Published Online
on June 10, 2002

A more recent version of this article appeared on July 1, 2002

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Submitted on April 3, 2002
Revised on April 16, 2002

Role of the _1D-Adrenegric Receptor in the Development of Salt-Induced Hypertension

Akito Tanoue; Masahiro Koba; Shigeki Miyawaki; Taka-aki Koshimizu; Chihiro Hosoda; Sayuri Oshikawa; and Gozoh Tsujimoto^*

^* To whom correspondence should be addressed. E-mail: gtsujimoto{at}nch.go.jp .

Abstract—In an attempt to elucidate whether there is a specific ₁-adrenergic receptor (₁-AR) subtype involved in the genesis or maintenance of hypertension, the _1D-AR subtype was evaluated in a model of salt-induced hypertension. The _1D-AR--deficient (_1D^-/-) and control (_1D^+/+) mice (n=8 to 14 in each group) were submitted to subtotal nephrectomy and given 1% saline as drinking water for 35 days. Blood pressure (BP) was monitored by tail-cuff readings and confirmed at the end point by direct intraarterial BP recording. The _1D^-/- mice had a significantly (P=0.0004) attenuated increase in BP response in this protocol (baseline 94.6±2.8 versus end point 107.4±4.5 mm Hg) compared with that of their wild-type counterparts (_1D^+/+), from a baseline 97.4±2.9 to an end point 139.4±4.5 mm Hg. Seven of 15 _1D^+/+ mice died with edema, probably owing to renal failure, whereas 14 of 15 _1D^-/- mice were maintained for 35 days. Body weight, renal remnant weight, and residual renal function were similar in the 2 groups, whereas the values of plasma catecholamines (epinephrine, norepinephrine, and dopamine) were higher in _1D^+/+ than in the _1D^-/- mice. These data suggest that _1D-AR plays an important role in developing a high BP in response to dietary salt-loading, and that agents having selective _1D-AR antagonism could have significant therapeutic potential in the treatment of hypertension.

Key words: receptors, adrenergic • mice • hypertension, sodium-dependent • nephrectomy

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