| First Author | Asico LD | Year | 1998 |
| Journal | J Clin Invest | Volume | 102 |
| Issue | 3 | Pages | 493-8 |
| PubMed ID | 9691085 | Mgi Jnum | J:115136 |
| Mgi Id | MGI:3690706 | Doi | 10.1172/JCI3685 |
| Citation | Asico LD, et al. (1998) Disruption of the dopamine D3 receptor gene produces renin-dependent hypertension. J Clin Invest 102(3):493-8 |
| abstractText | 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. |
