scholarly journals Rats are protected from the stress of chronic pressure overload compared with mice

2020 ◽  
Vol 318 (5) ◽  
pp. R894-R900 ◽  
Author(s):  
Koichi Nishimura ◽  
Marko Oydanich ◽  
Jie Zhang ◽  
Denis Babici ◽  
Diego Fraidenraich ◽  
...  
Keyword(s):  
Troponin I ◽  
Diastolic Pressure ◽  
Pressure Overload ◽  
Wall Stress ◽  
Left Ventricular ◽  
Pressure Gradients ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Systolic And Diastolic Function ◽  
Systolic Wall Stress

The goal of this investigation was to compare the effects of chronic (4 wk) transverse aortic constriction (TAC) in Sprague-Dawley rats and C57BL/6J mice. TAC, after 1 day, induced similar left ventricular (LV) pressure gradients in both rats ( n = 7) and mice ( n = 7) (113 ± 5.4 vs. 103 ± 11.5 mmHg), and after 4 wk, the percent increase in LV hypertrophy, as reflected by LV/tibial length (51% vs 49%), was similar in rats ( n = 12) and mice ( n = 12). After 4 wk of TAC, LV systolic and diastolic function were preserved in TAC rats. In contrast, in TAC mice, LV ejection fraction decreased by 31% compared with sham, along with increases in LV end-diastolic pressure (153%) and LV systolic wall stress (86%). Angiogenesis, as reflected by Ki67 staining of capillaries, increased more in rats ( n = 6) than in mice ( n = 6; 10 ± 2 vs. 6 ± 1 Ki67-positive cells/field). Myocardial blood flow fell by 55% and coronary reserve by 28% in mice with TAC ( n = 4), but they were preserved in rats ( n = 4). Myogenesis, as reflected by c-kit-positive myocytes staining positively for troponin I, is another mechanism that can confer protection after TAC. However, the c-kit-positive cells in rats with TAC were all negative for troponin I, indicating the absence of myogenesis. Thus, rats showed relative tolerance to severe pressure overload compared with mice, with mechanisms involving angiogenesis but not myogenesis.

Captopril prevents vascular and fibrotic changes but not cardiac hypertrophy in aortic-banded rats

1996 ◽  
Vol 271 (3) ◽  
pp. H906-H913 ◽  
Author(s):  
C. P. Regan ◽  
P. G. Anderson ◽  
S. P. Bishop ◽  
K. H. Berecek
Keyword(s):  
Cardiac Hypertrophy ◽  
Coronary Vessels ◽  
Pressure Overload ◽  
Renin Angiotensin System ◽  
Left Ventricular ◽  
Heart Weight ◽  
Sprague Dawley ◽  
Vessel Morphology ◽  
Sprague Dawley Rats ◽  
Quantitative Image

To determine the role of the renin-angiotensin system (RAS) on cardiovascular remodeling in a pressure overload model of cardiac hypertrophy, a subdiaphragmatic aortic band was placed in adult male, Sprague-Dawley rats. Rats were left untreated (AB) or given captopril (Cap, 400 mg/l) (AB-Cap). Sham-operated controls were either left untreated (S) or given Cap (S-Cap). After 4 wk, rats were catheterized, and carotid and femoral mean arterial pressures (CMAP and FMAP in mmHg, respectively) were recorded. Hearts were isolated, and minimal coronary resistance (MCR) was determined. Hearts were then perfusion fixed, total and regional heart weights were recorded, and sections were processed for vessel morphology. Changes in coronary artery medical thickness and perivascular fibrosis were assessed by quantitative image analysis. CMAP was significantly higher in AB and AB-Cap than S or S-Cap rats (P < 0.05). There was no difference in FMAP in AB vs. S rats, but AB-Cap and S-Cap had lower FMAP values than S rats. Total heart weight and left ventricular weight-to-body weight ratios were increased in AB and AB-Cap rats compared with S and S-Cap rats (P < 0.05). MCR of AB was greater than S and S-Cap rats. MCR of AB-Cap rats was significantly greater than S and S-Cap rats but was significantly less than AB rats. In coronary vessels, medial thickness was greatest in AB, whereas there was no difference among AB-Cap, S, and S-Cap rats. Similarly, the increase in perivascular fibrosis was greatest in AB rats, and there was no difference among AB-Cap, S, and S-Cap rats. These data suggest that the RAS, independent of increased arterial pressure, is critical for the development of the vascular and fibrotic changes that occur in this model of pressure overload hypertrophy.

