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Dr. Jonathan  Blau  Md image

Dr. Jonathan Blau Md

1814 Roseland Blvd Suite 200
Tyler TX 75701
903 936-6500
Medical School: Medical College Of Wisconsin - 1989
Accepts Medicare: Yes
Participates In eRX: Yes
Participates In PQRS: Yes
Participates In EHR: Yes
License #: J7721
NPI: 1942260567
Taxonomy Codes:
2081P2900X

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Awards & Recognitions

About Us

Practice Philosophy

Conditions

Dr. Jonathan Blau is associated with these group practices

Procedure Pricing

HCPCS Code Description Average Price Average Price
Allowed By Medicare
HCPCS Code:64635 Description:Destroy lumb/sac facet jnt Average Price:$1,158.67 Average Price Allowed
By Medicare:
$232.44
HCPCS Code:64493 Description:Inj paravert f jnt l/s 1 lev Average Price:$1,031.25 Average Price Allowed
By Medicare:
$121.71
HCPCS Code:64490 Description:Inj paravert f jnt c/t 1 lev Average Price:$1,035.76 Average Price Allowed
By Medicare:
$132.22
HCPCS Code:64633 Description:Destroy cerv/thor facet jnt Average Price:$1,100.00 Average Price Allowed
By Medicare:
$251.14
HCPCS Code:64483 Description:Inj foramen epidural l/s Average Price:$947.65 Average Price Allowed
By Medicare:
$112.94
HCPCS Code:62290 Description:Inject for spine disk x-ray Average Price:$900.00 Average Price Allowed
By Medicare:
$108.97
HCPCS Code:27096 Description:Inject sacroiliac joint Average Price:$720.25 Average Price Allowed
By Medicare:
$99.58
HCPCS Code:62311 Description:Inject spine l/s (cd) Average Price:$650.00 Average Price Allowed
By Medicare:
$84.28
HCPCS Code:64640 Description:Injection treatment of nerve Average Price:$635.73 Average Price Allowed
By Medicare:
$83.09
HCPCS Code:62310 Description:Inject spine c/t Average Price:$650.00 Average Price Allowed
By Medicare:
$102.94
HCPCS Code:20610 Description:Drain/inject joint/bursa Average Price:$579.14 Average Price Allowed
By Medicare:
$56.24
HCPCS Code:20610 Description:Drain/inject joint/bursa Average Price:$559.17 Average Price Allowed
By Medicare:
$37.03
HCPCS Code:64636 Description:Destroy l/s facet jnt addl Average Price:$558.81 Average Price Allowed
By Medicare:
$62.84
HCPCS Code:95886 Description:Musc test done w/n test comp Average Price:$540.00 Average Price Allowed
By Medicare:
$82.39
HCPCS Code:64634 Description:Destroy c/th facet jnt addl Average Price:$530.10 Average Price Allowed
By Medicare:
$73.43
HCPCS Code:76942 Description:Echo guide for biopsy Average Price:$565.00 Average Price Allowed
By Medicare:
$190.26
HCPCS Code:64491 Description:Inj paravert f jnt c/t 2 lev Average Price:$430.53 Average Price Allowed
By Medicare:
$74.36
HCPCS Code:64492 Description:Inj paravert f jnt c/t 3 lev Average Price:$429.74 Average Price Allowed
By Medicare:
$75.00
