Abstract 1: Male Sprague Dawley Rats Exposed To Perinatal Hypoxia Are More Susceptible To Angiotensin II-induced Hypertension In Adulthood Vs Females

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Lindsey A Ramirez ◽  
Terri Marin ◽  
Elizabeth Snyder ◽  
Michael W Brands ◽  
Jennifer C Sullivan
Keyword(s):  
Preterm Infants ◽  
Later Life ◽  
Pressure Effects ◽  
Light Cycle ◽  
Perinatal Hypoxia ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Dark Cycle ◽  
Induced Hypertension ◽  
Blood Pressure Effects

Preterm infants (born prior to 37 weeks (wks) gestation) are susceptible to hypoxia, which predisposes to hypertension in later life. Underdeveloped organs, including the kidney, prevent preterm infants from effectively regulating blood volume and O 2 delivery. Since rat nephrogenesis completes ~ postnatal day (PND) 8, we hypothesized that exposure to hypoxia before nephrogenesis is complete will promote hypertension in adulthood. Male and female Sprague Dawley pups were randomized to Ctrl (room air) or intermittent hypoxia (IH) at PND 1 (n=6/group). IH pups were exposed to ~10% O 2 three times a day, 10 minutes/session, from PND 1-8. O 2 saturation was measured at PND 6. Mean arterial pressure (MAP) was measured via telemetry from ~14 – 16 wks of age. To determine the MAP response to a cardiovascular challenge, osmotic minipumps containing angiotensin (Ang) II (400 ng/kg/min) were implanted at 15 wks of age. IH pups had lower O 2 saturation vs ctrl (P O2 <0.05). Light cycle (LC) and dark cycle (DC) MAP were similar in all groups at baseline. Following treatment, LC-MAP was higher in IH-M vs Ctrl-M, but similar among female groups (P Int . = 0.04). IH animals had higher DC-MAP vs ctrl (P O2 = 0.02). IH decreased blood oxygen, suggesting a global decrease in oxygen delivery to organs, similar to what is seen with hypoxia. Perinatal IH alone did not increase MAP. However, this exposure did increase MAP in response to Ang II. While both males and females exposed to perinatal hypoxia had higher Ang II-induced hypertension vs ctrls in the dark cycle, this effect was preserved only in males in the light cycle. This suggests males are more susceptible to blood pressure effects of perinatal IH.

scholarly journals Asymmetric dimethylarginine in angiotensin II-induced hypertension

2010 ◽  
Vol 298 (3) ◽  
pp. R740-R746 ◽  
Author(s):  
Jennifer M. Sasser ◽  
Natasha C. Moningka ◽  
Mark W. Cunningham ◽  
Byron Croker ◽  
Chris Baylis
Keyword(s):  
Nitric Oxide ◽  
Renal Injury ◽  
Asymmetric Dimethylarginine ◽  
Renal Cortex ◽  
Interstitial Fibrosis ◽  
Glomerular Sclerosis ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Plasma Adma ◽  
Induced Hypertension

Recent studies have shown that asymmetric dimethylarginine (ADMA), a nitric oxide synthase inhibitor, is increased in hypertension and chronic kidney disease. However, little is known about the effects of hypertension per se on ADMA metabolism. The purpose of this study was to test the hypothesis that ANG II-induced hypertension, in the absence of renal injury, is associated with increased oxidative stress and plasma and renal cortex ADMA levels in rats. Male Sprague-Dawley rats were treated with ANG II at 200 ng·kg−1·min−1 sc (by minipump) for 1 or 3 wk or at 400 ng·kg−1·min−1 for 6 wk. Mean arterial pressure was increased after 3 and 6 wk of ANG II; however, renal injury (proteinuria, glomerular sclerosis, and interstitial fibrosis) was only evident after 6 wk of treatment. Plasma thiobarbituric acid reactive substances concentration and renal cortex p22phox protein abundance were increased early (1 and 3 wk), but urinary excretion of isoprostane and H2O2 was only increased after 6 wk of ANG II. An increased in plasma ADMA after 6 wk of ANG II was associated with increased lung protein arginine methyltransferase-1 abundance and decreased renal cortex dimethylarginine dimethylaminohydrolase activity. No changes in renal cortex ADMA were observed. ANG II hypertension in the absence of renal injury is not associated with increased ADMA; however, when the severity and duration of the treatment were increased, plasma ADMA increased. These data suggest that elevated blood pressure alone, for up to 3 wk, in the absence of renal injury does not play an important role in the regulation of ADMA. However, the presence of renal injury and sustained hypertension for 6 wk increases ADMA levels and contributes to nitric oxide deficiency and cardiovascular disease.