Left ventricular adaptation to gradual renovascular hypertension in dogs

1993 ◽  
Vol 265 (1) ◽  
pp. H22-H38 ◽  
Author(s):  
T. N. Nguyen ◽  
A. C. Chagas ◽  
S. A. Glantz
Keyword(s):  
Pressure Overload ◽  
Wall Stress ◽  
Left Ventricular ◽  
Beta Blockade ◽  
Stroke Work ◽  
Adrenergic Stimulation ◽  
Lv Mass ◽  
Wall Mass ◽  
Systolic Wall Stress ◽  
Over Time

The left ventricle hypertrophies in response to chronic pressure overload. To determine whether increased beta-adrenergic stimulation, wall mass, intrinsic contractility, or a combination of these factors is responsible for improved left ventricular (LV) pump function during early development of pressure-overload hypertrophy and whether hypertrophy normalizes peak-systolic wall stress, as is commonly believed, we induced pressure overload in intact-chest dogs by gradual constriction of one renal artery and implanted radiopaque markers, via a catheter, in the LV endocardium to measure dimensions. Changes in hemodynamics, LV dimensions, contractility indexes, and circumferential wall stress were measured before and after acute beta-blockade for 12 wk. LV function improved over time in the unblocked state, indicated by increased cardiac output, systolic pressures, stroke work, and maximal elastance (Emax). Acute beta-blockade reduced stroke work, Emax, and maximal LV rate of pressure over time (dP/dtmax) relative to the unblocked state but all still increased significantly over time. dP/dtmax and Emax did not vary with increases in LV mass, but stroke work was borderline dependent on LV mass. These results suggest that beta-adrenergic stimulation contributes to improved LV pump function and that the remaining improvements are due to both increased intrinsic contractility and wall mass. In contrast to accepted theory, LV systolic wall stresses decreased significantly over time. End-diastolic wall stress increased after renal artery constriction, then returned to baseline values as the heart hypertrophied. These results suggest that hypertrophy normalizes end-diastolic, not peak-systolic, wall stress.

scholarly journals Effects of a myofilament calcium sensitizer on left ventricular systolic and diastolic function in rats with volume overload heart failure

2014 ◽  
Vol 307 (11) ◽  
pp. H1605-H1617 ◽  
Author(s):  
Kristin Wilson ◽  
Anuradha Guggilam ◽  
T. Aaron West ◽  
Xiaojin Zhang ◽  
Aaron J. Trask ◽  
...  
Keyword(s):  
Heart Failure ◽  
Troponin I ◽  
Regulatory Protein ◽  
Volume Overload ◽  
Left Ventricular ◽  
Lv Function ◽  
Stroke Work ◽  
Sprague Dawley ◽  
Diastolic Relaxation ◽  
Systolic And Diastolic Function

Aortocaval fistula (ACF)-induced volume overload (VO) heart failure (HF) results in progressive left ventricular (LV) dysfunction. Hemodynamic load reversal during pre-HF (4 wk post-ACF; REV) results in rapid structural but delayed functional recovery. This study investigated myocyte and myofilament function in ACF and REV and tested the hypothesis that a myofilament Ca2+ sensitizer would improve VO-induced myofilament dysfunction in ACF and REV. Following the initial sham or ACF surgery in male Sprague-Dawley rats (200–240 g) at week 0, REV surgery and experiments were performed at weeks 4 and 8, respectively. In ACF, decreased LV function is accompanied by impaired sarcomeric shortening and force generation and decreased Ca2+ sensitivity, whereas, in REV, impaired LV function is accompanied by decreased Ca2+ sensitivity. Intravenous levosimendan (Levo) elicited the best inotropic and lusitropic responses and was selected for chronic oral studies. Subsets of ACF and REV rats were given vehicle (water) or Levo (1 mg/kg) in drinking water from weeks 4–8. Levo improved systolic (% fractional shortening, end-systolic elastance, and preload-recruitable stroke work) and diastolic (τ, dP/d tmin) function in ACF and REV. Levo improved Ca2+ sensitivity without altering the amplitude and kinetics of the intracellular Ca2+ transient. In ACF-Levo, increased cMyBP-C Ser-273 and Ser-302 and cardiac troponin I Ser-23/24 phosphorylation correlated with improved diastolic relaxation, whereas, in REV-Levo, increased cMyBP-C Ser-273 phosphorylation and increased α-to-β-myosin heavy chain correlated with improved diastolic relaxation. We concluded that Levo improves LV function, and myofilament composition and regulatory protein phosphorylation likely play a key role in improving function.

