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The Spectrum of Subclinical Primary Aldosteronism and Incident Hypertension: A Cohort Study.
Brown JM, Robinson-Cohen C, Luque-Fernandez MA, Allison MA, Baudrand R, Ix JH, Kestenbaum B, de Boer IH, Vaidya A
(2017) Ann Intern Med 167: 630-641
MeSH Terms: Aged, Aged, 80 and over, Aldosterone, Cross-Sectional Studies, Female, Humans, Hyperaldosteronism, Hypertension, Incidence, Longitudinal Studies, Male, Middle Aged, Potassium, Receptors, Mineralocorticoid, Renin, Risk Factors
Show Abstract · Added October 24, 2017
Background - Primary aldosteronism is recognized as a severe form of renin-independent aldosteronism that results in excessive mineralocorticoid receptor (MR) activation.
Objective - To investigate whether a spectrum of subclinical renin-independent aldosteronism that increases risk for hypertension exists among normotensive persons.
Design - Cohort study.
Setting - National community-based study.
Participants - 850 untreated normotensive participants in MESA (Multi-Ethnic Study of Atherosclerosis) with measurements of serum aldosterone and plasma renin activity (PRA).
Measurements - Longitudinal analyses investigated whether aldosterone concentrations, in the context of physiologic PRA phenotypes (suppressed, ≤0.50 µg/L per hour; indeterminate, 0.51 to 0.99 µg/L per hour; unsuppressed, ≥1.0 µg/L per hour), were associated with incident hypertension (defined as systolic blood pressure ≥140 mm Hg, diastolic blood pressure ≥90 mm Hg, or initiation of antihypertensive medications). Cross-sectional analyses investigated associations between aldosterone and MR activity, assessed via serum potassium and urinary fractional excretion of potassium.
Results - A suppressed renin phenotype was associated with a higher rate of incident hypertension than other PRA phenotypes (incidence rates per 1000 person-years of follow-up: suppressed renin phenotype, 85.4 events [95% CI, 73.4 to 99.3 events]; indeterminate renin phenotype, 53.3 events [CI, 42.8 to 66.4 events]; unsuppressed renin phenotype, 54.5 events [CI, 41.8 to 71.0 events]). With renin suppression, higher aldosterone concentrations were independently associated with an increased risk for incident hypertension, whereas no association between aldosterone and hypertension was seen when renin was not suppressed. Higher aldosterone concentrations were associated with lower serum potassium and higher urinary excretion of potassium, but only when renin was suppressed.
Limitation - Sodium and potassium were measured several years before renin and aldosterone.
Conclusion - Suppression of renin and higher aldosterone concentrations in the context of this renin suppression are associated with an increased risk for hypertension and possibly also with increased MR activity. These findings suggest a clinically relevant spectrum of subclinical primary aldosteronism (renin-independent aldosteronism) in normotension.
Primary Funding Source - National Institutes of Health.
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16 MeSH Terms
Circulating concentrations of biomarkers and metabolites related to vitamin status, one-carbon and the kynurenine pathways in US, Nordic, Asian, and Australian populations.
