Copyright (C) 1998 Elsevier Science B.V.

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KW - Kidney function

KW - Sodium chloride intake

KW - Sympathetic nerves

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