scholarly journals Treatment With Lisinopril Prevents the Early Progression of Glomerular Injury in Obese Dahl Salt-Sensitive Rats Independent of Lowering Arterial Pressure

2021 ◽  
Vol 12 ◽  
Author(s):  
Andrea K. Brown ◽  
Alyssa Nichols ◽  
Chantell A. Coley ◽  
Ubong S. Ekperikpe ◽  
Kasi C. McPherson ◽  
...  
Keyword(s):  
Drinking Water ◽  
Arterial Pressure ◽  
Early Development ◽  
Chronic Treatment ◽  
Leptin Receptor ◽  
Glomerular Injury ◽  
Mesangial Expansion ◽  
Renal Inflammation ◽  
Early Progression ◽  
Receptor Mutant

Recently, we reported that obese Dahl salt-sensitive leptin receptor mutant (SSLepRmutant) rats develop glomerular injury and progressive proteinuria prior to puberty. Moreover, this early progression of proteinuria was associated with elevations in GFR. Therefore, the current study examined whether treatment with lisinopril to reduce GFR slows the early progression of proteinuria in SSLepRmutant rats prior to puberty. Experiments were performed on 4-week-old SS and SSLepRmutant rats that were either treated with vehicle or lisinopril (20 mg/kg/day, drinking water) for 4 weeks. We did not observe any differences in MAP between SS and SSLepRmutant rats treated with vehicle (148 ± 5 vs. 163 ± 6 mmHg, respectively). Interestingly, chronic treatment with lisinopril markedly reduced MAP in SS rats (111 ± 3 mmHg) but had no effect on MAP in SSLepRmutant rats (155 ± 4 mmHg). Treatment with lisinopril significantly reduced proteinuria in SS and SSLepRmutant rats compared to their vehicle counterparts (19 ± 5 and 258 ± 34 vs. 71 ± 12 and 498 ± 66 mg/day, respectively). Additionally, nephrin excretion was significantly elevated in SSLepRmutant rats versus SS rats, and lisinopril reduced nephrin excretion in both strains. GFR was significantly elevated in SSLepRmutant rats compared to SS rats, and lisinopril treatment reduced GFR in SSLepRmutant rats by 30%. The kidneys from SSLepRmutant rats displayed glomerular injury with increased mesangial expansion and renal inflammation versus SS rats. Chronic treatment with lisinopril significantly decreased glomerular injury and renal inflammation in the SSLepRmutant rats. Overall, these data indicate that inhibiting renal hyperfiltration associated with obesity is beneficial in slowing the early development of glomerular injury and renal inflammation.

scholarly journals Altered renal hemodynamics is associated with glomerular lipid accumulation in obese Dahl salt-sensitive leptin receptor mutant rats

2020 ◽  
Vol 318 (4) ◽  
pp. F911-F921 ◽  
Author(s):  
Kasi C. McPherson ◽  
Corbin A. Shields ◽  
Bibek Poudel ◽  
Ashley C. Johnson ◽  
Lateia Taylor ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Mutant Strain ◽  
Early Development ◽  
Lipid Accumulation ◽  
Leptin Receptor ◽  
Regulatory Protein ◽  
Pcr Analysis ◽  
Glomerular Injury ◽  
Receptor Mutant

The present study examined whether development of renal injury in the nondiabetic obese Dahl salt-sensitive leptin receptor mutant (SSLepRmutant) strain is associated with elevations in glomerular filtration rate and renal lipid accumulation. Baseline mean arterial pressure at 6 wk of age was similar between Dahl salt-sensitive wild-type (SSWT) and SSLepRmutant rats. However, by 18 wk of age, the SSLepRmutant strain developed hypertension, while the elevation in mean arterial pressure was not as severe in SSWT rats (192 ± 4 and 149 ± 6 mmHg, respectively). At baseline, proteinuria was fourfold higher in SSLepRmutant than SSWT rats and remained elevated throughout the study. The early development of progressive proteinuria was associated with renal hyperfiltration followed by a decline in renal function over the course of study in the SSLepRmutant compared with SSWT rats. Kidneys from the SSLepRmutant strain displayed more glomerulosclerosis and glomerular lipid accumulation than SSWT rats. Glomeruli were isolated from the renal cortex of both strains at 6 and 18 wk of age, and RNA sequencing was performed to identify genes and pathways driving glomerular injury. We observed significant increases in expression of the influx lipid transporters, chemokine (C-X-C motif) ligand 16 (Cxcl16) and scavenger receptor and fatty acid translocase (Cd36), respectively, and a significant decrease in expression of the efflux lipid transporter, ATP-binding cassette subfamily A member 2 ( Abca2; cholesterol efflux regulatory protein 2), in SSLepRmutant compared with SSWT rats at 6 and 18 wk of age, which were validated by RT-PCR analysis. These data suggest an association between glomerular hyperfiltration and glomerular lipid accumulation during the early development of proteinuria associated with obesity.

