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This Article Full Text Full Text (PDF) All Versions of this Article: 285/6/E1161    most recent 00570.2002v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Tachikawa, K. Articles by Oiso, Y. Search for Related Content PubMed PubMed Citation Articles by Tachikawa, K. Articles by Oiso, Y.

Altered cardiovascular regulation in arginine vasopressin-overexpressing transgenic rat

¹Department of Internal Medicine, Nagoya University Graduate School of Medicine, Nagoya 466-8550; ²Department of Teratology and Genetics, Research Institute of Environmental Medicine, Nagoya University, Nagoya 464-8601; and ³YS New Technology Institute Inc., Tochigi 329-0512, Japan

Submitted 24 December 2002 ; accepted in final form 10 August 2003

Although arginine vasopressin (AVP), an antidiuretic hormone, has been widely acknowledged to play an important role in cardiovascular regulation via V1a receptors (V1aR), its precise significance remains unclear. In this study, we investigated the effects of long-standing high plasma AVP status on cardiovascular regulation in the AVP-overexpressing transgenic (Tg) rat. Adult male homozygous Tg rats were compared with age-matched normal Sprague-Dawley rats as controls. There were no significant differences in mean arterial blood pressure (BP; MABP) or heart rate between Tg and control rats in the basal state. Subcutaneous injection of AVP significantly increased MABP in controls but did not cause any apparent increase in MABP in Tg rats. BP recovery from hemorrhage-induced hypotension was significantly delayed in Tg compared with control rats. Pretreatment with a selective V1aR antagonist, OPC-21268, which is thought to restore the downregulation of V1aR, markedly improved both of these impaired responses. Northern blot analysis confirmed that decreased expression of V1aR mRNA and pretreatment with V1aR antagonist significantly restored the downregulation of V1aR mRNA. These results suggest that the Tg rat has decreased sensitivity to the hypertensive effect of AVP due to downregulation of V1aR, which may function as an adaptive mechanism to maintain normal BP against chronic hypervasopressinemia. In addition, impaired restoration of BP after hemorrhage-induced hypotension in Tg rats supports a physiological role of AVP in cardiovascular regulation.

transgenic animal; desensitization; blood pressure

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