Submitted on September 7, 2007
Accepted on December 10, 2007
Dysregulation of Dopamine-dependent Mechanisms as a Determinant of Hypertension: Studies in Dopamine Receptor Knockout Mice
Chunyu Zeng1*, Ines Armando, Yingjin Luo, Gilbert M Eisner2, Robin A. Felder3, and Pedro A. Jose4
1 Cardiology, The Third Military Medical University, Daping Hospital, Department of Cardiology, Chongqing, 400042, China; , China
2 Department of Medicine, Georgetown University Medical Center, Washington, District of Columbia, United States
3 Department of Pathology, University of Virgina Medical Center, Charlottesville, Virginia, United States
4 Department of Pediatrics, Georgetown University Medical Center, Washington, District of Columbia, United States
* To whom correspondence should be addressed. E-mail: cyzeng1{at}hotmail.com.
Dopamine plays an important role in the pathogenesis of hypertension by regulating epithelial sodium transport and by interacting with vasoactive hormones/humoral factors, such as aldosterone, angiotensin, catecholamines, endothelin, oxytocin, prolactin pro-opiomelancortin, reactive oxygen species, renin, and vasopressin. Dopamine receptors are classified into D1-like (D1, D5) and D2-like (D2, D3, D4) subtypes based on their structure and pharmacology. In recent years, mice deficient in one or more of the five dopamine receptor subtypes have been generated, leading to a better understanding of the physiological role of each of the dopamine receptor subtypes. This review summarizes the results from studies of the various dopamine receptor mutant mice on the role of individual dopamine receptor subtypes and their interactions with other G protein-coupled receptors in the regulation of blood pressure.