HCPCS Code:64494 Description:Inj paravert f jnt l/s 2 lev Average Price:$412.83 Average Price Allowed
By Medicare:
$69.52
HCPCS Code:64495 Description:Inj paravert f jnt l/s 3 lev Average Price:$409.88 Average Price Allowed
By Medicare:
$70.30
HCPCS Code:27093 Description:Injection for hip x-ray Average Price:$362.18 Average Price Allowed
By Medicare:
$55.11
HCPCS Code:73525 Description:Contrast x-ray of hip Average Price:$196.00 Average Price Allowed
By Medicare:
$27.24
HCPCS Code:99144 Description:Mod cs by same phys 5 yrs + Average Price:$200.00 Average Price Allowed
By Medicare:
$33.73
HCPCS Code:99205 Description:Office/outpatient visit new Average Price:$320.00 Average Price Allowed
By Medicare:
$190.46
HCPCS Code:99203 Description:Office/outpatient visit new Average Price:$228.00 Average Price Allowed
By Medicare:
$99.68
HCPCS Code:99204 Description:Office/outpatient visit new Average Price:$280.00 Average Price Allowed
By Medicare:
$152.99
HCPCS Code:95903 Description:Motor nerve conduction test Average Price:$195.00 Average Price Allowed
By Medicare:
$70.26
HCPCS Code:72100 Description:X-ray exam of lower spine Average Price:$125.00 Average Price Allowed
By Medicare:
$11.11
HCPCS Code:95904 Description:Sense nerve conduction test Average Price:$142.00 Average Price Allowed
By Medicare:
$52.79
HCPCS Code:77002 Description:Needle localization by xray Average Price:$100.00 Average Price Allowed
By Medicare:
$26.35
HCPCS Code:72070 Description:X-ray exam of thoracic spine Average Price:$73.00 Average Price Allowed
By Medicare:
$10.56
HCPCS Code:95934 Description:H-reflex test Average Price:$115.00 Average Price Allowed
By Medicare:
$57.64
HCPCS Code:77003 Description:Fluoroguide for spine inject Average Price:$85.00 Average Price Allowed
By Medicare:
$29.01
HCPCS Code:72040 Description:X-ray exam of neck spine Average Price:$66.00 Average Price Allowed
By Medicare:
$11.11
HCPCS Code:99215 Description:Office/outpatient visit est Average Price:$165.00 Average Price Allowed
By Medicare:
$133.41
HCPCS Code:99214 Description:Office/outpatient visit est Average Price:$125.00 Average Price Allowed
By Medicare:
$99.13
HCPCS Code:99212 Description:Office/outpatient visit est Average Price:$55.00 Average Price Allowed
By Medicare:
$40.10
HCPCS Code:G0434 Description:Drug screen multi drug class Average Price:$30.00 Average Price Allowed
By Medicare:
$15.74
HCPCS Code:J1030 Description:Methylprednisolone 40 MG inj Average Price:$15.00 Average Price Allowed
By Medicare:
$3.56
HCPCS Code:99213 Description:Office/outpatient visit est Average Price:$78.00 Average Price Allowed
By Medicare:
$66.92
HCPCS Code:J1885 Description:Ketorolac tromethamine inj Average Price:$10.00 Average Price Allowed
By Medicare:
$0.24
HCPCS Code:J7325 Description:Synvisc or Synvisc-One Average Price:$12.93 Average Price Allowed
By Medicare:
$12.16

