Lack of effect of vasopressin replacement on renin hypersecretion in Brattleboro rats

Lack of effect of vasopressin replacement on renin hypersecretion in Brattleboro rats GOL, RAFFAELLO M. A., EIJI GOTOH, LANNY C. KEIL, ROY L. SHACKELFORD, AND WILLIAM F. GANONG. Lack of effect of vasopressreplacement on hypersecretion . Am. J. Physiol. 257 (Regulatory tegrative Comp. Physiol. 26): R1117-R1122, 1989.-To determe how the vasopress deficiency homozygous with diabetes sipidus produces creased secretion, homozygousand heterozygous were fused through subcutaneouslyimplanted Alzet mipumps for 1 wk with a doseof arge vasopressthat restored plasmavasopress to normal the homozygous animals. the homozygous animals, plasma activity (PRA) and the PRA response to immobilization remaed elevated compared with LongEvans controls. Propranolol reducedPRA to normal and markedly reduced the PRA responseto immobilization. PRA was normal heterozygous . The data dicate that the creased secretion homozygous is a result of creasedsympathetic activity, and becausecirculatg vasopress doesnot crossthe blood-bra barrier, it seemslikely that the creasedsympathetic activity is central orig. arge vasopress; plasma activity; angiotensogen VASOPRESS deficiency homozygous with diabetes sipidus (DI) is associated with elevated plasma activity (PRA) at rest and supernormal responses to stimuli that crease secretion (see Ref. 15). The hypersecretion could be due to the lack of a direct feedback effect of vasopress on the juxtaglomerular cells, because vasopress hibits the release of from isolated perfused kidneys and kidney slices http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Regulatory, Integrative and Comparative Physiology The American Physiological Society

Lack of effect of vasopressin replacement on renin hypersecretion in Brattleboro rats

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Publisher
The American Physiological Society
Copyright
Copyright © 1989 the American Physiological Society
ISSN
0363-6119
eISSN
1522-1490
Publisher site
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Abstract

GOL, RAFFAELLO M. A., EIJI GOTOH, LANNY C. KEIL, ROY L. SHACKELFORD, AND WILLIAM F. GANONG. Lack of effect of vasopressreplacement on hypersecretion . Am. J. Physiol. 257 (Regulatory tegrative Comp. Physiol. 26): R1117-R1122, 1989.-To determe how the vasopress deficiency homozygous with diabetes sipidus produces creased secretion, homozygousand heterozygous were fused through subcutaneouslyimplanted Alzet mipumps for 1 wk with a doseof arge vasopressthat restored plasmavasopress to normal the homozygous animals. the homozygous animals, plasma activity (PRA) and the PRA response to immobilization remaed elevated compared with LongEvans controls. Propranolol reducedPRA to normal and markedly reduced the PRA responseto immobilization. PRA was normal heterozygous . The data dicate that the creased secretion homozygous is a result of creasedsympathetic activity, and becausecirculatg vasopress doesnot crossthe blood-bra barrier, it seemslikely that the creasedsympathetic activity is central orig. arge vasopress; plasma activity; angiotensogen VASOPRESS deficiency homozygous with diabetes sipidus (DI) is associated with elevated plasma activity (PRA) at rest and supernormal responses to stimuli that crease secretion (see Ref. 15). The hypersecretion could be due to the lack of a direct feedback effect of vasopress on the juxtaglomerular cells, because vasopress hibits the release of from isolated perfused kidneys and kidney slices

Journal

AJP - Regulatory, Integrative and Comparative PhysiologyThe American Physiological Society

Published: Nov 1, 1989

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