Published online before print June 10, 2002, doi: 10.1161/01.HYP.0000022062.70639.1C
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(Hypertension. 2002;40:101.)
© 2002 American Heart Association, Inc.
Scientific Contributions |
Role of the 
1D-Adrenegric Receptor in the Development of Salt-Induced Hypertension
Department of Molecular, Cell Pharmacology, National Center for Child Health and Development Research Institute (A.T., T.K., C.H., S.O., G.T.), Tokyo, Japan; and Discovery Research Laboratories, Nippon Shinyaku Co (M.K., S.M.), Tsukuba City, Ibaraki, Japan.
Correspondence to Gozoh Tsujimoto, Department of Molecular, Cell Pharmacology, National Center for Child Health and Development Research Institute, 3-35-31, Taishi-do, Setagaya-Ku, Tokyo 154-8567, Japan. E-mail gtsujimoto{at}nch.go.jp
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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