Preservation of coronary reserve by ivabradine-induced reduction in heart rate in infarcted rats is associated with decrease in perivascular collagen

2007 ◽  
Vol 293 (1) ◽  
pp. H590-H598 ◽  
Author(s):  
Eduard I. Dedkov ◽  
Wei Zheng ◽  
Lance P. Christensen ◽  
Robert M. Weiss ◽  
Florence Mahlberg-Gaudin ◽  
...  
Keyword(s):  
Heart Rate ◽  
Myocardial Perfusion ◽  
Transforming Growth Factor ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Coronary Reserve ◽  
Osmotic Pumps ◽  
Sprague Dawley Rats

We tested the hypothesis that chronically reducing the heart rate in infarcted middle-aged rats using ivabradine (IVA) would induce arteriolar growth and attenuate perivascular collagen and, thereby, improve maximal perfusion and coronary reserve in the surviving myocardium. Myocardial infarction (MI) was induced in 12-mo-old male Sprague-Dawley rats, which were then treated with either IVA (10.5 mg·kg−1·day−1; MI + IVA) or placebo (MI) via intraperitoneal osmotic pumps for 4 wk. Four weeks of IVA treatment limited the increase in left ventricular end-diastolic pressure and the decrease in ejection fraction but did not affect the size of the infarct, the magnitude of myocyte hypertrophy, or the degree of arteriolar and capillary growth. However, treatment reduced interstitial and periarteriolar collagen in the surviving myocardium of MI + IVA rats. The reduced periarteriolar collagen content was associated with improvement in maximal myocardial perfusion and coronary reserve. Although the rates of proliferation of periarteriolar fibroblasts were similar in the MI and MI + IVA groups, the expression levels of the AT1 receptor and transforming growth factor (TGF)-β1 in the myocardium, as well as the plasma level of the ANG II peptide, were lower in treated rats 14 days after MI. Therefore, our data reveal that improved maximal myocardial perfusion and coronary reserve in MI + IVA rats are most likely the result of reduced periarteriolar collagen rather than enhanced arteriolar growth.

Chronic elevation of norepinephrine in conscious dogs produces hypertrophy with no loss of LV reserve

1992 ◽  
Vol 262 (2) ◽  
pp. H331-H339 ◽  
Author(s):  
J. M. Stewart ◽  
M. B. Patel ◽  
J. Wang ◽  
M. Ochoa ◽  
M. Gewitz ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Wall Stress ◽  
Left Ventricular ◽  
Plasma Catecholamine ◽  
Wall Function ◽  
Volume Loading ◽  
Norepinephrine Infusion ◽  
Pressure Maximum ◽  
Developed Pressure ◽  
Systolic Wall Stress

Elevated plasma catecholamine levels may cause both myocardial hypertrophy and tissue damage. To determine whether the left ventricle from dogs with chronic norepinephrine infusion can sustain additional functional loads, we altered ventricular preload or afterload and determined both global and left ventricular (LV) wall function. Dogs were instrumented to measure LV wall function, LV internal base diameter, and LV pressures and were allowed to fully recover. Preload was altered by volume loading and afterload by injection of phenylephrine. Osmotic infusion pumps were implanted to continuously release norepinephrine at 0.5 micrograms.kg-1.min-1 for 28 days, and the volume loading and phenylephrine were repeated on days 14 and 28. Heart rate decreased, whereas there were no differences in mean arterial pressure, maximum first derivative of LV pressure (dP/dt), LV dP/dt/developed pressure of 40 mmHg, LV dP/dt/end-diastolic circumference, slope of the pressure-diameter relation, peak systolic wall stress, LV/end-diastolic diameter, or LV/end-systolic diameter during norepinephrine infusion. Diastolic and systolic wall thickness and chamber weights were increased (P less than 0.05). Indexes of diastolic function, including end-diastolic pressure, end-diastolic pressure-end-diastolic diameter relationship, maximum negative dP/dt, and the time constant (tau) were unchanged after chronic norepinephrine infusion, although maximum end-diastolic pressure during volume loading was increased from 17.7 +/- 2.0 to 21.7 +/- 1.0 mmHg. Chronic norepinephrine infusion did not alter tau, and tau increased equivalently with phenylephrine injection in both normal (36 +/- 1 to 62 +/- 5 ms) dogs and in those chronically infused with norepinephrine (36 +/- 1 to 56 +/- 5 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract 149: Zoniporide Combined with α-Methylnorepinephrine Promotes Greater Hemodynamic Stability than Either Agent Alone During Chest Compression in Rats

