Fructose high-salt (FHS) diets increase blood pressure (BP) in an angiotensin II (Ang II)-dependent manner. Ang II stimulates aldosterone release, which acting on the mineralocorticoid receptor (MR) regulates Na+ reabsorption by the aldosterone-sensitive distal nephron (ASDN). The MR can be transactivated by glucocorticoids, including those locally produced by 11β-HSD1. The epithelial sodium channel (ENaC) is a key transporter regulated MRs. We hypothesized that fructose-induced salt-sensitive hypertension depends in part on abnormal activation of MRs in the ASDN with consequent increases in ENaC expression. We found that aldosterone-upregulated genes in mice ASDN, significantly overlapped with 74 genes upregulated by FHS in the rat kidney cortex (13/74; p≤1x10-8), and that these 74 genes are prominently expressed in rat ASDN cells. Additionally, the average z-score expression of mice-aldosterone-upregulated genes is highly correlated with FHS compared to glucose high-salt (GHS) in the rat kidney cortex (Pearson correlation; r=0.66; p≤0.005). There were no significant differences in plasma aldosterone concentrations between the FHS and GHS. However, 11β-HSD1 transcripts were upregulated by FHS (log2FC=0.26, p≤0.02). FHS increased BP by 23±6 mmHg compared to GHS, and blocking MRs with eplerenone prevented this increase. Additionally, inhibiting ENaC with amiloride significantly reduced BP in FHS from 148±6 to 134±5 mmHg (p≤0.019). Compared to GHS, FHS increased total and cleaved αENaC protein by 89±14 % (p≤0.03) and 47±16 % (p≤0.01) respectively. FHS did not change β- or γ-subunit expression. These results suggest that fructose-induced salt-sensitive hypertension depends, in part, on abnormal Na+ retention by ENaC, resulting from the activation of MRs by glucocorticoids.
@article{ZhangEtAl2024_AldoFruc,
author = {Zhang, R. and Shi, S. and Jadhav, D. A. and Kim, N. and Brostek, A. and Forester, B. R. and Shukla, R. and Qu, C. and Kramer, B. K. and Garvin, J. L. and Kleyman, T. R. and A. Gonzalez-Vicente, Agustin},
title = {[PRE-PRINT] Abnormal activation of the mineralocorticoid receptor in the aldosterone-sensitive distal nephron contributes to fructose-induced salt-sensitive hypertension},
journal = {BioRxiv},
elocation-id = {2024.08.19.608663},
year = {2024},
month = aug,
doi = {10.1101/2024.08.19.608663},
publisher = {Cold Spring Harbor Laboratory},
}BACKGROUND: A fructose high-salt (FHS) diet increases systolic blood pressure and Ang II (angiotensin II)–stimulated proximal tubule (PT) superoxide (O2−) production. These increases are prevented by scavenging O2− or an Ang II type 1 receptor antagonist. SGLT4 (sodium glucose-linked cotransporters 4) and SGLT5 are implicated in PT fructose reabsorption, but their roles in fructose-induced hypertension are unclear. We hypothesized that PT fructose reabsorption by SGLT5 initiates a genetic program enhancing Ang II–stimulated oxidative stress in males and females, thereby causing fructose-induced salt-sensitive hypertension. METHODS: We measured systolic blood pressure in male and female Sprague-Dawley (wild type [WT]), SGLT4 knockout (−/−), and SGLT5−/− rats. Then, we measured basal and Ang II–stimulated (37 nmol/L) O2− production by PTs and conducted gene coexpression network analysis. RESULTS: In male WT and female WT rats, FHS increased systolic blood pressure by 15±3 (n=7; P<0.0027) and 17±4 mm Hg (n=9; P<0.0037), respectively. Male and female SGLT4−/− had similar increases. Systolic blood pressure was unchanged by FHS in male and female SGLT5−/−. In male WT and female WT fed FHS, Ang II stimulated O2− production by 14±5 (n=6; P<0.0493) and 8±3 relative light units/µg protein/s (n=7; P<0.0218), respectively. The responses of SGTL4−/− were similar. Ang II did not stimulate O2− production in tubules from SGLT5−/−. Five gene coexpression modules were correlated with FHS. These correlations were completely blunted in SGLT5−/− and partially blunted by chronically scavenging O2− with tempol. CONCLUSIONS: SGLT5-mediated PT fructose reabsorption is required for FHS to augment Ang II–stimulated proximal nephron O2− production, and increases in PT oxidative stress likely contribute to FHS-induced hypertension.