scholarly journals Depletion of macrophages slows the early progression of renal injury in obese Dahl salt-sensitive leptin receptor mutant rats

2020 ◽  
Vol 318 (6) ◽  
pp. F1489-F1499
Author(s):  
Bibek Poudel ◽  
Corbin A. Shields ◽  
Andrea K. Brown ◽  
Ubong Ekperikpe ◽  
Tyler Johnson ◽  
...  
Keyword(s):  
Metabolic Disease ◽  
Glucose Tolerance ◽  
Mutant Strain ◽  
Renal Injury ◽  
Renal Fibrosis ◽  
Leptin Receptor ◽  
Glomerular Injury ◽  
Mesangial Expansion ◽  
Early Progression ◽  
Receptor Mutant

Recently, we reported that obese Dahl salt-sensitive (SS) leptin receptor mutant (SSLepRmutant) rats display progressive renal injury. The present study demonstrated that the early development of renal injury in the SSLepRmutant strain is associated with an increase in the renal infiltration of macrophages compared with lean SS rats. We also examined whether depletion of macrophages with clodronate would reduce the early progression of renal injury in the SSLepRmutant strain. Four-week-old SS and SSLepRmutant rats were treated with either vehicle (PBS) or clodronate (50 mg/kg ip, 2 times/wk) for 4 wk. While the administration of clodronate did not reduce renal macrophage infiltration in SS rats, clodronate decreased macrophages in the kidneys of SSLepRmutant rats by >50%. Interestingly, clodronate significantly reduced plasma glucose, insulin, and triglyceride levels and markedly improved glucose tolerance in SSLepRmutant rats. Treatment with clodronate had no effect on the progression of proteinuria or renal histopathology in SS rats. In the SSLepRmutant strain, proteinuria was markedly reduced during the first 2 wk of treatment (159 ± 32 vs. 303 ± 52 mg/day, respectively). However, after 4 wk of treatment, the effect of clodronate was no longer observed in the SSLepRmutant strain (346 ± 195 vs. 399 ± 50 mg/day, respectively). The kidneys from SSLepRmutant rats displayed glomerular injury with increased mesangial expansion and renal fibrosis versus SS rats. Treatment with clodronate significantly decreased glomerular injury and renal fibrosis in the SSLepRmutant strain. Overall, these data indicate that the depletion of macrophages improves metabolic disease and slows the early progression of renal injury in SSLepRmutant rats.

Abstract MP15: Treatment With IL-25 Slows The Early Progression Of Proteinuria In Obese Dahl Salt-sensitive Rats

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Bibek Poudel ◽  
Corbin A Shields ◽  
Ubong Ekperikpe ◽  
Andrea K Brown ◽  
Denise C Cornelius ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Renal Disease ◽  
Mutant Strain ◽  
Treated Group ◽  
Macrophage Infiltration ◽  
M2 Macrophages ◽  
M1 Macrophages ◽  
Renal Inflammation ◽  
Early Progression ◽  
Group 1