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Lorissa Lamoureux ◽  
Herbert K Whitehouse ◽  
Jeejabai Radhakrishnan ◽  
Raúl J Gazmuri
Keyword(s):  
Chest Compression ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Sprague Dawley ◽  
Blood Flows ◽  
Compression Time ◽  
Sprague Dawley Rats ◽  
Sodium Hydrogen Exchanger ◽  
Ventricular Distensibility ◽  
Over Time

Background: We have reported in animal models of cardiac arrest that sodium hydrogen exchanger-1 (NHE-1) inhibition - by attenuating reperfusion injury - helps preserve left ventricular distensibility yielding higher forward blood flows during chest compression. Others have reported that α-methylnorepinephrine (α-MNE) - a selective peripheral α2-adrenoreceptor agonist - is superior to epinephrine given its lack of β-agonist effect that intensifies myocardial ischemia. We examined in a rat model of VF the effects of combining the NHE-1 inhibitor zoniporide (ZNP) with α-MNE during CPR, expecting to elicit a vasopressor effect (α-MNE) that is better maintained over time because of ZNP. Methods: VF was electrically induced in 32 male retired breeder Sprague-Dawley rats and left untreated for 8 minutes. Chest compression was then initiated, gradually increasing the depth of compression (maximum 17 mm) to attain an aortic diastolic pressure of 28 mmHg by the end of minute 2, maintaining such level for the remaining 6 minutes of chest compression, time at which defibrillation was attempted. The rats were randomized 1:1:1:1 to receive a 3 mg/kg bolus of ZNP or 0.9% NaCl before starting chest compression and a 100 μg/kg bolus of α-MNE or its vehicle at minute 2 of chest compression with the investigators blind to the assignment. Results: The ratio between the aortic diastolic pressure and depth of compression (Figure) was higher - as expected - in rats that received α-MNE(+) given its vasopressor effect. The effect, however, was not maintained and declined over time; but to a significantly lesser degree in rats that also received ZNP; i.e., α-MNE(+)/ZNP(+) group. Conclusions: The findings support a favorable interaction between α-MNE and ZNP; the first prompting needed peripheral vasoconstriction - likely with less concomitant myocardial injury - and the latter preserving left ventricular distensibility, which combined enhance the hemodynamic efficacy of chest compression.

Abstract 17904: Deficiency of Yes-associated Protein Promotes Cardiac Dysfunction in Response to Pressure Overload in the Mouse Heart

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Jaemin Byun ◽  
Dominic P Del Re ◽  
Peiyong Zhai ◽  
Akihiro Shirakabe ◽  
Junichi Sadoshima
Keyword(s):  
Cardiac Hypertrophy ◽  
Mammalian Cells ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Pressure Overload ◽  
Wall Stress ◽  
Left Ventricular ◽  
Lv Function ◽  
Mouse Heart ◽  
And Control