scholarly journals Angiotensin II-mediated hypertension impairs nitric oxide-induced NKCC2 inhibition in thick ascending limbs

2016 ◽  
Vol 310 (8) ◽  
pp. F748-F754 ◽  
Author(s):  
Vanesa D. Ramseyer ◽  
Pablo A. Ortiz ◽  
Oscar A. Carretero ◽  
Jeffrey L. Garvin
Keyword(s):  
Nitric Oxide ◽  
Pde5 Inhibitor ◽  
Cell Types ◽  
No Production ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
No Donor ◽  
Induced Hypertension ◽  
Stimulation Of

In thick ascending limbs (THALs), nitric oxide (NO) decreases NaCl reabsorption via cGMP-mediated inhibition of Na-K-2Cl cotransporter (NKCC2). In angiotensin (ANG II)-induced hypertension, endothelin-1 (ET-1)-induced NO production by THALs is impaired. However, whether this alters NO's natriuretic effects and the mechanisms involved are unknown. In other cell types, ANG II augments phosphodiesterase 5 (PDE5)-mediated cGMP degradation. We hypothesized that NO-mediated inhibition of NKCC2 activity and stimulation of cGMP synthesis are blunted via PDE5 in ANG II-induced hypertension. Sprague-Dawley rats were infused with vehicle or ANG II (200 ng·kg−1·min−1) for 5 days. ET-1 reduced NKCC2 activity by 38 ± 13% ( P < 0.05) in THALs from vehicle-treated rats but not from ANG II-hypertensive rats (Δ: −9 ± 13%). A NO donor yielded similar results as ET-1. In contrast, dibutyryl-cGMP significantly decreased NKCC2 activity in both vehicle-treated and ANG II-hypertensive rats (control: Δ−44 ± 15% vs. ANG II: Δ−41 ± 10%). NO increased cGMP by 2.08 ± 0.36 fmol/μg protein in THALs from vehicle-treated rats but only 1.06 ± 0.25 fmol/μg protein in ANG II-hypertensive rats ( P < 0.04). Vardenafil (25 nM), a PDE5 inhibitor, restored NO's ability to inhibit NKCC2 activity in THALs from ANG II-hypertensive rats (Δ: −60 ± 9%, P < 0.003). Similarly, NO's stimulation of cGMP was also restored by vardenafil (vehicle-treated: 1.89 ± 0.71 vs. ANG II-hypertensive: 2.02 ± 0.32 fmol/μg protein). PDE5 expression did not differ between vehicle-treated and ANG II-hypertensive rats. We conclude that NO-induced inhibition of NKCC2 and increases in cGMP are blunted in ANG II-hypertensive rats due to PDE5 activation. Defects in the response of THALs to NO may enhance NaCl retention in ANG II-induced hypertension.

scholarly journals Serelaxin reduces oxidative stress and asymmetric dimethylarginine in angiotensin II-induced hypertension

2014 ◽  
Vol 307 (12) ◽  
pp. F1355-F1362 ◽  
Author(s):  
Jennifer M. Sasser ◽  
Mark W. Cunningham ◽  
Chris Baylis
Keyword(s):  
Oxidative Stress ◽  
Asymmetric Dimethylarginine ◽  
Oxidation Products ◽  
No Oxidation ◽  
Kidney Cortex ◽  
High Dose ◽  
Protective Effects ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Induced Hypertension