HCPCS Code Definitions

62311
Injection(s), of diagnostic or therapeutic substance(s) (including anesthetic, antispasmodic, opioid, steroid, other solution), not including neurolytic substances, including needle or catheter placement, includes contrast for localization when performed, epidural or subarachnoid; lumbar or sacral (caudal)
99204
Office or other outpatient visit for the evaluation and management of a new patient, which requires these 3 key components: A comprehensive history; A comprehensive examination; Medical decision making of moderate complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of moderate to high severity. Typically, 45 minutes are spent face-to-face with the patient and/or family.
20610
Arthrocentesis, aspiration and/or injection; major joint or bursa (eg, shoulder, hip, knee joint, subacromial bursa)
62310
Injection(s), of diagnostic or therapeutic substance(s) (including anesthetic, antispasmodic, opioid, steroid, other solution), not including neurolytic substances, including needle or catheter placement, includes contrast for localization when performed, epidural or subarachnoid; cervical or thoracic
20610
Arthrocentesis, aspiration and/or injection; major joint or bursa (eg, shoulder, hip, knee joint, subacromial bursa)
27096
Injection procedure for sacroiliac joint, anesthetic/steroid, with image guidance (fluoroscopy or CT) including arthrography when performed
62290
Injection procedure for discography, each level; lumbar
99215
Office or other outpatient visit for the evaluation and management of an established patient, which requires at least 2 of these 3 key components: A comprehensive history; A comprehensive examination; Medical decision making of high complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of moderate to high severity. Typically, 40 minutes are spent face-to-face with the patient and/or family.
27093
Injection procedure for hip arthrography; without anesthesia
99203
Office or other outpatient visit for the evaluation and management of a new patient, which requires these 3 key components: A detailed history; A detailed examination; Medical decision making of low complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of moderate severity. Typically, 30 minutes are spent face-to-face with the patient and/or family.
64483
Injection(s), anesthetic agent and/or steroid, transforaminal epidural, with imaging guidance (fluoroscopy or CT); lumbar or sacral, single level
64634
Destruction by neurolytic agent, paravertebral facet joint nerve(s), with imaging guidance (fluoroscopy or CT); cervical or thoracic, each additional facet joint (List separately in addition to code for primary procedure)
64490
Injection(s), diagnostic or therapeutic agent, paravertebral facet (zygapophyseal) joint (or nerves innervating that joint) with image guidance (fluoroscopy or CT), cervical or thoracic; single level
64493
Injection(s), diagnostic or therapeutic agent, paravertebral facet (zygapophyseal) joint (or nerves innervating that joint) with image guidance (fluoroscopy or CT), lumbar or sacral; single level
64491
Injection(s), diagnostic or therapeutic agent, paravertebral facet (zygapophyseal) joint (or nerves innervating that joint) with image guidance (fluoroscopy or CT), cervical or thoracic; second level (List separately in addition to code for primary procedure)
64492
Injection(s), diagnostic or therapeutic agent, paravertebral facet (zygapophyseal) joint (or nerves innervating that joint) with image guidance (fluoroscopy or CT), cervical or thoracic; third and any additional level(s) (List separately in addition to code for primary procedure)
64633
Destruction by neurolytic agent, paravertebral facet joint nerve(s), with imaging guidance (fluoroscopy or CT); cervical or thoracic, single facet joint
64495
Injection(s), diagnostic or therapeutic agent, paravertebral facet (zygapophyseal) joint (or nerves innervating that joint) with image guidance (fluoroscopy or CT), lumbar or sacral; third and any additional level(s) (List separately in addition to code for primary procedure)
64494
Injection(s), diagnostic or therapeutic agent, paravertebral facet (zygapophyseal) joint (or nerves innervating that joint) with image guidance (fluoroscopy or CT), lumbar or sacral; second level (List separately in addition to code for primary procedure)
64636
Destruction by neurolytic agent, paravertebral facet joint nerve(s), with imaging guidance (fluoroscopy or CT); lumbar or sacral, each additional facet joint (List separately in addition to code for primary procedure)
77003
Fluoroscopic guidance and localization of needle or catheter tip for spine or paraspinous diagnostic or therapeutic injection procedures (epidural or subarachnoid)
64640
Destruction by neurolytic agent; other peripheral nerve or branch
76942
Ultrasonic guidance for needle placement (eg, biopsy, aspiration, injection, localization device), imaging supervision and interpretation
77002
Fluoroscopic guidance for needle placement (eg, biopsy, aspiration, injection, localization device)
73525
Radiologic examination, hip, arthrography, radiological supervision and interpretation
72100
Radiologic examination, spine, lumbosacral; 2 or 3 views
72070
Radiologic examination, spine; thoracic, 2 views
95886
Needle electromyography, each extremity, with related paraspinal areas, when performed, done with nerve conduction, amplitude and latency/velocity study; complete, five or more muscles studied, innervated by three or more nerves or four or more spinal levels (List separately in addition to code for primary procedure)
64635
Destruction by neurolytic agent, paravertebral facet joint nerve(s), with imaging guidance (fluoroscopy or CT); lumbar or sacral, single facet joint
G0434
Drug screen, other than chromatographic; any number of drug classes, by clia waived test or moderate complexity test, per patient encounter
99214
Office or other outpatient visit for the evaluation and management of an established patient, which requires at least 2 of these 3 key components: A detailed history; A detailed examination; Medical decision making of moderate complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of moderate to high severity. Typically, 25 minutes are spent face-to-face with the patient and/or family.
99213
Office or other outpatient visit for the evaluation and management of an established patient, which requires at least 2 of these 3 key components: An expanded problem focused history; An expanded problem focused examination; Medical decision making of low complexity. Counseling and coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of low to moderate severity. Typically, 15 minutes are spent face-to-face with the patient and/or family.
99205
Office or other outpatient visit for the evaluation and management of a new patient, which requires these 3 key components: A comprehensive history; A comprehensive examination; Medical decision making of high complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of moderate to high severity. Typically, 60 minutes are spent face-to-face with the patient and/or family.
72040
Radiologic examination, spine, cervical; 2 or 3 views
99212
Office or other outpatient visit for the evaluation and management of an established patient, which requires at least 2 of these 3 key components: A problem focused history; A problem focused examination; Straightforward medical decision making. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are self limited or minor. Typically, 10 minutes are spent face-to-face with the patient and/or family.
J7325
Hyaluronan or derivative, synvisc or synvisc-one, for intra-articular injection, 1 mg
J1885
Injection, ketorolac tromethamine, per 15 mg
J1030
Injection, methylprednisolone acetate, 40 mg