Midttun Ø, Theofylaktopoulou D, McCann A, Fanidi A, Muller DC, Meyer K, Ulvik A, Zheng W, Shu XO, Xiang YB, Prentice R, Thomson CA, Pettinger M, Giles GG, Hodge A, Cai Q, Blot WJ, Wu J, Johansson M, Hultdin J, Grankvist K, Stevens VL, McCullough ML, Weinstein SJ, Albanes D, Langhammer A, Hveem K, Næss M, Sesso HD, Gaziano JM, Buring JE, Lee IM, Severi G, Zhang X, Han J, Stampfer MJ, Smith-Warner SA, Zeleniuch-Jacquotte A, le Marchand L, Yuan JM, Butler LM, Koh WP, Wang R, Gao YT, Ericson U, Sonestedt E, Ziegler RG, Freedman ND, Visvanathan K, Jones MR, Relton C, Brennan P, Johansson M, Ueland PM
(2017) Am J Clin Nutr 105: 1314-1326
MeSH Terms: Aged, Asia, Australia, Biomarkers, Carbon, Cross-Sectional Studies, Dietary Supplements, Female, Humans, Kynurenine, Laboratories, Male, Middle Aged, Scandinavian and Nordic Countries, Tryptophan, United States, Vitamin A, Vitamin B Complex, Vitamin D, alpha-Tocopherol
Show Abstract · Added April 21, 2017
Circulating concentrations of biomarkers that are related to vitamin status vary by factors such as diet, fortification, and supplement use. Published biomarker concentrations have also been influenced by the variation across laboratories, which complicates a comparison of results from different studies. We robustly and comprehensively assessed differences in biomarkers that are related to vitamin status across geographic regions. The trial was a cross-sectional study in which we investigated 38 biomarkers that are related to vitamin status and one-carbon and tryptophan metabolism in serum and plasma from 5314 healthy control subjects representing 20 cohorts recruited from the United States, Nordic countries, Asia, and Australia, participating in the Lung Cancer Cohort Consortium. All samples were analyzed in a centralized laboratory. Circulating concentrations of riboflavin, pyridoxal 5'-phosphate, folate, vitamin B-12, all- retinol, 25-hydroxyvitamin D, and α-tocopherol as well as combined vitamin scores that were based on these nutrients showed that the general B-vitamin concentration was highest in the United States and that the B vitamins and lipid soluble vitamins were low in Asians. Conversely, circulating concentrations of metabolites that are inversely related to B vitamins involved in the one-carbon and kynurenine pathways were high in Asians. The high B-vitamin concentration in the United States appears to be driven mainly by multivitamin-supplement users. The observed differences likely reflect the variation in intake of vitamins and, in particular, the widespread multivitamin-supplement use in the United States. The results provide valuable information about the differences in biomarker concentrations in populations across continents.
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20 MeSH Terms
20-Hydroxyeicosatetraenoic Acid (HETE)-dependent Hypertension in Human Cytochrome P450 (CYP) 4A11 Transgenic Mice: NORMALIZATION OF BLOOD PRESSURE BY SODIUM RESTRICTION, HYDROCHLOROTHIAZIDE, OR BLOCKADE OF THE TYPE 1 ANGIOTENSIN II RECEPTOR.
Savas Ü, Wei S, Hsu MH, Falck JR, Guengerich FP, Capdevila JH, Johnson EF
(2016) J Biol Chem 291: 16904-19
MeSH Terms: Angiotensins, Animals, Blood Pressure, Cytochrome P-450 CYP4A, Female, Humans, Hydroxyeicosatetraenoic Acids, Hypertension, Losartan, Male, Mice, Mice, Inbred BALB C, Mice, Transgenic, Receptor, Angiotensin, Type 1, Renin-Angiotensin System, Sodium Chloride, Dietary, Solute Carrier Family 12, Member 3
Show Abstract · Added March 14, 2018
Male and female homozygous 129/Sv mice carrying four copies of the human cytochrome P450 4A11 gene (CYP4A11) under control of its native promoter (B-129/Sv-4A11(+/+)) develop hypertension (142 ± 8 versus 113 ± 7 mm Hg systolic blood pressure (BP)), and exhibit increased 20-hydroxyeicosatetraenoic acid (20-HETE) in kidney and urine. The hypertension is reversible by a low-sodium diet and by the CYP4A inhibitor HET0016. B-129/Sv-4A11(+/+) mice display an 18% increase of plasma potassium (p < 0.02), but plasma aldosterone, angiotensin II (ANGII), and renin activities are unchanged. This phenotype resembles human genetic disorders with elevated activity of the sodium chloride co-transporter (NCC) and, accordingly, NCC abundance is increased by 50% in transgenic mice, and NCC levels are normalized by HET0016. ANGII is known to increase NCC abundance, and renal mRNA levels of its precursor angiotensinogen are increased 2-fold in B-129/Sv-4A11(+/+), and blockade of the ANGII receptor type 1 with losartan normalizes BP. A pro-hypertensive role for 20-HETE was implicated by normalization of BP and reversal of renal angiotensin mRNA increases by administration of the 20-HETE antagonists 2-((6Z,15Z)-20-hydroxyicosa-6,15-dienamido)acetate or (S)-2-((6Z,15Z)-20-hydroxyicosa-6,15-dienamido)succinate. SGK1 expression is also increased in B-129/Sv-4A11(+/+) mice and paralleled increases seen for NCC. Losartan, HET0016, and 20-HETE antagonists each normalized SGK1 mRNA expression. These results point to a potential 20-HETE dependence of intrarenal angiotensinogen production and ANGII receptor type 1 activation that are associated with increases in NCC and SGK1 and identify elevated P450 4A11 activity and 20-HETE as potential risk factors for salt-sensitive human hypertension by perturbation of the renal renin-angiotensin axis.