Recent findings suggest the therapeutic action of relaxin during hypertension is dependent on nitric oxide synthase (NOS) activation; however, the mechanisms underlying the beneficial effects of relaxin on the NOS system have not been fully elucidated. We hypothesized that the protective effects of relaxin include reducing both oxidative stress and the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA). We examined the effect of Serelaxin [human recombinant relaxin-2 (RLX)] in male Sprague-Dawley rats given high-dose angiotensin (ANG) II (400 ng·kg−1·min−1 sc) for 6 wk or shams. RLX was administered (4 μg/h sc) to half of the rats in each group after 2 wk of ANG II for the remaining 4 wk. ANG II induced hypertension and proteinuria, reduced NO oxidation products (NOx), and increased oxidative stress (NADPH oxidase activity, thiobarbituric acid-reactive substances, and 8-isoprostane excretion) and plasma ADMA. While RLX had no effect on sham rats, RLX attenuated the ANG II-dependent hypertension (165 ± 5 vs. 135 ± 13 mmHg, P < 0.05) and proteinuria at 6 wk (62 ± 6 vs. 41 ± 4 mg·day−1·100 g−1, P < 0.05) and normalized oxidative stress and circulating ADMA, in association with restored NOx excretion and kidney cortex NOx. We found that RLX had no impact on the ADMA-regulatory enzymes protein arginine methyltransferase and dimethylarginine-dimethylaminohydrolase (DDAH). Furthermore, RLX treatment did not increase DDAH activity in kidney cortex or liver. These data suggest that benefits of RLX treatment include reduced ADMA levels and increased NO bioavailability, possibly due to its antioxidant effects.

ACE2 and ANG-(1-7) in the rat uterus during early and late gestation

2008 ◽  
Vol 294 (1) ◽  
pp. R151-R161 ◽  
Author(s):  
Liomar A. A. Neves ◽  
Kathryn Stovall ◽  
JaNae Joyner ◽  
Gloria Valdés ◽  
Patricia E. Gallagher ◽  
...  
Keyword(s):  
Early Pregnancy ◽  
Perfusion Pressure ◽  
Late Pregnancy ◽  
Late Gestation ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Induced Hypertension ◽  
Uteroplacental Blood Flow ◽  
Uterine Perfusion

The present study was designed to determine ANG peptide content [ANG I, ANG II, ANG-(1-7)], ACE2 mRNA, and the immunocytochemical distribution of ANG-(1-7) and ACE2 in the uteroembryonic unit during early and late gestation in Sprague-Dawley rats and in a rat model of pregnancy-induced hypertension, the reduced uterine perfusion pressure (RUPP) model. At early pregnancy ANG-(1-7) and ACE2 staining were localized in the primary and secondary decidual zone and luminal and glandular epithelial cells. During late gestation, ANG-(1-7) and ACE2 staining was visualized in the labyrinth placenta and amniotic and yolk sac epithelium. Uterine ANG II concentration at early pregnancy was significantly decreased by 21–55% in the implantation and interimplantation sites compared with virgin rats, whereas ANG-(1-7) levels were maintained at prepregnancy levels. At late gestation, uterine concentrations of ANG I and ANG II were significantly increased (30% and 25%, respectively). In RUPP animals, ANG-(1-7) concentration is significantly reduced in the uterus (181 ± 16 vs. 372 ± 74 fmol/g of tissue) and placenta (143 ± 26 vs. 197 ± 20 fmol/g of tissue). ACE2 mRNA increased in the uterus of early pregnant compared with virgin rats, yet within the implantation site it was downregulated. At late pregnancy, ACE2 mRNA is elevated by 58% in the uterus and decreased by 59% in RUPP animals. The regulation of ANG-(1-7) and ACE2 in early and late pregnancy supports the hypothesis that ANG-(1-7) and ACE2 may act as a local autocrine/paracrine regulator throughout pregnancy, participating in the early (angiogenesis, apoptosis, and growth) and late (uteroplacental blood flow) events of pregnancy.

Abstract 224: Differential Actions of Angiotensin II on Proximal Tubule Transport

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Carolina Panico ◽  
Earl H Rudolph ◽  
Roland C Blantz ◽  
Giovambattista Capasso ◽  
Christopher S Wilcox ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Filtration Fraction ◽  
Fluid Uptake ◽  
Sd Rats ◽  
Luminal Side ◽  
Induced Hypertension ◽  
Single Nephron

Studies with the proximal tubule-specific angiotensin type 1 receptor (AT 1 R) knockout mouse have shown that the proximal tubule (PT) contributes to Ang II-induced hypertension. Ang II levels in the PT fluid are 100- to 1000-fold higher than in plasma, yet the function of the AT 1 -Rs on the luminal side of the PT is unclear. Moreover, hemodynamic actions of Ang II that raise the filtration fraction and the peritubular fluid uptake forces also stimulate PT fluid uptake. We tested the effects of Ang II and AT 1 -Rs on PT fluid uptake in rats. Ang II (200 ng/kg/min) delivered for 2 weeks increased MAP (Con: 95±9 vs Ang II: 140±5 mmHg, p<0.001), single nephron GFR (snGFR)(Con: 36±3 vs Ang II: 43±3, p<0.05) and absolute proximal reabsorption (APR) (Con: 20±3 vs Ang II: 34.5±6.5 nl/min, p<0.01), measured by free flow collections in the S2 segments of the PT in Sprague Dawley (SD) rats. These effects were normalized by acute reduction of MAP via a supra-renal aortic clamp. In a separate group of Munich Wistar Frömter (MWF) rats, which have surface glomeruli, Ang II increased snGFR and APR in the S1 segment (Con: 19±4 vs AngII: 44±5 nl/min, p<0.01; +125±9 %) substantially more than in the S2 segment (Con: 25±6 vs Ang II 37±7 nl/min, p<0.01; +48±6 %). In microperfusion and recollection experiments, in which snGFR was controlled, fluid uptake (Jv) in the PT of SD rats was reduced dose-dependently by Ang II delivered directly into the lumen of S2 segments. Ang II (10 -9 M) at physiological levels reduced Jv by 60±7%. This effect on Jv was blocked by co-perfusion of an AT 1 R blocker. Ang II (10 -9 M), microperfused directly into the S2 reduced Jv in MWF rats as well by 44±5%. Ang II in cultured PT cells at higher concentrations (10 -7 to 10 -9 M) also reduced 22 Na + uptake by 20-35%. In conclusion, enhanced PT fluid reabsorption by Ang II is due to hemodynamic enhancement that likely entails peritubular fluid uptake primarily in the S1 segment. However, luminal Ang II acting on AT 1 -Rs in the S1 and S2 segments of the PT reduces fluid uptake. This effect could be overridden by the hemodynamic effect of systemic Ang II to increase reabsorption especially in the S1 segment.

Abstract T P81: Long-Term Activity Levels Vary by Rat Strain Following Stroke: A Disruption of the Circadian Rhythm?

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Allison Kunze ◽  
Dannielle Zierath ◽  
Olga Drogomiretskiy ◽  
Brett Jaspers ◽  
Tessa Barclay ◽  
...  
Keyword(s):  
Circadian Rhythm ◽  
Infarct Volume ◽  
Therapeutic Interventions ◽  
Stroke Severity ◽  
Light Cycle ◽  
Sprague Dawley ◽  
Dark Cycle ◽  
Lewis Rats ◽  
Sd Rats

Background: Assessment of long-term behavioral outcome after experimental cerebral ischemia is important for evaluating potential therapeutic interventions. In this study, we explored strain related differences in baseline behavior and in response to stroke. Methods: Spontaneous cage activity was monitored (cm moved per hr) and analyzed before and after 2 hour middle cerebral artery occlusion (MCAO) in male Lewis, Wistar, and Sprague Dawley (SD) rats using the Noldus PhenoTyper® cages and EthoVision® Software system. Stroke severity was assessed using the neuroscore, foot fault errors, and performance on the rotarod. Infarct volume at 24 hours was determined in a second cohort of animals. Animals were sacrificed 56 days after MCAO. Data are analyzed using non-parametric statistics. Results: Prior to stroke, the median distance moved per hour during the dark was similar among the 3 strains, but Lewis rats were more active during the light cycle (P=0.001). Neuroscores did not differ between strains at 3 hrs after MCAO nor did infarct volumes at 24 hours after MCAO. Lewis rats, however, performed worse on the rotarod in the month following MCAO (P<0.05 at each time point). Foot fault errors were similar throughout the study period. After stroke, Lewis rats became more active during the dark cycle while Wistar and SD rats became more active during the light cycle (Figure). Summary: The 3 strains of rats evaluated in this study had different patterns in the change in activity after MCAO. Lewis rats showed an increase in activity during the dark cycle while Wistar and SD rats showed an increase in activity during the light cycle. This observation suggests that there are genetic differences in the response to stroke that may alter the circadian rhythm after stroke.

scholarly journals Computer Pattern Recognition: Spontaneous Motor Activity Studies of Rats Following Acute Exposure to Triethyltin