Medical Malpractice Cases

None Found

Medical Board Sanctions

None Found

Referrals

NPI
Doctor Name
Specialty
Count
1164535142
Neurosurgery
4,688
1740287838
Internal Medicine
2,234
1396707121
Interventional Pain Management
1,632
1316903982
Diagnostic Radiology
903
1902896863
Family Practice
835
1750341269
Diagnostic Radiology
788
1740280510
Internal Medicine
711
1083669246
Diagnostic Radiology
685
1245291202
Diagnostic Radiology
628
1780658112
Urology
486
*These referrals represent the top 10 that Dr. Blau has made to other doctors

Publications

A 0.7 Mb de novo duplication at 7q21.3 including the genes DLX5 and DLX6 in a patient with split-hand/split-foot malformation. - American journal of medical genetics. Part A
Split-hand/split-foot malformation (SHFM1) has been reported to be caused by deletions, duplications or rearrangements involving the 7q21.3 region harboring DSS1, DLX5, and DLX6. We report on a female patient with unilateral syndactyly of the third and fourth fingers of the right hand and overgrowth and lateral deviation of the right great toe. There was a split foot malformation on the right, with absent fifth toe. The left hand was apparently normal and left foot was intact. The patient has no hearing loss. We performed conventional G-banding karyotype analysis, array comparative genomic hybridization (aCGH) and fluorescence in situ hybridization (FISH). G-banding karyotype result was normal 46,XX. However, a duplication of 719 kb (96,303,736-97,022,335; NCBI build36/hg18, March 2006) was identified at the 7q21.3 region by aCGH. The array result was also confirmed by FISH analysis. The duplicated region harbors only DLX5 and DLX6, which are known for their role in SHFM1. Additionally, FISH analysis of parental samples showed de novo origin of this abnormality in the patient. This is the first report that highlights the duplication of 719 kb at 7q21.3, harboring only DLX5 and DLX6 associated with the SHFM1 phenotype.Copyright © 2012 Wiley Periodicals, Inc.
Transfusion-related acute gut injury: feeding, flora, flow, and barrier defense. - Seminars in perinatology
TRAGI (transfusion-related acute gut injury) is an acronym we proposed to characterize a severe neonatal gastrointestinal reaction temporally related to a transfusion of packed blood red cells (PRBCs) for anemia in very low birth weights. The following are in support of a causative relationship: (1) the timing of necrotizing enterocolitis after a PRBC transfusion not being random, (2) traditional risk factors for necrotizing enterocolitis are often absent, (3) significant anemia appears to be a universal finding, (4) the age of donor blood is often slightly older than controls, (5) TRAGI is not postnatal age dependent, and (6) TRAGI does not show a centering at 31 weeks' postconceptual age as does nontransfusion-related NEC. Although TRAGI is linked to the timing of PRBC transfusions, we propose a novel hypothesis that the convergence at 31 weeks' postconceptual age for classic NEC approximates the age of presentation of other oxygen delivery and neovascularization syndromes (eg, retinopathy of prematurity), suggesting its etiologic link to a generalized systemic maturational mechanism or another common developmental theme. This report will begin by reviewing the history of the clinical presentation and discovery of TRAGI and will then analyze various pathophysiologic mechanisms that may account for the phenomenon when clinicians render therapies. We will end by a call to action for randomized clinical trials to test various etiologic theories.Copyright © 2012 Elsevier Inc. All rights reserved.
Transfusion-related acute gut injury: necrotizing enterocolitis in very low birth weight neonates after packed red blood cell transfusion. - The Journal of pediatrics