Recently, we reported that the early progression of proteinuria in the obese Dahl salt-sensitive (SS LepR mutant) strain was associated with increased renal macrophage infiltration in the absence of hyperglycemia and elevations in arterial pressure. Macrophages (MØ) can be divided into two distinct phenotypes: M1-macrophages (classical; pro-inflammatory), and M2-macrophages (alternative; anti-inflammatory). M1-macrophages induce renal inflammation and fibrosis whereas M2-macrophages reduce renal inflammation and fibrosis. Moreover, previous studies have demonstrated that interlukin-25 (IL-25) converts resting MØ and M1 macrophages into M2 macrophages. Therefore, the objective of the current study was to examine whether treatment with IL-25 would reduce the early progression of proteinuria in SS LepR mutant rats by increasing renal M2 macrophages. Four week-old SS LepR mutant rats were separated into two groups (n=5/group): (1) vehicle (PBS) and (2) IL-25 (1μg/day, i.p.) for the first 10 days of the study. At baseline, proteinuria was similar in vehicle and IL-25 treated rats (81±18 vs. 66±8 mg/day, respectively). After 2 weeks, proteinuria was markedly reduced in the IL-25-treated group compared to the values measured in the vehicle treated rats (191±37 vs. 365±55 mg/day respectively; p<0.05 vs. vehicle). Interestingly, treatment with IL-25 was no longer effective in inhibiting the progression of proteinuria after 4 weeks (508±83 and 521±73 mg/day). When examining the possible phenotypes of the infiltrated macrophages in the kidneys, we did not detect any differences in M1 versus M2 macrophages between vehicle and IL-25 treated groups after 4 weeks. However, after 2 weeks of treatment, we did observe a tendency for M2 macrophages to be elevated in the kidneys of the IL-25 group. Overall, these data support our previous finding that the early progression of proteinuria in the obese SS LepR mutant strain is associated with renal macrophage infiltration and also suggest that IL-25 may be considered a therapeutic target for renal disease associated with obesity. This study was supported by DK109133. Key Words: Obesity, Renal Disease, Macrophages, IL-25

scholarly journals Early development of podocyte injury independently of hyperglycemia and elevations in arterial pressure in nondiabetic obese Dahl SS leptin receptor mutant rats

2016 ◽  
Vol 311 (4) ◽  
pp. F793-F804 ◽  
Author(s):  
Kasi C. McPherson ◽  
Lateia Taylor ◽  
Ashley C. Johnson ◽  
Sean P. Didion ◽  
Aron M. Geurts ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Mutant Strain ◽  
Leptin Receptor ◽  
Systolic Arterial Pressure ◽  
Zinc Finger Nucleases ◽  
Glomerular Injury ◽  
Podocyte Injury ◽  
Entire Study ◽  
Glucose Levels ◽  
Plasma Insulin Levels

The current study examined the effect of obesity on the development of renal injury within the genetic background of the Dahl salt-sensitive rat with a dysfunctional leptin receptor derived from zinc-finger nucleases (SSLepRmutant strain). At 6 wk of age, body weight was 35% higher in the SSLepRmutant strain compared with SSWT rats and remained elevated throughout the entire study. The SSLepRmutant strain exhibited impaired glucose tolerance and increased plasma insulin levels at 6 wk of age, suggesting insulin resistance while SSWT rats did not. However, blood glucose levels were normal throughout the course of the study. Systolic arterial pressure (SAP) was similar between the two strains from 6 to 10 wk of age. However, by 18 wk of age, the development of hypertension was more severe in the SSLepRmutant strain compared with SSWT rats (201 ± 10 vs. 155 ± 3 mmHg, respectively). Interestingly, proteinuria was substantially higher at 6 wk of age in the SSLepRmutant strain vs. SSWT rats (241 ± 27 vs. 24 ± 2 mg/day, respectively) and remained elevated until the end of the study. The kidneys from the SSLepRmutant strain displayed significant glomerular injury, including podocyte foot process effacement and lipid droplets compared with SSWT rats as early as 6 wk of age. By 18 wk of age, plasma creatinine levels were twofold higher in the SSLepRmutant strain vs. SSWT rats, suggesting the presence of chronic kidney disease (CKD). Overall, these results indicate that the SSLepRmutant strain develops podocyte injury and proteinuria independently of hyperglycemia and elevated arterial pressure that later progresses to CKD.

