Why the study?
Does the lack of renal dopamine D5 receptors promote hypertension in a mouse model?
Does the lack of renal dopamine D5 receptors promote hypertension in a mouse model?
Renal dopamine D5 receptors play a crucial role in blood pressure homeostasis and the pathogenesis of hypertension, independent of extrarenal D5 receptors.
Renal D5 receptor loss promotes hypertension in this mouse model; leaves open translation to human disease or therapy.
Disruption of the dopamine D(5) receptor gene in mice increases BP and causes salt sensitivity. To determine the role of renal versus extrarenal D(5) receptors in BP regulation, we performed cross-renal transplantation experiments. BP was similar between wild-type mice and wild-type mice transplanted with wild-type kidneys, indicating that the transplantation procedure did not affect BP. BP was lower among D(5)(-/-) mice transplanted with wild-type kidneys than D(5)(-/-) kidneys, demonstrating that the renal D(5) receptors are important in BP control. BP was higher in wild-type mice transplanted with D(5)(-/-) kidneys than wild-type kidneys but not significantly different from syngenic transplanted D(5)(-/-) mice, indicating the importance of the kidney in the development of hypertension. On a high-salt diet, all mice with D(5)(-/-) kidneys excreted less sodium than mice with wild-type kidneys. Transplantation of a wild-type kidney into a D(5)(-/-) mouse decreased the renal expression of AT(1) receptors and Nox-2. Conversely, transplantation of a D(5)(-/-) kidney into a wild-type mouse increased the expression of both, suggesting that both renal and extrarenal factors are important in the regulation of AT(1) receptor and Nox-2 expression. These results highlight the role of renal D(5) receptors in BP homeostasis and the pathogenesis of hypertension.
No takes yet. Share an insight, caveat, or question.
Asico et al. (2010) studied this question.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: