Hypertension is elicited by chronic, low dose intracerebroventricular (ICV) angiotensin II (AII) infusion in rats raised from weaning on relatively high sodium chloride diet (250 mEq kg-1 food). This experimental model of hypertension is dependent upon renal innervation and associated with neurogenic sodium retention. The present study determined whether this neurogenic ICV AII hypertension is mediated by central α-adrenoceptors. Rats were weaned at 21 days of age and fed a 1.5% (250 mg kg-1 food) sodium chloride diet for 10-12 weeks. At adulthood, animals were instrumented with central nervous system (CNS) lateral ventricular cannulas, femoral artery and vein catheters and housed in metabolic pens for chronic study. Low dose ICV AII infusion (20 ng min-1) increased mean arterial pressure (MAP) from 121±4 to 140±6 mm Hg on the day of ICV infusion. This increase in arterial pressure was associated with 3 consecutive days of decreased urinary sodium excretion. Subsequent ICV α-adrenoceptor blockade with phentolamine (AII+phentolamine) abolished the pressor and antinatriuretic responses to low dose chronic ICV AII infusion. Resumption of ICV AII infusion alone increased in MAP toward pre-α-adrenergic blockade values (133±5 mm Hg) on day 8. Following cessation of ICV AII infusion, arterial pressure and sodium excretion returned to values not significantly different from control. This model of hypertension was not dependent on circulating plasma renin activity (PRA), since PRA decreased during ICV AII infusion. These data confirm that low dose ICV AII causes hypertension and sodium retention in rats raised from weaning on moderately elevated sodium intake. We conclude that AII mediated neurogenic hypertension and antinatriuresis is elicited by stimulation of AT1 receptors on neurons which interact with noradrenergic cell bodies in cardiovascular and autonomic centers that may modulate renal sympathetic outflow via α-adrenoceptors. Copyright (C) 1999 Elsevier Science B.V.
|Number of pages||7|
|Journal||Journal of the Autonomic Nervous System|
|State||Published - Apr 16 1999|
Bibliographical noteFunding Information:
We 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, Ms Kelly Zanoni, Mr Harold Eick and Mr David Eick. This work was supported in part by an NIH Minority Graduate Assistant Supplement and by NHLBI RO1-40137.
- Angiotensin II
- Central nervous system
- Sodium chloride intake
ASJC Scopus subject areas
- Neuroscience (all)
- Clinical Neurology