Role of oxidative stress in age-related reduction of NO-cGMP-mediated vascular relaxation in SHR

2003 ◽  
Vol 285 (3) ◽  
pp. R542-R551 ◽  
Author(s):  
Jason A. Payne ◽  
Jane F. Reckelhoff ◽  
Raouf A. Khalil
Keyword(s):  
Oxidative Stress ◽  
Drinking Water ◽  
Arterial Pressure ◽  
Vascular Relaxation ◽  
Adult Rats ◽  
Vascular Contraction ◽  
Aging Rats ◽  
Age Related ◽  
Nitrite Nitrate ◽  
Late Stages

The incidence of hypertension increases during the late stages of aging; however, the vascular mechanisms involved are unclear. We investigated whether the late stages of aging are associated with impaired nitric oxide (NO)-mediated vascular relaxation and enhanced vascular contraction and whether oxidative stress plays a role in the age-related vascular changes. Aging (16 mo) male spontaneously hypertensive rats (SHR) nontreated or treated for 8 mo with the antioxidant tempol (1 mM in drinking water) or vitamin E (E; 5,000 IU/kg chow) and vitamin C (C; 100 mg · kg-1· day-1in drinking water) and adult (12 wk) male SHR were used. After the arterial pressure was measured, aortic strips were isolated from the rats for measurement of isometric contraction. The arterial pressure and phenylephrine (Phe)-induced vascular contraction were enhanced, and the ACh-induced vascular relaxation and nitrite/nitrate production were reduced in aging compared with adult rats. In aging rats, the arterial pressure was nontreated (188 ± 4), tempol-treated (161 ± 6), and E + C-treated (187 ± 1 mmHg). Phe (10-5M) caused an increase in active stress in nontreated aging rats (14.3 ± 1.0) that was significantly ( P < 0.05) reduced in tempol-treated (9.0 ± 0.7) and E + C-treated rats (9.8 ± 0.6 × 104N/m2). ACh produced a small relaxation of Phe contraction in nontreated aging rats that was enhanced ( P < 0.05) in tempol- and E + C-treated rats. l-NAME (10-4M), inhibitor of NO synthase, or ODQ (10-5M), inhibitor of cGMP production in smooth muscle, inhibited ACh relaxation and enhanced Phe contraction in tempol- and E + C-treated but not the nontreated aging rats. ACh-induced vascular nitrite/nitrate production was not different in nontreated, tempol- and E + C-treated aging rats. Relaxation of Phe contraction with sodium nitroprusside, an exogenous NO donor, was smaller in aging than adult rats but was not different between nontreated, tempol- and E + C-treated aging rats. Thus, during the late stages of aging in SHR rats, an age-related inhibition of a vascular relaxation pathway involving not only NO production by endothelial cells but also the bioavailability of NO and the smooth muscle response to NO is partially reversed during chronic treatment with the antioxidants tempol and vitamins E and C. The data suggest a role for oxidative stress in the reduction of vascular relaxation and thereby the promotion of vascular contraction and hypertension during the late stages of aging.

scholarly journals Fluoxetine exposure in adolescent and adult female mice decreases cocaine and sucrose preference later in life

2018 ◽  
Vol 33 (1) ◽  
pp. 145-153 ◽  
Author(s):  
Francisco J Flores-Ramirez ◽  
Israel Garcia-Carachure ◽  
David O Sanchez ◽  
Celene Gonzalez ◽  
Samuel A Castillo ◽  
...  
Keyword(s):  
Drinking Water ◽  
Conditioned Place Preference ◽  
Early Development ◽  
Adult Female ◽  
Model System ◽  
Psychotropic Medications ◽  
Sucrose Preference ◽  
Female Mice ◽  
Male Subjects ◽  
Conditioned Place Preference Paradigm