This is a repeat cohort study in which we sought to determine whether an association of necrotizing enterocolitis (NEC) <48 hours of a packed red blood cells (PRBC) transfusion was a prior sampling artifact.All very low birth weight neonates with NEC Stage ≥ IIB admitted over an 18-month period were categorized for NEC: (1) <48 hours after a PRBC transfusion; (2) unrelated to the timing of PRBCs; and (3) never transfused.Eight hundred eighty-three admissions over 18 months were reviewed; 256 were very low birth weight that resulted in 36 NEC cases and 25% were associated with PRBC (n = 9). PRBC-associated cases had lower birth weight, hematocrit, and rapid onset of signs (<5 hours). The timing of association of PRBC transfusion and NEC differed from random, showing a distribution that was not uniform over time (χ(2) = 170.7, df = 40; P < .000001) consistent with the possibility of a causative relationship in certain cases of NEC. Current weight at onset of NEC did not differ; however, the more immature the neonate the later the onset of NEC creating a curious centering of occurrence at a median of 31 weeks postconceptual age.We conclude that PRBC-related NEC exists. Transfusion-related acute gut injury is an acronym we propose to characterize a severe neonatal gastrointestinal reaction proximal to a transfusion of PRBCs for anemia. The convergence at 31 weeks postconceptual age approximates the age of presentation of other O(2) delivery and neovascularization syndromes, suggesting a link to a generalized systemic maturational mechanism.Copyright © 2011 Mosby, Inc. All rights reserved.
Effects of protein/nonprotein caloric intake on parenteral nutrition associated cholestasis in premature infants weighing 600-1000 grams. - JPEN. Journal of parenteral and enteral nutrition
Parenteral nutrition-associated cholestasis (PNAC) has historically been a significant cause of morbidity and mortality in neonates undergoing parenteral feeding. Studies examining the causes of cholestasis in the PN-dependent neonate have produced a wide range of data, with some conflicting results. Increased protein/nonprotein calorie ratios, increased glucose concentrations, and increased lipid concentrations have all been implicated as possible causes of PNAC. However, these studies were done in the pre-TrophAmine (neonatal-specific amino acid parenteral nutrition [PN] formulation) era. With the introduction of TrophAmine, infants are now receiving higher concentrations of protein, often being advanced rapidly even when nonprotein calories may not be sufficiently advanced to meet the infants' caloric needs. To the best of our knowledge, no studies have been conducted to evaluate the protein/nonprotein calorie ratio as a cause of PNAC in the TrophAmine era.A retrospective chart review of 25 cholestatic and 25 noncholestatic PN-dependent premature neonates was conducted. All neonates weighed between 600 and 1000 g. Cholestasis was defined as a serum total bilirubin (TB) >or=2.0 mg/dL, with a serum direct bilirubin (DB) >or=20% of the TB. Neonates with major congenital anomalies or who underwent major surgery were excluded. PN macronutrient compositions were analyzed to examine if the different amounts of protein concentrations and protein/nonprotein calorie ratios played a role in the development of PNAC. Statistical analysis was performed using Student's t-tests. p Values < .05 were considered statistically significant.All measured nutrition parameters did not differ significantly between the cholestatic and noncholestatic groups. Protein intake, the protein/nonprotein calorie ratio, and renal function as evaluated by blood urea nitrogen (BUN) and creatinine did not differ between the 2 study groups. The only parameters that differed significantly between the groups were the duration of PN therapy and length of hospital stay.Protein to nonprotein calorie ratio was not an etiology in the development of cholestasis in infants (600-1000 g) receiving PN. Renal function elicited not to have an impact on cholestasis status of these infants. Therefore, providing adequate protein calories should not be limited in this patient population, as suggested by previous studies in the pre-TrophAmine era. We found that increased duration of PN therapy and increased length of hospital stay were associated with PNAC.
Acute antihypertensive action of nitroxides in the spontaneously hypertensive rat. - American journal of physiology. Regulatory, integrative and comparative physiology