© 2016 by The American Society for Biochemistry and Molecular Biology, Inc.
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17 MeSH Terms
Effects of losartan treatment on the physicochemical properties of diabetic rat bone.
Donmez BO, Unal M, Ozdemir S, Ozturk N, Oguz N, Akkus O
(2017) J Bone Miner Metab 35: 161-170
MeSH Terms: Absorptiometry, Photon, Angiotensin II Type 1 Receptor Blockers, Animals, Biomechanical Phenomena, Bone Density, Bone and Bones, Diabetes Mellitus, Experimental, Female, Losartan, Rats, Rats, Wistar, Renin-Angiotensin System, Spectroscopy, Fourier Transform Infrared
Show Abstract · Added March 3, 2017
Inhibitors of the renin-angiotensin system used to treat several diseases have also been shown to be effective on bone tissue, suggesting that angiotensin-converting enzyme inhibitors and angiotensin receptor blockers may reduce fracture risk. The present study investigated the effects of losartan on the physicochemical and biomechanical properties of diabetic rat bone. Losartan (5 mg/kg/day) was administered via oral gavage for 12 weeks. Bone mineral density (BMD) was measured using dual-energy X-ray absorptiometry. Whole femurs were tested under tension to evaluate the biomechanical properties of bone. The physicochemical properties of bone were analyzed by Fourier transform infrared spectroscopy. Although losartan did not recover decreases in the BMD of diabetic bone, it recovered the physicochemical (mineral and collagen matrix) properties of diabetic rat bone. Furthermore, losartan also recovered ultimate tensile strength of diabetic rat femurs. Losartan, an angiotensin II type 1 receptor blocker, has a therapeutic effect on the physicochemical properties of diabetic bone resulting in improvement of bone strength at the material level. Therefore, specific inhibition of this pathway at the receptor level shows potential as a therapeutic target for diabetic patients suffering from bone diseases such as osteopenia.
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13 MeSH Terms
Chronic Angiotensin-(1-7) Improves Insulin Sensitivity in High-Fat Fed Mice Independent of Blood Pressure.
Williams IM, Otero YF, Bracy DP, Wasserman DH, Biaggioni I, Arnold AC
(2016) Hypertension 67: 983-91
MeSH Terms: Analysis of Variance, Angiotensin I, Animals, Blood Glucose, Blood Pressure Determination, Body Composition, Cardiovascular Diseases, Diet, High-Fat, Disease Models, Animal, Dose-Response Relationship, Drug, Drug Administration Schedule, Glucose Clamp Technique, Heart Function Tests, Hemodynamics, Hypertension, Infusions, Subcutaneous, Insulin Resistance, Male, Mice, Mice, Inbred C57BL, Obesity, Peptide Fragments, Random Allocation, Reference Values, Renin-Angiotensin System
Show Abstract · Added May 5, 2016
Angiotensin-(1-7) improves glycemic control in animal models of cardiometabolic syndrome. The tissue-specific sites of action and blood pressure dependence of these metabolic effects, however, remain unclear. We hypothesized that Ang-(1-7) improves insulin sensitivity by enhancing peripheral glucose delivery. Adult male C57BL/6J mice were placed on standard chow or 60% high-fat diet for 11 weeks. Ang-(1-7) (400 ng/kg per minute) or saline was infused subcutaneously during the last 3 weeks of diet, and hyperinsulinemic-euglycemic clamps were performed at the end of treatment. High-fat fed mice exhibited modest hypertension (systolic blood pressure: 137 ± 3 high fat versus 123 ± 5 mm Hg chow;P=0.001), which was not altered by Ang-(1-7) (141 ± 4 mm Hg;P=0.574). Ang-(1-7) did not alter body weight or fasting glucose and insulin in chow or high-fat fed mice. Ang-(1-7) increased the steady-state glucose infusion rate needed to maintain euglycemia in high-fat fed mice (31 ± 5 Ang-(1-7) versus 16 ± 1 mg/kg per minute vehicle;P=0.017) reflecting increased whole-body insulin sensitivity, with no effect in chow-fed mice. The improved insulin sensitivity in high-fat fed mice was because of an enhanced rate of glucose disappearance (34 ± 5 Ang-(1-7) versus 20 ± 2 mg/kg per minute vehicle;P=0.049). Ang-(1-7) enhanced glucose uptake specifically into skeletal muscle by increasing translocation of glucose transporter 4 to the sarcolemma. Our data suggest that Ang-(1-7) has direct insulin-sensitizing effects on skeletal muscle, independent of changes in blood pressure. These findings provide new insight into mechanisms by which Ang-(1-7) improves insulin action, and provide further support for targeting this peptide in cardiometabolic disease.
