Pathogenesis of Hypertension in Rats with Chronic Aortic Baroreceptor Deafferentation

SUMMARY In an attempt to produce a form of chronic neorogenlc hypertension without the Increased blood pressure lability which b characteristic of total baroreceptor removal, selective aortic baroreceptor deafferentation (ABD) was performed In rats. Blood pressure, Mood pressure variability, heart r...

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Veröffentlicht in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 1980-05, Vol.2 (3), p.319-325
Hauptverfasser: FINK, GREGORY D, KENNEDY, FIDELMA, BRYAN, WILLIAM J, WERBER, ANDREW
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Sprache:eng
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Zusammenfassung:SUMMARY In an attempt to produce a form of chronic neorogenlc hypertension without the Increased blood pressure lability which b characteristic of total baroreceptor removal, selective aortic baroreceptor deafferentation (ABD) was performed In rats. Blood pressure, Mood pressure variability, heart rate, plasma and extracellular fluid volumes, and the effect of total autonomk blockade were determined in male rats 1 month following ABD. Rats with ABD had significantly higher systolic, diastollc, and mean arterial blood pressures than did sham-operated animals, but the standard deviation of pressure measured repetitively over a 1-hour period was not significantly greater. Total autonomk blockade with atroplne, propranolol, and pnentolamine lowered blood pressure and heart rate to a similar level In ABD and sham-operated rats. Extracellular fluid volume was not different In the two groups of rats, but plasma volume was significantly lower in rats with ABD. Despite the overall reduction in plasma volume, there was a significant positive correlation between plasma volume and blood pressure In ABD rats; no such correlation was observed in sham-operated rats. It was concluded that ABD produces a mild, chronic hypertension in rats without marked pressure lability. Although the hypertension appears to be 'neurogenic' In that it is abolished by autonomic blockade, volume factors also may contribute to the increased blood pressure.
ISSN:0194-911X
1524-4563
DOI:10.1161/01.HYP.2.3.319