Effects of paraventricular nucleus lesions on chronic renal hypertension

T. C. Herzig, R. A. Buchholz and J. R. Haywood Department of Pharmacology, University of Texas Health Science Center, San Antonio 78284-7764. The contribution of the paraventricular nucleus region of the hypothalamus (PVN) to the maintenance of one-kidney, figure-8 renal wrap hypertension was determ...

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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 1991-09, Vol.261 (3), p.H860-H867
Hauptverfasser: Herzig, T. C, Buchholz, R. A, Haywood, J. R
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Sprache:eng
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Zusammenfassung:T. C. Herzig, R. A. Buchholz and J. R. Haywood Department of Pharmacology, University of Texas Health Science Center, San Antonio 78284-7764. The contribution of the paraventricular nucleus region of the hypothalamus (PVN) to the maintenance of one-kidney, figure-8 renal wrap hypertension was determined in this study. Electrolytic ablation of the PVN was performed 4 wk after the production of hypertension or sham operation. Ablation of the PVN region significantly reduced mean arterial pressure (MAP) from 150 +/- 9 to 110 +/- 3 mmHg in the hypertensive rats. In the sham-hypertensive group, the lesion decreased MAP from 118 +/- 2 to 99 +/- 4 mmHg. In both groups of animals MAP from 118 +/- 2 to 99 +/- 4 mmHg. In both groups of animals MAP returned to prelesion values by day 7 postlesion. When ganglionic blockade was performed on day 7 postlesion, the fall in MAP was greater in hypertensive rats (-44 +/- 5 mmHg) than in normotensive rats (-26 +/- 3 mmHg). In a separate group of rats studied 3 days after PVN ablation, ganglionic blockade produced similar decreases in MAP in the wrapped and sham-operated animals. These studies suggest that the PVN contributes to the increased functional sympathetic nervous system associated with one-kidney, figure-8 renal hypertension. Although ablation of the PVN region decreases MAP, neural mechanisms compensate to return MAP to hypertensive levels.
ISSN:0363-6135
0002-9513
1522-1539
DOI:10.1152/ajpheart.1991.261.3.h860