© 2016 American Heart Association, Inc.
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25 MeSH Terms
Plasma FGF23 and Calcified Atherosclerotic Plaque in African Americans with Type 2 Diabetes Mellitus.
Freedman BI, Divers J, Russell GB, Palmer ND, Bowden DW, Carr JJ, Wagenknecht LE, Hightower RC, Xu J, Smith SC, Langefeld CD, Hruska KA, Register TC
(2015) Am J Nephrol 42: 391-401
MeSH Terms: Adult, African Americans, Aged, Albuminuria, Blood Pressure, Bone Density, Carotid Arteries, Coronary Vessels, Cross-Sectional Studies, Diabetes Mellitus, Type 2, Female, Fibroblast Growth Factors, Follow-Up Studies, Glomerular Filtration Rate, Glycated Hemoglobin A, Humans, Iliac Artery, Kidney Function Tests, Male, Middle Aged, Phosphates, Plaque, Atherosclerotic, Renin-Angiotensin System, Risk Factors, Tomography, X-Ray Computed, Vitamin D
Show Abstract · Added September 29, 2016
BACKGROUND - Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone implicated in disorders of serum phosphorus concentration and vitamin D. The role of FGF23 in vascular calcification remains controversial.
METHODS - Relationships between FGF23 and coronary artery calcified atherosclerotic plaque (CAC), aortoiliac calcified plaque (CP), carotid artery CP, volumetric bone mineral density (vBMD), albuminuria, and estimated glomerular filtration rate (eGFR) were determined in 545 African Americans with type 2 diabetes (T2D) and preserved kidney function in African American-Diabetes Heart Study participants. Generalized linear models were fitted to test associations between FGF23 and cardiovascular, bone, and renal phenotypes, and change in measurements over time, adjusting for age, gender, African ancestry proportion, body mass index, diabetes duration, hemoglobin A1c, blood pressure, renin-angiotensin-system inhibitors, statins, calcium supplements, serum calcium, and serum phosphate.
RESULTS - The sample was 56.7% female with a mean (SD) age of 55.6 (9.6) years, diabetes duration of 10.3 (8.2) years, eGFR 90.9 (22.1) ml/min/1.73 m2, urine albumin:creatinine ratio (UACR) 151 (588) (median 13) mg/g, plasma FGF23 161 (157) RU/ml, and CAC 637 (1,179) mg. In fully adjusted models, FGF23 was negatively associated with eGFR (p < 0.0001) and positively associated with UACR (p < 0.0001) and CAC (p = 0.0006), but not with carotid CP or aortic CP. Baseline FGF23 concentration did not associate with changes in vBMD or CAC after a mean of 5.1 years follow-up.
CONCLUSIONS - Plasma FGF23 concentrations were independently associated with subclinical coronary artery disease, albuminuria, and kidney function in the understudied African American population with T2D. Findings support relationships between FGF23 and vascular calcification, but not between FGF23 and bone mineral density, in African Americans lacking advanced nephropathy.
© 2016 S. Karger AG, Basel.
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26 MeSH Terms
Immunomodulatory metabolites released by the frog-killing fungus Batrachochytrium dendrobatidis.
