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Research Article Free access | 10.1172/JCI3685

Disruption of the dopamine D3 receptor gene produces renin-dependent hypertension.

L D Asico, C Ladines, S Fuchs, D Accili, R M Carey, C Semeraro, F Pocchiari, R A Felder, G M Eisner, and P A Jose

Department of Pediatrics, Georgetown University Medical Center, Washington, D.C. 20007, USA.

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Department of Pediatrics, Georgetown University Medical Center, Washington, D.C. 20007, USA.

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Department of Pediatrics, Georgetown University Medical Center, Washington, D.C. 20007, USA.

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Department of Pediatrics, Georgetown University Medical Center, Washington, D.C. 20007, USA.

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Department of Pediatrics, Georgetown University Medical Center, Washington, D.C. 20007, USA.

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Department of Pediatrics, Georgetown University Medical Center, Washington, D.C. 20007, USA.

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Department of Pediatrics, Georgetown University Medical Center, Washington, D.C. 20007, USA.

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Department of Pediatrics, Georgetown University Medical Center, Washington, D.C. 20007, USA.

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Department of Pediatrics, Georgetown University Medical Center, Washington, D.C. 20007, USA.

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Department of Pediatrics, Georgetown University Medical Center, Washington, D.C. 20007, USA.

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Published August 1, 1998 - More info

Published in Volume 102, Issue 3 on August 1, 1998
J Clin Invest. 1998;102(3):493–498. https://doi.org/10.1172/JCI3685.
© 1998 The American Society for Clinical Investigation
Published August 1, 1998 - Version history
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Abstract

Since dopamine receptors are important in the regulation of renal and cardiovascular function, we studied the cardiovascular consequences of the disruption of the D3 receptor, a member of the family of D2-like receptors, expressed in renal proximal tubules and juxtaglomerular cells. Systolic and diastolic blood pressures were higher (approximately 20 mmHg) in heterozygous and homozygous than in wild-type mice. An acute saline load increased urine flow rate and sodium excretion to a similar extent in wild-type and heterozygous mice but the increase was attenuated in homozygous mice. Renal renin activity was much greater in homozygous than in wild-type mice; values for heterozygous mice were intermediate. Blockade of angiotensin II subtype-1 receptors decreased systolic blood pressure for a longer duration in mutant than in wild-type mice. Thus, disruption of the D3 receptor increases renal renin production and produces renal sodium retention and renin-dependent hypertension.

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