1991 ◽  
Vol 10 (6) ◽  
pp. 705-718 ◽  
Author(s):  
W. J. Kernan ◽  
D. L. Hopper ◽  
M. P. Bowes
Keyword(s):  
Pattern Recognition ◽  
Red Light ◽  
Recognition System ◽  
Exposed Group ◽  
Light Cycle ◽  
Light Conditions ◽  
Sprague Dawley ◽  
Dark Cycle ◽  
Sprague Dawley Rats ◽  
Normal Light

A computer pattern recognition system, RAPID, was used to measure the spontaneous activity of male Sprague-Dawley rats during six observational periods distributed over 11 days after a single oral dose of triethyltin bromide (TET) at 3 or 5 mg/kg. These observational periods were distributed between those taken under red light conditions during the animals normal dark cycle (Days 2, 7, and 10 after exposure) and those taken under white light conditions during the animals normal light cycle (Days 3, 6, and 11 after exposure). Significant disruption of the normal behavioral patterns were observed on Days 2 and 7 for the 3 mg/kg-exposed group and on Days 2, 3, 6, 7, and 10 for the 5 mg/kg-exposed group.

Blood pressure effects of iontophoretically applied bioactive hormones in the anterior forebrain of the rat

1993 ◽  
Vol 265 (4) ◽  
pp. R826-R833 ◽  
Author(s):  
S. N. Thornton ◽  
S. Nicolaidis
Keyword(s):  
Blood Pressure ◽  
Systemic Blood Pressure ◽  
Antagonistic Effect ◽  
Pressure Effects ◽  
Ang Ii ◽  
Ventral Region ◽  
Male Wistar Rats ◽  
Anterior Forebrain ◽  
Blood Pressure Effects ◽  
Blood Pressure Responses

In the course of electrophysiological investigations using iontophoresis, we observed that in specific regions of the forebrain even these minute applications of peptide and steroid hormones can influence systemic blood pressure. In urethan-anesthetized male Wistar rats, with a catheter in the femoral artery, iontophoretic application of the peptide hormones angiotensin II (ANG II), vasopressin (AVP), and atrial natriuretic peptide (ANP) and the steroid hormone aldosterone (ALDO) was effective at locations in the midline septum, the triangularis nucleus of the septum, and the subfornical organ (SFO). Increases in blood pressure (of up to 15 mmHg) were observed after ANG II and AVP, decreases after ALDO, and either an increase or a decrease, depending on the location, after ANP. There was no clear evidence of an antagonistic effect of ANP on ANG II-induced neuronal or blood pressure responses. In addition to demonstrating the potency of these hormones even when they are restricted to tiny volumes of tissue, the present results demonstrate that the medial ventral region of the anterior forebrain may be included in the same baroreceptive circuit as the SFO (and organ vasculosum of the lamina terminalis) and hence be involved in the regulation of blood volume and perhaps in the sensing of and corrective responses to extracellular thirst.

scholarly journals Augmentation of endogenous intrarenal angiotensin II levels in Val5-ANG II-infused rats

2009 ◽  
Vol 296 (5) ◽  
pp. F1067-F1071 ◽  
Author(s):  
Weijian Shao ◽  
Dale M. Seth ◽  
L. Gabriel Navar
Keyword(s):  
Angiotensin Ii ◽  
De Novo ◽  
Excretion Rate ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Osmotic Minipump ◽  
Relative Contribution ◽  
Sprague Dawley Rats ◽  
Induced Hypertension ◽  
Stimulation Of

