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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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

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.[1]

References

  1. Disruption of the dopamine D3 receptor gene produces renin-dependent hypertension. Asico, L.D., Ladines, C., Fuchs, S., Accili, D., Carey, R.M., Semeraro, C., Pocchiari, F., Felder, R.A., Eisner, G.M., Jose, P.A. J. Clin. Invest. (1998) [Pubmed]
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