Tempol is an amphipathic radical nitroxide (N) that acutely reduces blood pressure (BP) and heart rate (HR) in the spontaneously hypertensive rat (SHR). We investigated the hypothesis that the response to nitroxides is determined by SOD mimetic activity or lipophilicity. Groups (n = 6-10) of anesthetized SHRs received graded intravenous doses of Ns: tempol (T), 4-amino-tempo (AT), 4-oxo-tempo (OT), 4-trimethylammonium-2,2,6,6-tetramethylpiperidine-1-oxyl iodide (CAT-1), 3-carbamoyl-proxyl (3-CP), or 3-carboxy-proxyl (3-CTPY). Others received native or liposomal (L) Cu/Zn SOD. T and OT are uncharged, AT is positively charged and cell-permeable, and CAT-1 is positively charged and cell-impermeable. 3-CP and 3-CTPY have five-member pyrrolidine rings, whereas T, AT, OT, and CAT-1 have six-member piperidine rings. T and AT reduced mean arterial pressure (MAP) similarly (-48 +/- 2 mmHg and -55 +/- 8 mmHg) but more (P < 0.05) than OT and CAT-1. 3-CP and 3-CTPY were ineffective. The group mean change in MAP with piperidine Ns correlated with SOD activity (r = -0.94), whereas their ED(50) correlated with lipophilicity (r = 0.89). SOD and L-SOD did not lower BP acutely but reduced it after 90 min (-32 +/- 5 and -31 +/- 6 mmHg; P < 0.05 vs. vehicle). Pyrrolidine nitroxides are ineffective antihypertensive agents. The antihypertensive response to piperidine Ns is predicted by SOD mimetic action, and the sensitivity of response is by hydrophilicity. SOD exerts a delayed hypotensive action that is not enhanced by liposome encapsulation, suggesting it must diffuse to an extravascular site.
Antihypertensive response to prolonged tempol in the spontaneously hypertensive rat. - Kidney international
Tempol is a permeant nitroxide superoxide dismutase (SOD) mimetic that lowers mean arterial pressure (MAP) in spontaneously hypertensive rats (SHRs). We investigated the hypothesis that the antihypertensive response entails a negative salt balance, blunting of plasma renin activity (PRA), endothelin-1 (ET-1), or catecholamines or correction of oxidative stress as indexed by 8-isoprostane prostaglandin F(2alpha) (PGF(2alpha)) (8-Iso).Groups (N= 6 to 8) of SHRs were infused for 2 weeks with vehicle or tempol (200 nmol/kg/min) or given tempol (2 mmol/L) in drinking water.Tempol infusion reduced the MAP of anesthetized SHRs (150 +/- 5 vs. 126 +/- 6 mm Hg) (P < 0.005). Oral tempol did not change the heart rate but reduced the MAP of conscious SHRs (-23 +/- 6 mm Hg) (P < 0.01) but not Wistar-Kyoto (WKY) rats. Tempol infusion increased the PRA (2.2 +/- 0.2 vs. 5.0 +/- 0.9 ng/mL/hour) (P < 0.005), did not change excretion of nitric oxide (NO) [NO(2)+ NO(3) (NOx)], ET-1, or catecholamines but reduced excretion of 8-Iso (13.2 +/- 1.4 vs. 9.6 +/- 0.9 ng/24 hours; P < 0.01). Cumulative Na(+) balance and gain in body weight were unaltered by tempol infusion. Tempol prevented a rise in MAP with high salt intake.Tempol corrects hypertension without a compensatory sympathoadrenal activation or salt retention. The response is independent of nitric oxide, endothelin, or catecholamines and occurs despite increased PRA. It is accompanied by a reduction in oxidative stress and is maintained during increased salt intake.
Angiotensin-induced defects in renal oxygenation: role of oxidative stress. - American journal of physiology. Heart and circulatory physiology
We tested the hypothesis that superoxide anion (O(2)(-).) generated in the kidney by prolonged angiotensin II (ANG II) reduces renal cortical Po(2) and the use of O(2) for tubular sodium transport (T(Na):Q(O(2))). Groups (n = 8-11) of rats received angiotensin II (ANG II, 200 ng.kg(-1).min(-1) sc) or vehicle for 2 wk with concurrent infusions of a permeant nitroxide SOD mimetic 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (Tempol, 200 nmol.kg(-1).min(-1)) or vehicle. Rats were studied under anesthesia with measurements of renal oxygen usage and Po(2) in the cortex and tubules with a glass electrode. Compared with vehicle, ANG II increased mean arterial pressure (107 +/- 4 vs. 146 +/- 6 mmHg; P < 0.001), renal vascular resistance (42 +/- 3 vs. 65 +/- 7 mmHg.ml(-1).min(-1).100 g(-1); P < 0.001), renal cortical NADPH oxidase