@article{BeauEtAl2024SGLT5WGCNAHypertension,
title = {Knocking out sodium glucose-linked transporter 5 prevents fructose-induced renal oxidative stress and salt-sensitive hypertension},
author = {Forester, B. R. and Zhang, R. and Schuhler, B. and Brostek, A. and Gonzalez-Vicente, A. and Garvin, J. L.},
year = {2024},
month = jun,
journal = {Hypertension},
volume = {81},
number = {6},
pages = {1296--1307},
publisher = {Am Heart Assoc},
pubmedid = {38545789},
doi = {10.1161/HYPERTENSIONAHA.123.22535},
}Introduction: The kidney tubule comprises distinct segments with specialized epithelium, including proximal tubules (PT) subsegments S1, S2, and S3, descending (DTL) and ascending (ATL) thin limbs, thick ascending limb (TAL) medullary (MTAL) and cortical (CTAL) subsegments, distal convoluted tubule (DCT), connecting tubule (CNT), and collecting ducts (CD) containing principal (PC) and intercalated (IC) cells. Single-cell RNA sequencing (scRNAseq) is a crucial tool in kidney research. However, it assigns cells to nephron segments based on transcriptome similarity, disregarding anatomical context and spatial information, critical for kidney function. Hypothesis: We hypothesized that cellular deconvolution of microdissected tubule segment transcriptomes would identify mixed cell populations coexisting on different parts of the nephron. Methods: We employed CibersortX to estimate cell proportions in microdissected rat nephron segment transcriptomes (GSE56743), using rat kidney epithelial cell transcriptomes from a scRNAseq dataset (GSE137869) as reference. Raw sequencing files from the Sequence Read Archive (SRA) were downloaded and reprocessed. The number of detected genes was 34,322 for bulk RNAseq and 15,282 for scRNAseq, with a shared gene space of 13,373 used for deconvolution. Results: We discovered that PT.S1 segments primarily consist of S1 cells (81%) and some S2 cells (12%). Microdissected PT.S2 segments contain a mix of S1 (18%), S2 (58%), and S3 (19%) cells. PT.S3 segments were primarily composed of S3 cells (75%). DTL and ATL segments displayed a high percentage of the corresponding cell type. Microdissected MTAL segments were a mix of MTAL (25%) and CTAL (69%) cells, while microdissected CTAL segments were almost exclusively composed of MTAL cells (95%). DCT segments exhibited 80% DCT cells with some principal (2%) and intercalated (1%) cells. In CNT, CCD, and OMCD, we observed a continuous increase in PC abundance (58%, 72%, and 78%, respectively) along with a decrease in IC (32%, 23%, and 11%, respectively). Microdissected IMCD contained PC (58%), IC (4%), and 18% of a distinct cell type with IC characteristics not found in other segments. Conclusions: Our analysis supports the well-established cell heterogeneity in connecting tubules and the collecting duct system, including the existence of a specialized IMCD cell. Additionally, we identified mixed cell populations in the S2 segment of the proximal tubule and the medullary thick ascending limb. In the case of S2, the high proportion of cells from adjacent S1 and S3 segments suggests a differentiation continuum from S1 to S3 with diffused anatomical boundaries. We identified two different TAL cell types, the MTAL phenotype restricted to the MTAL and the CTAL phenotype present in higher abundance in both subsegments. These cell types may correspond to the medullary "rough surface" and cortical "smooth surface" cells described in rat TAL. In summary, the terminology used in scRNAseq cluster assignment referring to specific nephron segments is misleading, as it encompasses anatomical regions with multiple coexisting cell types. This highlights the need for caution when interpreting such data.
