Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2011 Jan;57(1):11-7.
doi: 10.1161/HYPERTENSIONAHA.110.157727. Epub 2010 Nov 22.

Dopamine receptors: important antihypertensive counterbalance against hypertensive factors

Affiliations
Review

Dopamine receptors: important antihypertensive counterbalance against hypertensive factors

Chunyu Zeng et al. Hypertension. 2011 Jan.
No abstract available

PubMed Disclaimer

Figures

Figure 1
Figure 1. Synthesis and metabolism of dopamine in neural and renal proximal tubule cells
The catecholamines (dopamine, norepinephrine and epinephrine) are synthesized from the same precursors, the amino acid tyrosine and its hydroxylated product L-3, 4 dihydroxyphenylalanine(L-DOPA). Dopamine synthesis differs between neural and renal proximal tubule (RPT) cells. Neural cells express tyrosine hydroxylase (TH), which converts tyrosine to L-DOPA, which is decarboxylated to dopamine, via aromatic acid decarboxylase (AADC). Dopamine is converted to norepinephrine by dopamine β–hydroxylase (DBH). In tissues expressing phenylethanolamine-N-methyl transferase (PNMT) (e.g., adrenal medulla, heart, and some areas of the brain) norepinephrine is converted to epinephrine. In contrast, RPT cells do not express TH or DBH; dopamine, synthesized from L-DOPA taken up from the glomerular filtrate and the circulation, is not converted to norepinephrine.
Figure 2
Figure 2. Dysfunction of renal D1-like receptors in hypertension
In hypertension, constitutively active GRK4 gene variants (R65L, A142V, and A486V) increase the phosphorylation of D1 receptors uncoupling them from their G protein/effector complex. This results in impairment in the ability of the D1 receptor to increase production of second messengers and inhibit the activity of sodium transporters/pump (e.g., NHE3, Na+-K+ ATPase).
Figure 3
Figure 3. Dopamine counterbalances the prohypertensive effects of α–adrenergic nervous and renin-angiotensin systems
Stimulation of dopamine receptors inhibits catecholamine and renin release*, AT1 receptor (and probably α-adrenergic)-mediated sodium reabsorption. Actions of dopamine receptors, by themselves, and by counterbalancing the prohypertensive effects of α-adrenergic nervous and renin-angiotensin systems, keep the blood pressure in the normal range. *D1 receptors inhibit renin release but can stimulate it in the absence of COX2.

References

    1. Hall JE. The kidney, hypertension, and obesity. Hypertension. 2003;41:625–633. - PubMed
    1. Hussain T, Lokhandwala MF. Renal dopamine receptors and hypertension. Exp Biol Med (Maywood) 2003;228:134–142. - PubMed
    1. Venkatakrishnan U, Chen C, Lokhandwala MF. The role of intrarenal nitric oxide in the natriuretic response to dopamine-receptor activation. Clin Exp Hypertens. 2000;22:309–324. - PubMed
    1. Khan F, Spicarová Z, Zelenin S, Holtbäck U, Scott L, Aperia A. Negative reciprocity between angiotensin II type 1 and dopamine D1 receptors in rat renal proximal tubule cells. Am J Physiol Renal Physiol. 2008;295:F1110–F1116. - PubMed
    1. Pinho MJ, Serrão MP, Gomes P, Hopfer U, Jose PA, Soares-da-Silva P. Over-expression of renal LAT1 and LAT2 and enhanced L-DOPA uptake in SHR immortalized renal proximal tubular cells. Kidney Int. 2004;66:216–226. - PubMed

Publication types