Rollins-Smith LA, Fites JS, Reinert LK, Shiakolas AR, Umile TP, Minbiole KP
(2015) Infect Immun 83: 4565-70
MeSH Terms: Adenosine, Animals, Apoptosis, Cell Survival, Chytridiomycota, Drug Synergism, Host-Pathogen Interactions, Humans, Jurkat Cells, Kynurenine, Lymphocytes, Mycoses, Skin, Thionucleosides, Tryptophan, Xenopus laevis
Show Abstract · Added April 18, 2017
Batrachochytrium dendrobatidis is a fungal pathogen in the phylum Chytridiomycota that causes the skin disease chytridiomycosis. Chytridiomycosis is considered an emerging infectious disease linked to worldwide amphibian declines and extinctions. Although amphibians have well-developed immune defenses, clearance of this pathogen from the skin is often impaired. Previously, we showed that the adaptive immune system is involved in the control of the pathogen, but B. dendrobatidis releases factors that inhibit in vitro and in vivo lymphocyte responses and induce lymphocyte apoptosis. Little is known about the nature of the inhibitory factors released by this fungus. Here, we describe the isolation and characterization of three fungal metabolites produced by B. dendrobatidis but not by the closely related nonpathogenic chytrid Homolaphlyctis polyrhiza. These metabolites are methylthioadenosine (MTA), tryptophan, and an oxidized product of tryptophan, kynurenine (Kyn). Independently, both MTA and Kyn inhibit the survival and proliferation of amphibian lymphocytes and the Jurkat human T cell leukemia cell line. However, working together, they become effective at much lower concentrations. We hypothesize that B. dendrobatidis can adapt its metabolism to release products that alter the local environment in the skin to inhibit immunity and enhance the survival of the pathogen.
Copyright © 2015, American Society for Microbiology. All Rights Reserved.
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16 MeSH Terms
Atherosclerosis following renal injury is ameliorated by pioglitazone and losartan via macrophage phenotype.
Yamamoto S, Zhong J, Yancey PG, Zuo Y, Linton MF, Fazio S, Yang H, Narita I, Kon V
(2015) Atherosclerosis 242: 56-64
MeSH Terms: Angiotensin Receptor Antagonists, Animals, Aortic Diseases, Apolipoproteins E, Apoptosis, Atherosclerosis, Cell Line, Cytokines, Disease Models, Animal, Drug Evaluation, Preclinical, Drug Synergism, Drug Therapy, Combination, Female, Hyperlipidemias, Inflammation, Losartan, Macrophages, Mice, Mice, Inbred C57BL, Mice, Knockout, Nephrectomy, PPAR gamma, Phenotype, Pioglitazone, Renal Insufficiency, Chronic, Renin-Angiotensin System, Thiazolidinediones
Show Abstract · Added April 10, 2018
OBJECTIVE - Chronic kidney disease (CKD) amplifies atherosclerosis, which involves renin-angiotensin system (RAS) regulation of macrophages. RAS influences peroxisome proliferator-activated receptor-γ (PPARγ), a modulator of atherogenic functions of macrophages, however, little is known about its effects in CKD. We examined the impact of combined therapy with a PPARγ agonist and angiotensin receptor blocker on atherogenesis in a murine uninephrectomy model.
METHODS - Apolipoprotein E knockout mice underwent uninephrectomy (UNx) and treatment with pioglitazone (UNx + Pio), losartan (UNx + Los), or both (UNx + Pio/Los) for 10 weeks. Extent and characteristics of atherosclerotic lesions and macrophage phenotypes were assessed; RAW264.7 and primary peritoneal mouse cells were used to examine pioglitazone and losartan effects on macrophage phenotype and inflammatory response.
RESULTS - UNx significantly increased atherosclerosis. Pioglitazone and losartan each significantly reduced the atherosclerotic burden by 29.6% and 33.5%, respectively; although the benefit was dramatically augmented by combination treatment which lessened atherosclerosis by 55.7%. Assessment of plaques revealed significantly greater macrophage area in UNx + Pio/Los (80.7 ± 11.4% vs. 50.3 ± 4.2% in UNx + Pio and 57.2 ± 6.5% in UNx + Los) with more apoptotic cells. The expanded macrophage-rich lesions of UNx + Pio/Los had more alternatively activated, Ym-1 and arginine 1-positive M2 phenotypes (Ym-1: 33.6 ± 8.2%, p < 0.05 vs. 12.0 ± 1.1% in UNx; arginase 1: 27.8 ± 0.9%, p < 0.05 vs. 11.8 ± 1.3% in UNx). In vitro, pioglitazone alone and together with losartan was more effective than losartan alone in dampening lipopolysaccharide-induced cytokine production, suppressing M1 phenotypic change while enhancing M2 phenotypic change.