@inproceedings{JadhavEtAl2024Abs,
author = {Jadhav, D. A. and Zhang, R. and Kramer, B. K. and Gonzalez-Vicente, A.},
title = {[ABSTRACT] Transcript Deconvolution Reveals Heterogeneous Cell Populations in Microdissected Nephron Segments of the Rat Kidney},
booktitle = {Physiology},
volume = {39},
number = {S1},
pages = {831},
year = {2024},
month = may,
doi = {10.1152/physiol.2024.39.S1.831},
url = {https://doi.org/10.1152/physiol.2024.39.S1.831},
}Single-cell RNA sequencing (scRNAseq) is a crucial tool in kidney research. These technologies cluster cells based on transcriptome similarity, irrespective of the anatomical location and order within the nephron. Thus, a transcriptome cluster may obscure the heterogeneity of the cell population within a nephron segment. Elevated dietary fructose leads to salt-sensitive hypertension, in part, through fructose reabsorption in the proximal tubule (PT). However, the organization of the four known fructose transporters in apical PTs (SGLT4, SGLT5, GLUT5, and NaGLT1) remains poorly understood. We hypothesized that cells within each subsegment of the proximal tubule exhibit complex, heterogeneous fructose transporter expression patterns. To test this hypothesis, we analyzed rat kidney transcriptomes and proteomes from publicly available scRNAseq and tubule microdissection databases. We found that microdissected PT-S1 segments consist of 81% ± 12% cells with scRNAseq-derived transcriptional characteristics of S1, whereas PT-S2 express a mixture of 18% ± 9% S1, 58% ± 8% S2, and 19% ± 5% S3 transcripts, and PT-S3 consists of 75% ± 9% S3 transcripts. The expression of all four fructose transporters was detectable in all three PT segments, but key fructose transporters SGLT5 and GLUT5 progressively increased from S1 to S3, and both were significantly upregulated in S3 vs. S1/S2 (Slc5a10: 1.9 log2FC, p < 1 × 10−299; Scl2a5: 1.4 log2FC, p < 4 × 10−105). A similar distribution was found in human kidneys. These data suggest that S3 is the primary site of fructose reabsorption in both humans and rats. Finally, because of the multiple scRNAseq transcriptional phenotypes found in each segment, our findings also imply that anatomical labels applied to scRNAseq clusters may be misleading.
@article{ZhangEtAl2024SGLTLocation,
author = {Zhang, R. and Jadhav, D. A. and Kim, N. and Kramer, B. K. and Gonzalez-Vicente, A.},
title = {Profiling Cell Heterogeneity and Fructose Transporter Expression in the Rat Nephron by Integrating Single-Cell and Microdissected Tubule Segment Transcriptomes},
journal = {International Journal of Molecular Sciences},
volume = {25},
year = {2024},
month = mar,
number = {5},
article-number = {3071},
pubmedid = {38474316},
issn = {1422-0067},
doi = {10.3390/ijms25053071},
}Single-cell RNA sequencing (scRNAseq) is a crucial tool in kidney research. These technologies cluster cells according to transcriptome similarity, irrespective of the anatomical location and ordering within the nephron. Thus, a cluster transcriptome may obscure heterogeneity of the cell population within a nephron segment. Elevated dietary fructose leads to salt-sensitive hypertension, in part by fructose reabsorption in the proximal tubule (PT). However, organization of the four known fructose transporters in apical PTs (SGLT4, SGLT5, GLUT5 and NaGLT1) remains poorly understood. We hypothesized that cells within each subsegment of the proximal tubule exhibit complex, heterogenous fructose transporter expression patterns. To test this hypothesis we analyzed rat and kidney transcriptomes and proteomes from publicly available scRNAseq and tubule microdissection databases. We found that microdissected PT-S1 segments consist of 81±12% cells with scRNAseq-derived transcriptional characteristics of S1, whereas PT-S2 express a mixture of 18±9% S1, 58±8% S2, and 19±5% S3 transcripts, and PT-S3 consists of 75±9% S3 transcripts. The expression of all four fructose transporters was detectable in all three PT segments, but key fructose transporters SGLT5 and GLUT5 progressively increased from S1 to S3, and both were significantly upregulated in S3 vs. S1/S2 (Slc5a10: 1.9 log2FC, p<1×10^-299; Scl2a5: 1.4 log2FC, p<4×10^-105). A similar distribution was found in human kidneys. These data suggest that S3 is the primary site of fructose reabsorption in both humans and rats. Finally, because of the multiple scRNAseq transcriptional phenotypes found in each segment our findings also imply that anatomic labels applied to scRNAseq clusters may be misleading.