Background: Preclinical evidence from male subjects indicates that exposure to psychotropic medications, during early development, results in long-lasting altered responses to reward-related stimuli. However, it is not known if exposure to the antidepressant fluoxetine, in female subjects specifically, changes sensitivity to natural and drug rewards, later in life. Aims: The aim of this work was to investigate if exposure to fluoxetine mediates enduring changes in sensitivity to the rewarding properties of cocaine and sucrose, using female mice as a model system. Methods: We exposed C57BL/6 female mice to fluoxetine (250 mg/L in their drinking water) for 15 consecutive days, either during adolescence (postnatal day 35–49) or adulthood (postnatal day 70–84). Twenty-one days later, mice were examined on their behavioral reactivity to cocaine (0, 2.5, 5, 7.5 mg/kg) using the conditioned place preference paradigm, or assessed on the two-bottle sucrose (1%) test. Results: We found that regardless of age of antidepressant exposure, female mice pre-exposed to fluoxetine displayed reliable conditioning to the cocaine-paired compartment. However, when compared to respective age-matched controls, antidepressant pre-exposure decreased the magnitude of conditioning at the 5 and 7.5 mg/kg cocaine doses. Furthermore, fluoxetine pre-exposure reduced sucrose preference without altering total liquid intake. Conclusions: The data suggest that pre-exposure to fluoxetine, during adolescence or adulthood, results in a prolonged decrease in sensitivity to the rewarding properties of both natural and drug rewards in female C57BL/6 mice.

Abstract 254: Inflammasome Activity Is Essential For Deoxycorticosterone Acetate/salt-induced Hypertension In Mice

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Shalini M Krishnan ◽  
Christopher G Sobey ◽  
Barbara Kemp-Harper ◽  
Christopher T Chan ◽  
Henry Diep ◽  
...  
Keyword(s):  
Drinking Water ◽  
Receptor Protein ◽  
Salt Treatment ◽  
Deoxycorticosterone Acetate ◽  
Renal Inflammation ◽  
Protein Levels ◽  
Caspase 1 ◽  
Induced Hypertension ◽  
The Impact ◽  
Inflammasome Activity

Inflammasomes are signalling complexes comprised of a NOD-like receptor protein (NLRP), an adapter protein (ASC) and caspase-1. Inflammasomes detect host-derived danger signals and induce inflammation via activation of caspase-1, which in turn cleaves the cytokines pro-interleukin(IL)-1β and pro-IL-18 into their active, pro-inflammatory forms. Hypertension is associated with chronic renal inflammation, but the role of the inflammasome in this process is not known. Hence, we tested whether deoxycorticosterone acetate (DOCA)/salt-induced hypertension in mice is associated with increased expression and/or activation of the inflammasome in the kidney, and assessed the impact of inhibition of inflammasome activity on blood pressure (BP) and markers of renal inflammation and fibrosis. Male C57BL6/J (wild type) and ASC -/- mice were uninephrectomised, implanted with a DOCA pellet (2.4 mg/d, 21 d, s.c. ) and had their drinking water replaced with 1% saline (1K/DOCA/salt). Control mice had a kidney removed but received a placebo pellet and normal drinking water. 1K/DOCA/salt-treated mice had elevated systolic BP (146±4 mmHg) compared to control mice (115±2 mmHg; n=13-16; P<0.05). 1K/DOCA/salt-induced hypertension was associated with increased renal mRNA expression (fold-change vs control; n=7-9; P<0.05) of inflammasome subunits NLRP3 (2.3±0.2), ASC (2.8±0.6) and pro-caspase-1 (2.6±0.5), and the cytokine, pro-IL-1 (4.0±0.8). Moreover, protein levels of cleaved (active) caspase-1 and IL-1 were increased by 1.6±0.2- and 2.1±0.3-fold, respectively in kidneys of 1K/DOCA/salt vs control mice (n=6; P<0.05). ASC -/- mice, which lack an active inflammasome complex, displayed blunted hypertensive responses to 1K/DOCA/salt-treatment (140±3 mmHg) compared to wild types (155±8 mmHg; n=8-9; P<0.05). ASC -/- mice were also protected from 1K/DOCA/salt-induced increases in renal expression of the inflammatory genes IL-6, IL-17a, CCL2, ICAM-1 and VCAM-1, and accumulation of collagen. Thus, renal inflammation, fibrosis and elevated BP in response to 1K/DOCA/salt-treatment are critically dependent on inflammasome activity, highlighting this signalling complex and its cytokine products as potential therapeutic targets to treat hypertension.

