G Protein-Coupled Receptor Kinase 4

Yang, Jian; Villar, Van Anthony M.; Jones, John E.; José, Pedro A.; Zeng, Chunyu

doi:10.1161/hypertensionaha.115.05189

Cited by 31 publications

(44 citation statements)

References 71 publications

(117 reference statements)

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“…The major mechanism for the increase in renal dopamine production with salt loading has been suggested to be caused by neural L-DOPA spill-over into the circulation (84, 85). Dopamine, produced in the kidney, and not converted to norepinephrine, is responsible for at least 50% of sodium excretion during conditions of moderate sodium excess (32–34). However, gastrin secreted by G-cells in the stomach and duodenum and released into the circulation (39, 86) may aid in this process.…”

Section: Gut Microbiota and Gastrorenal Axismentioning

confidence: 99%

Gut microbiota in hypertension

José

Raj²

2015

Current Opinion in Nephrology and Hypertension

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159

109

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Purpose of review Hypertension, which is present in about one quarter of the world’s population, is responsible for about 41% of the number one cause of death, cardiovascular disease. Not included in these statistics is the effect of sodium intake on blood pressure, even though an increase or a marked decrease in sodium intake can increase blood pressure. This review deals with the interaction of gut microbiota and the kidney with genetics and epigenetics in the regulation of blood pressure and salt sensitivity. Recent findings The abundance of the gut microbes, Firmicutes and Bacteroidetes, is associated with increased blood pressure in several models of hypertension, including the spontaneously hypertensive and Dahl salt-sensitive rats. Decreasing gut microbiota by antibiotics can increase or decrease blood pressure that is influenced by genotype. The biological function of probiotics may also be a consequence of epigenetic modification, related, in part, to microRNA. Products of the fermentation of nutrients by gut microbiota can influence blood pressure by regulating expenditure of energy, intestinal metabolism of catecholamines, and gastrointestinal and renal ion transport, and thus, salt sensitivity. Summary The beneficial or deleterious effects of gut microbiota on blood pressure is a consequence of several variables, including genetics, epigenetics, lifestyle, and intake of antibiotics. These variables may influence the ultimate level of blood pressure and control of hypertension.

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Section: Gut Microbiota and Gastrorenal Axismentioning

confidence: 99%

Gut microbiota in hypertension

José

Raj²

2015

Current Opinion in Nephrology and Hypertension

Self Cite

159

109

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“…As noted previously, GRK2, GRK3, GRK5, and GRK6 are ubiquitously expressed, whereas GRK4 is expressed in a limited number of tissues. GRK4, for example, is abundantly expressed in the testes and human myometrium and, to a lesser extent, in a few other tissues, including the artery, brain, kidney, and intestine, but has minimal expression in the normal heart . The distinct distribution of GRK4 indicates its vital role in the regulation of blood pressure.…”

Section: Role Of Grks In the Regulation Of Blood Pressurementioning

confidence: 99%

“…The dopaminergic system and the renin–angiotensin system are important regulators of sodium balance and blood pressure, which are relevant to the pathogenesis and/or maintenance of hypertension . The dopaminergic system exerts a paracrine regulatory role on renal sodium transport in the proximal tubule via its 5 receptor subtypes.…”

Section: Role Of Grks In the Regulation Of Blood Pressurementioning

confidence: 99%

G Protein–Coupled Receptor Kinases: Crucial Regulators of Blood Pressure

Yang

Villar

Armando

et al. 2016

JAHA

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“…Wild-type GRK4 is important in the desensitization and recycling of D 1 R and D 3 R to the plasma membrane of renal proximal tubules (41, 63). GRK4 plays a vital role in regulating dopamine-mediated natriuresis and renin-angiotensin system-mediated antinatriuresis (41, 61). However, a role of GRK4 in the regulation of CCKBR has not been reported.…”

Section: Gastrin As the Effector Of Gut Sodium Sensormentioning

confidence: 99%

“…The reasons leading to the differences among studies are not known. However, the negative studies could be the consequence of not taking into account salt sensitivity (GRK4 R65L and A486V, in particular) or assessing the role of GRK4 in conjunction with other single nucleotide polymorphisms of GRK4 and other genes (41, 61). It should be stated that GRK4 gene variants have also been associated with obesity associated with increased sodium intake (GRK4 486A>V), lower values of eGFR (GRK4 rs2488815, intronic), and hypertension in some diabetic subjects (78-80).…”

Section: Gastrin As the Effector Of Gut Sodium Sensormentioning

confidence: 99%