@article{ZhangEtAl2023SGLTLocation,
title = {[PRE-PRINT] Profiling cellular heterogeneity and fructose transporter expression in the rat nephron by integrating single-cell and microdissected tubule segment transcriptomes},
author = {Zhang, R. and Aatmaram-Jadhav, D. and Kramer, B. K. and Gonzalez-Vicente, A.},
year = {2023},
month = dec,
journal = {BioRxiv},
publisher = {Cold Spring Harbor Laboratory},
doi = {https://doi.org/10.1101/2023.12.20.572656},
}@inproceedings{ZhangEtAl2023Abs_ENaC,
title = {[ABSTRACT] Increased Epithelial Sodium Channel (ENaC) Activity Mediates Fructose-Induced Salt-Sensitive Hypertension},
author = {Zhang, R. and Shi, S. and Kleyman, T. R. and Gonzalez-Vicente, A.},
year = {2023},
month = nov,
volume = {34},
booktitle = {Journal of the American Society of Nephrology},
doi = {10.1681/ASN.20233411S1514c},
url = {https://journals.lww.com/jasn/citation/2023/11001/increased_epithelial_sodium_channel__enac_.1822.aspx},
}Sexual dimorphism is a key biological variable in different organ systems. Although a growing body of evidence at single cell-resolution highlights sex differences in the kidneys of humans and mice, information regarding rats is limited. We integrated publicly available datasets to construct a single-cell RNA sequencing atlas of the rat kidney, incorporating data from 3 females and 3 males. Transcriptomes from the tubular epithelial cell clusters, exhibited strong correlation with those from rat-kidney microdissected tubule segments and single-cell RNA sequencing of human kidney biopsies. We hypothesize that transcriptomes of rat tubular epithelial cells present sexual dimorphism. To test this hypothesis, we identified genes that were differentially expressed between sexes (DEGs: log2FC >= 1; adjusted-p <= 0.05) in proximal tubules (PT), thick ascending limbs (TAL), distal convoluted tubules (DCT), principal cells (PC) and intercalated cells A and B (IC-A and IC-B, respectively). Gene enrichments of PT DEGs were conducted using WikiPathways. The number of genes positively enriched in males was as follows: 43 PT, 9 TAL, 16 DCT, 23 PC, 12 I-CA and 19 I-CB. While females presented 44 PT, 4 TAL, 4 DCT, 3 PC, 1 IC-A and 3 IC-B. Four transcripts were upregulated in all male segments, 1) glutathione peroxidase 3 (Gpx3), 2) lysozyme 2 (Lyz2), 3) locus A1 (RT1-A1) which enables beta-2-microglobulin and peptide binding activity, and 4) AABR07060872.1 an Ig-like domain-containing protein. Only one long non-coding RNA (AABR07039356.2) was upregulated in all female segments. The three most enriched pathways in male PT were: 1) Proximal tubule transport (WP4917; p < 1x1e-14), 2) Glycolysis and gluconeogenesis (WP534; p < 2x1e-12) and 3) Metabolic reprograming in colon cancer (WP4290; p < 8x1e-9). In females, the most enriched pathways were: 1) Trans-sulfuration and one-carbon metabolism (WP2525; p < 6x1e-9), 2) One-carbon metabolism related pathways (WP3940; p < 1x10-8) and 3) Amino acid metabolism (WP3925; p < 7x1e-8). Our results show the presence of sex-related transcriptional differences across the rat nephron, but predominantly in PT. These differences impact key metabolic functions of PT such amino acids and carbohydrates metabolism and transport processes.
