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Blood Pressure and Sodium Chloride Intake Regulation in Borderline Neurogenic Hypertensive BN/SHR Backcross Rats
Author(s) -
Fain Aaron,
Osborn Jeffrey L.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1206
Subject(s) - endocrinology , medicine , blood pressure , angiotensin ii , sodium , thirst , offspring , chemistry , biology , organic chemistry , pregnancy , genetics
Lifetime elevation of sodium chloride intake elicits hypertension in rats infused intracerebroventricularly with angiotensin II (AII) at doses that are subpressor in rats fed normal sodium diets. This sensitization of brain structures to AII may result from upregulation of hypothalamic angiotensin receptors. We hypothesize that hypothalamic AII receptor expression is increased in rats genetically predisposed to hypertension. Elevation of sodium chloride intake from weaning further increases brain AII receptors leading to neurogenic hypertension. Backcross borderline hypertensive rats were derived from an Okamoto SHR – Brown Norway cross followed by F1 generation matings of hypertensive offspring. These rats were raised from weaning to adulthood on high (4%) or normal (0.8%) salt diets. Hypertension (BP > 110 mmHg) was determined by tail cuff plethysmography. Animals were placed in metabolic pens and provided distilled water, hypertonic saline (2%) and sodium free chow to measure blood pressure and daily intakes of water, salt and food for 5 days. Rats raised on 0.8% salt increased their mean blood pressure by 10 mmHg (systolic hypertension) whereas blood pressures of rats raised on 4% sodium chloride were unchanged despite a reduction in body mass averaging 9g, and increased sodium and water intake over the 5 days. Body mass of rats raised on 0.8% sodium chloride remained unchanged. These results suggest that raising rats genetically predisposed to borderline hypertension on high salt intakes alters chronic regulation of both salt and water intake which may contribute to further elevations in blood pressure. (Supported by APS Undergraduate Summer Research Fellowship to A. Fain)