CONCLUSION - Combination of pioglitazone and losartan is more effective in reducing renal injury-induced atherosclerosis than either treatment alone. This benefit reflects mitigation in macrophage cytokine production, enhanced apoptosis, and a shift toward an anti-inflammatory phenotype.
Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
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27 MeSH Terms
Activation of the Endogenous Renin-Angiotensin-Aldosterone System or Aldosterone Administration Increases Urinary Exosomal Sodium Channel Excretion.
Qi Y, Wang X, Rose KL, MacDonald WH, Zhang B, Schey KL, Luther JM
(2016) J Am Soc Nephrol 27: 646-56
MeSH Terms: Adult, Aldosterone, Cross-Over Studies, Epithelial Sodium Channels, Exosomes, Female, Humans, Male, Renin-Angiotensin System, Sodium, Dietary
Show Abstract · Added November 30, 2015
Urinary exosomes secreted by multiple cell types in the kidney may participate in intercellular signaling and provide an enriched source of kidney-specific proteins for biomarker discovery. Factors that alter the exosomal protein content remain unknown. To determine whether endogenous and exogenous hormones modify urinary exosomal protein content, we analyzed samples from 14 mildly hypertensive patients in a crossover study during a high-sodium (HS, 160 mmol/d) diet and low-sodium (LS, 20 mmol/d) diet to activate the endogenous renin-angiotensin-aldosterone system. We further analyzed selected exosomal protein content in a separate cohort of healthy persons receiving intravenous aldosterone (0.7 μg/kg per hour for 10 hours) versus vehicle infusion. The LS diet increased plasma renin activity and aldosterone concentration, whereas aldosterone infusion increased only aldosterone concentration. Protein analysis of paired urine exosome samples by liquid chromatography-tandem mass spectrometry-based multidimensional protein identification technology detected 2775 unique proteins, of which 316 exhibited significantly altered abundance during LS diet. Sodium chloride cotransporter (NCC) and α- and γ-epithelial sodium channel (ENaC) subunits from the discovery set were verified using targeted multiple reaction monitoring mass spectrometry quantified with isotope-labeled peptide standards. Dietary sodium restriction or acute aldosterone infusion similarly increased urine exosomal γENaC[112-122] peptide concentrations nearly 20-fold, which correlated with plasma aldosterone concentration and urinary Na/K ratio. Urine exosomal NCC and αENaC concentrations were relatively unchanged during these interventions. We conclude that urinary exosome content is altered by renin-angiotensin-aldosterone system activation. Urinary measurement of exosomal γENaC[112-122] concentration may provide a useful biomarker of ENaC activation in future clinical studies.
Copyright © 2016 by the American Society of Nephrology.
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10 MeSH Terms
Antihypertensive mechanisms of intra-renal dopamine.
Zhang MZ, Harris RC
(2015) Curr Opin Nephrol Hypertens 24: 117-22
MeSH Terms: Animals, Antihypertensive Agents, Blood Pressure, Dopamine, Humans, Hypertension, Kidney, Renin-Angiotensin System
Show Abstract · Added February 12, 2015
PURPOSE OF REVIEW - This review will highlight recent findings concerning the regulation and signalling of the intrarenal dopaminergic system and the emerging evidence for its importance in blood pressure regulation.
RECENT FINDINGS - There is an increasing evidence that the intrarenal dopaminergic system plays an important role in the regulation of blood pressure, and defects in dopamine signalling appear to be involved in the development of hypertension. Recent experimental models have definitively demonstrated that abnormalities in intrarenal dopamine production or receptor signalling can predispose to salt-sensitive hypertension and a dysregulated renin-angiotensin system. There are also new results indicating the importance of dopamine receptor mediated regulation of salt and water homeostasis along the nephron, and new studies indicating the role that the intrarenal dopaminergic system plays to mitigate the production of reactive oxygen species and progression of chronic renal disease.
SUMMARY - New studies underscore the importance of the intrarenal dopaminergic system in the regulation of renal function and indicate how alterations in dopamine production or signalling may underlie the development of hypertension and kidney injury.
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8 MeSH Terms