@inproceedings{KramerEtAl2023Abs_SexDimorphicTubeEpiCell,
title = {[ABSTRACT] Sexually dimorphic transcriptional phenotypes in tubular epithelial cells of the rat kidney},
author = {Kramer, B. K. and Zhang, R. and Gonzalez-Vicente, A.},
booktitle = {Hypertension},
year = {2023},
month = oct,
volume = {80},
}Proximal tubules (PT) reabsorb fructose via a Na-dependent mechanism. Knocking out the Sodium-Linked Cotransporter 5 (SGLT5, Slc5A10) increases urinary fructose. Elevated dietary fructose increases transport rates in PT, contributing to salt-sensitive hypertension. Whether dietary fructose also elevates transport in other segments of the nephron that do not express known fructose transporters, is a matter of debate. The aldosterone-sensitive distal tubule (ASDT) consists of the late distal convoluted tubule, connecting tubule and collecting duct, and it is essential for regulating fluid volume and blood pressure. We hypothesize that fructose metabolism in PT could affect aldosterone signaling in the distal tubule of rats fed a high-salt diet. We obtained kidney-cortex bulk RNAseq transcriptomes from wild-type and SGLT5 (-/-) Sprague Dawley rats fed a solid diet containing 4 percent NaCl and either 20 percent fructose (FHS) or glucose (GHS). We used Weighted Correlation Network Analysis (WGCNA) to: 1st) create a gene coexpression network of the kidney cortex, and 2nd) identify genes whose expression changes in response to fructose in both wild-type and SGLT5 (-/-). Then, we used open source transcriptomes from mouse ASDT epithelial cells (PMID: 29521601) treated with and without aldosterone to map genes whose expression changes in response to aldosterone to the coexpression modules correlated with dietary fructose. The mouse transcriptome contained 8619 genes that mapped to the rat kidney transcriptome. Of these genes, 454 were significantly changed by aldosterone (ALDO). WGCNA yielded 35 coexpression modules. Five modules were significantly associated with dietary fructose in wild-type. These correlations were blunted in SGLT5 (-/-). Enrichment analysis indicated that 4 of the 35 modules were enriched for ALDO, 2 of which (Paleturquoise: p<5x10-6 and Orange: p<3x10-2) were also correlated with fructose in wild-type (Paleturquoise: p<3x10-2 and Orange: p<4x10-2). Paleturquoise contained 108 genes of which 74 mapped to the mouse transcriptome, and 15 to ALDO. Ontology enrichments in Paleturquoise indicate that it contains genes involved in Na, Cl and HCO3 transport. Importantly, the Amiloride-Sensitive Epithelial Sodium Channel Alpha Subunit (ENaCα; Scnn1a) and the Thiazide-Sensitive Sodium-Chloride Cotransporter (NCC; Slc12a3) belong in this module. Orange contained 148 genes, of which 34 mapped to mouse transcriptomes, and only 5 to ALDO. Orange’s ontology enrichment was largely immune processes, which explain the low number of mapping genes, as ALDO is a tubular epithelial cell signature. We conclude that even on a high-salt diet, kidneys from rats given fructose present higher transcriptional activation of aldosterone-responsive genes than those given glucose. In addition, Orange may be mediating proinflammatory actions of fructose. These effects depend on fructose reabsorption by PTs, as SGLT5 deletion blunts the effects of HSF on ALDO-enriched modules.
@inproceedings{ZhangEtAl2023Abs_AldoFruc,
title = {[ABSTRACT] Addition of fructose to a high-salt diet increases the expression of aldosterone-response genes},
author = {Zhang, R. and Gonzalez-Vicente, A.},
booktitle = {Physiology},
year = {2023},
month = may,
volume = {38},
url = {https://journals.physiology.org/doi/abs/10.1152/physiol.2023.38.S1.5733301},
}Kidneys of healthy individuals filter 4 to 25 g of fructose (FRU) a day, equivalent to 10 percent of the filtered glucose. FRU reabsorbed by proximal tubules (PTs) is mostly used in gluconeogenesis. Elevated dietary FRU alters hormonal signaling in PTs and increases oxidative stress, which overtime, leads to salt-sensitive hypertension, tubulointerstitial injury, and glomerular damage. Four apical transporters could transport FRU at physiological concentrations: SGLT5 (km0.62 mM), NAGLT1 (km4.5 mM), GLUT5 (km12.6 mM) and SGLT4 (undetermined km). We hypothesize that single-cell (sc) transcriptional phenotypes correspond to anatomical features and could inform FRU transport in PTs. We used scRNAseq rat kidney transcriptomes (3 males & 3 females) to measure the expression of FRU transporters in cell clusters corresponding to the S1, S2, and S3 PT segments. We integrated cell transcriptional phenotypes with spatial and structural features using quantitative proteomics and transcriptomics from microdissected PT segments. Clusters S1, S2, and S3 had 1281, 2123 and 1441 cells, respectively. More than 90 percent of cells in all clusters expressed KHK, the first enzyme in FRU metabolism (expression: S1