activity (2.3 +/- 0.2 vs. 3.6 +/- 0.4 nmol O(2)(-)..min(-1).mg(-1) protein; P < 0.05), mRNA and protein expression for p22(phox) (2.1- and 1.8-fold respectively; P < 0.05) and reduced the mRNA for extracellular (EC)-SOD (-1.8 fold; P < 0.05). ANG II reduced the Po(2) in the proximal tubule (39 +/- 1 vs. 34 +/- 2 mmHg; P < 0.05) and throughout the cortex and reduced the T(Na):Q(O(2)) (17 +/- 1 vs. 9 +/- 2 mumol/mumol; P < 0.001). Tempol blunted or prevented all these effects of ANG II. The effects of prolonged ANG II to cause hypertension, renal vasoconstriction, renal cortical hypoxia, and reduced efficiency of O(2) usage for Na(+) transport, activation of NADPH oxidase, increased expression of p22(phox), and reduced expression of EC-SOD can be ascribed to O(2)(-). generation because they are prevented by an SOD mimetic.
Salt intake, oxidative stress, and renal expression of NADPH oxidase and superoxide dismutase. - Journal of the American Society of Nephrology : JASN
The hypothesis that a high salt (HS) intake increases oxidative stress was investigated and was related to renal cortical expression of NAD(P)H oxidase and superoxide dismutase (SOD). 8-Isoprostane PGF(2alpha) and malonyldialdehyde were measured in groups (n = 6 to 8) of conscious rats during low-salt, normal-salt, or HS diets. NADPH- and NADH-stimulated superoxide anion (O(2)(.-)) generation was assessed by chemiluminescence, and expression of NAD(P)H oxidase and SOD were assessed with real-time PCR. Excretion of 8-isoprostane and malonyldialdehyde increased incrementally two- to threefold with salt intake (P < 0.001), whereas prostaglandin E(2) was unchanged. Renal cortical NADH- and NADPH-stimulable O(2)(.-) generation increased (P < 0.05) 30 to 40% with salt intake. Compared with low-salt diet, HS significantly (P < 0.005) increased renal cortical mRNA expression of gp91(phox) and p47(phox) and decreased expression of intracellular CuZn (IC)-SOD and mitochondrial (Mn)-SOD. Despite suppression of the renin-angiotensin system, salt loading enhances oxidative stress. This is accompanied by increased renal cortical NADH and NADPH oxidase activity and increased expression of gp91(phox) and p47(phox) and decreased IC- and Mn-SOD. Thus, salt intake enhances generation of O(2)(.-) accompanied by enhanced renal expression and activity of NAD(P)H oxidase with diminished renal expression of IC- and Mn-SOD.
Effects of ANG II type 1 and 2 receptors on oxidative stress, renal NADPH oxidase, and SOD expression. - American journal of physiology. Regulatory, integrative and comparative physiology
Oxidative stress accompanies angiotensin (ANG) II infusion, but the role of ANG type 1 vs. type 2 receptors (AT1-R and AT2-R, respectively) is unknown. We infused ANG II subcutaneously in rats for 1 wk. Excretion of 8-isoprostaglandin F2alpha (8-Iso) and malonyldialdehyde (MDA) were related to renal cortical mRNA abundance for subunits of NADPH oxidase and superoxide dismutases (SODs) using real-time PCR. Subsets of ANG II-infused rats were given the AT1-R antagonist candesartan cilexetil (Cand) or the AT2-R antagonist PD-123,319 (PD). Compared to vehicle (Veh), ANG II increased 8-Iso excretion by 41% (Veh, 5.4 +/- 0.8 vs. ANG II, 7.6 +/- 0.5 pg/24 h; P < 0.05). This was prevented by Cand (5.6 +/- 0.5 pg/24 h; P < 0.05) and increased by PD (15.8 +/- 2.0 pg/24 h; P < 0.005). There were similar changes in MDA excretion. Compared to Veh, ANG II significantly (P < 0.005) increased the renal cortical mRNA expression of p22phox (twofold), Nox-1 (2.6-fold), and Mn-SOD (1.5-fold) and decreased expression of Nox-4 (2.1-fold) and extracellular (EC)-SOD (2.1-fold). Cand prevented all of these changes except for the increase in Mn-SOD. PD accentuated changes in p22phox and Nox-1 and increased p67phox. We conclude that ANG II infusion stimulates oxidative stress via AT1-R, which increases the renal cortical mRNA expression of p22phox and Nox-1 and reduces abundance of Nox-4 and EC-SOD. This is offset by strong protective effects of AT2-R, which are accompanied by decreased expression of p22phox, Nox-1, and p67phox.

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