In angiotensin II (ANG II)-induced hypertension, intrarenal ANG II levels are increased by AT1 receptor-mediated ANG II internalization and endogenous ANG II generation. The objective of the present study was to determine the relative contribution of de novo formation of endogenous ANG II. Male Sprague-Dawley rats were divided into three groups: sham operated ( n = 6), Val5-ANG II infused ( n = 16), and Ile5-ANG II infused ( n = 6). Val5-ANG II and Ile5-ANG II were infused at 80 ng/min via subcutaneous osmotic minipump for 13 days, followed by harvesting of blood and kidney samples. In six Val5-ANG II-infused rats, urine was collected on the day before infusion and on day 12 of infusion. Extracted samples were subjected to HPLC to separate Val5-ANG II from Ile5-ANG II followed by RIA. Systolic blood pressure increased significantly from 121 ± 2 to 206 ± 4 mmHg in the Val5-ANG II-infused rats and from 124 ± 3 to 215 ± 5 mmHg in the Ile5-ANG II-infused rats. In the Val5-ANG II-infused rats, the plasma Ile5-ANG II levels increased 196.2 ± 70.1% compared with sham plasma Ile5-ANG II concentration. Val5-ANG II levels were 150.0 ± 28.2 fmol/ml which accounted for 53.5 ± 10.1% of the total ANG II in plasma. The kidney Ile5-ANG II levels in the Val5-ANG II-infused rats increased 69.9 ± 30.7% compared with sham kidney Ile5-ANG II concentrations. Intrarenal accumulation of Val5-ANG II accounted for 52.5 ± 5.3% of the total kidney ANG II during Val5-ANG II infusion while endogenous Ile5-ANG II accounted for 47.5 ± 8.6%. The urinary Ile5-ANG II excretion rate on day 12 increased 93.2 ± 32.1% compared with preinfusion level indicating increased formation of endogenous ANG II. Thus, the increases in intrarenal ANG II levels during chronic ANG II infusions involve substantial stimulation of endogenous ANG II formation which contributes to overall augmentation of intrarenal ANG II.

Abstract 493: Impact of Renal Vasoconstriction on the Relationship Between Blood Pressure and Renal Injury in Angiotensin II-induced Hypertensive Rats

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Aaron J Polichnowski ◽  
Maria Picken ◽  
Jianrui Long ◽  
Geoffrey Williamson ◽  
Karen Griffin ◽  
...  
Keyword(s):  
Renal Injury ◽  
Left Kidney ◽  
Separate Experiment ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Osmotic Minipump ◽  
Renal Vasoconstriction ◽  
Sprague Dawley Rats ◽  
Induced Hypertension ◽  
The Relationship

Ang II is thought to play a prominent role in the development of hypertension-induced renal disease via BP dependent and independent pathways; however the quantitative relationships between BP and renal injury have not been rigorously examined in Ang II-induced hypertension. The major goals of the present study were to assess: 1) the relationship between BP and renal injury in rats with hypertension induced by Ang II vs. renal mass reduction (RMR) and 2) the pressure-flow relationships in conscious Ang II-infused rats. One group of male Sprague-Dawley rats (Charles River) were implanted with a BP radiotransmitter and 10 days later administered Ang II (n=12; 500 ng/kg/min via osmotic minipump) or subjected to 3/4 RMR via right uninephrectomy + infarction of ∼ 1/2 of the left kidney (RKI, n=5). BP was measured continuously and kidneys were perfused fixed at 6 weeks for the assessment of renal injury. In a separate experiment, MAP and RBF (Transonic) were measured in conscious chronically instrumented rats. After recovery from surgery (∼7 days), baseline MAP and RBF were assessed (∼4 hours @ 200 Hz) on 2 consecutive days. Subsequently, rats were administered Ang II (n=6; 500 ng/kg/min) or saline (n=7; sham) via osmotic minipump and MAP and RBF were again assessed every 2-3 days for 10 days. Despite a higher average systolic BP over 6 weeks in Ang II (174±3 mmHg) vs. RKI (165±6 mmHg) rats, glomerulosclerosis (GS) was higher (p<0.05) in RKI (15±7% out of 100 glomeruli) vs. Ang II (6±1% out of 100 glomeruli) rats. Moreover, the slope of the relationship between BP and %GS (Δ%GS/ΔmmHg) was greater in RKI vs. Ang II rats. Both MAP (98±2 vs. 99±3 mmHg) and RBF (8.1±1vs. 8.2±1 ml/min) were similar at baseline in Ang II and sham rats, respectively. MAP was elevated by day 3 (123±6 mmHg) and further increased to 157±5 mmHg by day 10 in Ang II rats. Conversely, RBF was decreased at day 3 (6.6±0.6 ml/min) and the vasoconstriction persisted over the experimental protocol as RBF further decreased to 5.6±0.7 ml/min at day 10 in Ang II rats. In conclusion, Ang II-induced hypertension is associated with a diminished susceptibility to renal injury as compared to rats with RMR likely due, in part, to the AngII-induced vasoconstriction, which reduces BP transmission to the renal microvasculature.

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