@inproceedings{ZhangEtAl2023Abs_PTSegment,
title = {[ABSTRACT] Single-cell transcriptional phenotypes linked to anatomical localization of fructose transporters in rat proximal tubule segments},
author = {Gonzalez-Vicente, A. and Zhang, R.},
booktitle = {Physiology},
year = {2023},
month = may,
volume = {38},
url = {https://journals.physiology.org/doi/abs/10.1152/physiol.2023.38.S1.5725750},
}Proximal tubule fructose metabolism is key to fructose-induced hypertension, but the roles of sex and stress are unclear. We hypothesized that females are resistant to the salt-sensitive hypertension caused by low amounts of dietary fructose compared to males and that the magnitude of the increase in blood pressure (BP) depends, in part, on amplification of the stress response of renal sympathetic nerves. We measured systolic BP (SBP) in rats fed high salt with either no sugar (HS), 20 percent glucose (GHS) or 20 percent fructose (FHS) in the drinking water for 7-8 days. FHS increased SBP in both males (Δ22±9 mmHg; p<0.046) and females (Δ16±3 mmHg; p<0.0007), while neither GHS nor HS alone induced changes in SBP in either sex. The FHS-induced increase in SBP as measured by telemetry in the absence of added stress (8±2 mmHg) was significantly lower than that measured by plethysmography (24±5 mmHg) (p<0.014). However, when BP was measured by telemetry simulating the stress of plethysmography, the increase in SBP was significantly greater (15±3 mmHg) than under low stress (8±1 mmHg) (p<0.014). Moderate-stress also increased telemetric diastolic (p < 0.006) and mean BP (p<0.006) compared to low-stress in FHS-fed animals. Norepinephrine excretion was greater in FHS-fed rats than HS-fed animals (Male: 6.4±1.7 vs.1.8±0.4 nmole/Kg/day; p<0.02. Female 54±18 vs. 1.2±0.6; p<0.02). We conclude that fructose-induced salt-sensitive hypertension is similar in males and females unlike other forms of hypertension, and the increase in blood pressure depends in part on an augmented response of the sympathetic nervous system to stress.
@article{BrostekEtAl2022PR,
title = {Independent effects of sex and stress on fructose-induced salt-sensitive hypertension},
author = {Brostek, A. and Hong, N. J. and Zhang, R. and Forester, B. R. and Barmore, L. E. and Kaydo, L. and Kluge, N. and Smith, C. and Garvin, J. L. and Gonzalez-Vicente, A.},
year = {2022},
month = oct,
volume = {10},
journal = {Physiological Reports},
publisher = {John Wiley & Sons Inc.},
doi = {10.14814/phy2.15489},
}Proximal tubule fructose metabolism is key to fructose-induced hypertension, but the roles of sex and stress are unclear. We hypothesized that females are resistant to the salt-sensitive hypertension caused by low amounts of dietary fructose compared to males and that the magnitude of the increase in blood pressure (BP) depends, in part, on amplification of the stress response of renal sympathetic nerves. We measured systolic BP (SBP) in rats fed high salt with either no sugar (HS), 20% glucose (GHS) or 20% fructose (FHS) in the drinking water for 7-8 days. FHS increased SBP (p<0.03 vs basal) but neither GHS nor high salt alone raised SBP. FHS increased SBP significantly and similarly in both (male: Δ25±8 mm Hg; female: Δ19±2 mm Hg). FHS increased SBP by 24±5 mm Hg but only by 8±2 mm Hg when measured by plethysmography and telemetry, respectively (p<0.004). When SBP was measured by telemetry under low stress, FHS increased SBP by 8±1 mm Hg; on the contrary, when measured by telemetry under moderate stress conditions (simulating stress of plethysmography), FHS increased SBP by 15±3 mm Hg, a significantly greater increase (p<0.008). Norepinephrine excretion in rats subjected to moderate stress was 63±17 nmole/Kg/day for animals fed FHS but only 19±40 nmole/Kg/day for controls fed HS (p<0.02). We conclude that fructose-induced salt-sensitive hypertension is similar in males and females unlike other forms of hypertension, and the increase in blood pressure depends in part on an augmented response of the sympathetic nervous system to stress.
@inproceedings{BrostekEtAl2022Abs_PR,
title = {[ABSTRACT] Sex And Stress In Fructose-induced Salt-sensitive Hypertension},
author = {Brostek, A. and Hong, N. J. and Zhang, R. and Forester, B. R. and Barmore, L. E. and Kaydo, L. and Kluge, N. and Smith, C. and Garvin, J. L. and Gonzalez-Vicente, A.},
booktitle = {Hypertension},
volume = {79},
number = {Suppl\_1},
pages = {A076-A076},
year = {2022},
month = sep,
}