Effect of baroreceptor denervation on stimulation of drinking by angiotensin II in conscious dogs

1991 ◽  
Vol 260 (3) ◽  
pp. E333-E337 ◽  
Author(s):  
C. K. Klingbeil ◽  
V. L. Brooks ◽  
E. W. Quillen ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Plasma Osmolality ◽  
Plasma Angiotensin ◽  
High Doses ◽  
Stimulation Of

Angiotensin II causes marked stimulation of drinking when it is injected centrally but is a relatively weak dipsogen when administered intravenously. However, it has been proposed that the dipsogenic action of systemically administered angiotensin II may be counteracted by the pressor action of the peptide. To test this hypothesis, the dipsogenic action of angiotensin II was investigated in dogs, in which low and high baroreceptor influences had been eliminated by denervation of the carotid sinus, aortic arch, and heart. In five sham-operated dogs, infusion of angiotensin II at 10 and 20 ng.kg-1.min-1 increased plasma angiotensin II concentration to 109.2 +/- 6.9 and 219.2 +/- 38.5 pg/ml and mean arterial pressure by 20 and 29 mmHg, respectively, but did not induce drinking. In four baroreceptor-denervated dogs, the angiotensin II infusions produced similar increases in plasma angiotensin II concentration and mean arterial pressure but, in contrast to the results in the sham-operated dogs, produced a dose-related stimulation of drinking. Water intake with the low and high doses of angiotensin II was 111 +/- 44 and 255 +/- 36 ml, respectively. The drinking responses to an increase in plasma osmolality produced by infusion of hypertonic sodium chloride were not different in the sham-operated and baroreceptor-denervated dogs. These results demonstrate that baroreceptor denervation increases the dipsogenic potency of intravenous angiotensin II and provides further support for the hypothesis that the dipsogenic action of intravenous angiotensin II is counteracted by the rise in blood pressure.

Pulmonary vascular iNOS induction participates in the onset of chronic hypoxic pulmonary hypertension

2006 ◽  
Vol 290 (1) ◽  
pp. L11-L20 ◽  
Author(s):  
Václav Hampl ◽  
Jana Bíbová ◽  
Alena Baňasová ◽  
Jiří Uhlík ◽  
Dana Miková ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Drinking Water ◽  
Arterial Pressure ◽  
Tissue Injury ◽  
Vascular Wall ◽  
Systemic Arterial Pressure ◽  
No Production ◽  
Hypoxic Pulmonary Hypertension ◽  
Inos Inhibitor ◽  
Inos Induction

Pathogenesis of hypoxic pulmonary hypertension is initiated by oxidative injury to the pulmonary vascular wall. Because nitric oxide (NO) can contribute to oxidative stress and because the inducible isoform of NO synthase (iNOS) is often upregulated in association with tissue injury, we hypothesized that iNOS-derived NO participates in the pulmonary vascular wall injury at the onset of hypoxic pulmonary hypertension. An effective and selective dose of an iNOS inhibitor, l- N6-(1-iminoethyl)lysine (l-NIL), for chronic peroral treatment was first determined (8 mg/l in drinking water) by measuring exhaled NO concentration and systemic arterial pressure after LPS injection under ketamine+xylazine anesthesia. A separate batch of rats was then exposed to hypoxia (10% O2) and given l-NIL or a nonselective inhibitor of all NO synthases, NG-nitro-l-arginine methyl ester (l-NAME, 500 mg/l), in drinking water. Both inhibitors, applied just before and during 1-wk hypoxia, equally reduced pulmonary arterial pressure (PAP) measured under ketamine+xylazine anesthesia. If hypoxia continued for 2 more wk after l-NIL treatment was discontinued, PAP was still lower than in untreated hypoxic controls. Immunostaining of lung vessels showed negligible iNOS presence in control rats, striking iNOS expression after 4 days of hypoxia, and return of iNOS immunostaining toward normally low levels after 20 days of hypoxia. Lung NO production, measured as NO concentration in exhaled air, was markedly elevated as early as on the first day of hypoxia. We conclude that transient iNOS induction in the pulmonary vascular wall at the beginning of chronic hypoxia participates in the pathogenesis of pulmonary hypertension.

Treatment with lisinopril slows the early progression of proteinuria in obese Dahl salt‐sensitive rats independent of lowering arterial pressure and GFR

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Alyssa P. Pennington ◽  
Bibek P. Poudel ◽  
Corbin A. Shields ◽  
Willie Thompson ◽  
Jan M. Williams
Keyword(s):  
Arterial Pressure ◽  
Early Progression
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