Yes-Associated Protein (YAP), a downstream effector of the Hippo pathway, plays an important role in regulating cell proliferation and survival in mammalian cells. We have shown that cardiac-specific loss of YAP leads to increased cardiomyocyte (CM) apoptosis and impaired hypertrophy during chronic myocardial infarction in the mouse heart. However, it remains unclear whether YAP mediates hypertrophy of individual CMs under stress conditions in vivo. We hypothesized that endogenous YAP plays an essential role in mediating hypertrophy and survival of CMs in response to pressure overload (PO). Three-month-old YAP+/fl;α-MHC-Cre (YAP-cKO) and YAP+/fl (control) mice were subjected to transverse aortic constriction (TAC). Two weeks later, YAP-cKO and control mice developed similar levels of cardiac hypertrophy (left ventricular (LV) weight/tibia length: 7.27±0.38, 6.93±0.29) compared to sham (5.08±0.14, 4.07±0.33). LV CM cross sectional area was similarly increased by TAC in YAP-cKO and control mice compared to their respective shams. Induction of fetal-type genes, such as Anf and Myh7, was also similar in YAP-cKO and control mice. YAP-cKO and control mice exhibited similar baseline LV systolic function (ejection fraction (EF): 75, 76%). YAP-cKO mice had significantly decreased LV function after TAC compared to Sham-control mice (EF: 51%, 76%, p<0.05) and TAC-control mice (75%, p<0.05). LV end diastolic pressure (LVEDP, mmHg) was significantly increased (19.3 ±3.2, 9.8±1.6, p<0.05), and LV +dP/dt (mmHg/s, 7250±588, 9500±453, p<0.01) and -dP/dt (mmHg/s, 6000±433, 7781± 314, p<0.05) were significantly decreased in YAP-cKO compared to in control mice after TAC. LV end diastolic diameter (mm) was significantly greater in YAP-cKO than in control mice after TAC (3.95±0.11, 3.35±0.15, p<0.05), whereas LV pressure was similar, suggesting that LV wall stress was elevated in YAP-cKO compared to in control mice. Since cardiac hypertrophy in YAP-cKO mice is similar to that in control mice despite elevated wall stress, the lack of YAP appears to limit the extent of cardiac hypertrophy in response to increased wall stress. These data suggest that endogenous YAP plays an important role in mediating adaptive hypertrophy and protecting the heart against PO.

scholarly journals Effects of cardiac overexpression of type 6 adenylyl cyclase affects on the response to chronic pressure overload

2010 ◽  
Vol 299 (3) ◽  
pp. H707-H712 ◽  
Author(s):  
Aziz Guellich ◽  
Shumin Gao ◽  
Chull Hong ◽  
Lin Yan ◽  
Thomas E. Wagner ◽  
...  
Keyword(s):  
Adenylyl Cyclase ◽  
Contractile Function ◽  
Weight Ratio ◽  
Pressure Overload ◽  
Wall Stress ◽  
Left Ventricular ◽  
Body Weight Ratio ◽  
Aortic Constriction ◽  
Cross Sectional ◽  
Systolic Wall Stress

Adenylyl cyclase (AC) type 5 (AC5) and AC type 6 (AC6) are the two major AC isoforms in the heart. Cardiac overexpression of AC6 has been shown to be protective in response to several interventions. In this investigation, we examined the effects of chronic pressure overload in AC6 transgenic (TG) mice. In the absence of any stress, AC6 TG mice exhibited enhanced contractile function compared with their wild-type (WT) littermates, i.e., increased ( P < 0.05) left ventricular (LV) ejection fraction (EF) (75 ± 0.9 vs. 71 ± 0.5%) and LV dP/d t (7,850 ± 526 vs. 6,374 ± 315 mmHg/s). Forskolin (25 μg·kg−1·min−1 for 5 min) increased LVEF more ( P < 0.05) in AC6 TG mice (14.8 ± 1.0%) than in WT mice (7.7 ± 1.0%). Also, isoproterenol (0.04 μg·kg−1·min−1 for 5 min) increased LVEF more ( P < 0.05) in AC6 TG mice (18.0 ± 1.2%) than in WT mice (11.6 ± 2.1%). Pressure overload, induced by 4 wk of transverse aortic constriction (TAC), increased the LV weight-to-body weight ratio and myocyte cross-sectional area similarly in both groups, but reduced LVEF more in AC6 TG mice (22%) compared with WT mice (9%), despite the higher starting level of LVEF in AC6 TG mice. LV systolic wall stress increased more in AC6 TG mice than in WT mice, which could be responsible for the reduced LVEF in AC6 TG mice with chronic pressure overload. In addition, LV dP/d t was no longer elevated in AC6 TG mice after TAC compared with WT mice. LV end-diastolic diameter was also greater ( P < 0.05) in AC6 TG mice (3.8 ± 0.07 mm) than in WT mice (3.6 ± 0.05 mm) after TAC. Thus, in contrast to other interventions previously reported to be salutary with cardiac AC6 overpression, the response to chronic pressure overload was not; actually, AC6 TG mice fared worse than WT mice. The mechanism may be due to the increased LV systolic wall stress in AC6 TG mice with chronic pressure overload.

scholarly journals Renal denervation improves cardiac function in rats with chronic heart failure: Effects on expression of β-adrenoceptors

2016 ◽  
Vol 311 (2) ◽  
pp. H337-H346 ◽  
Author(s):  
Hong Zheng ◽  
Xuefei Liu ◽  
Neeru M. Sharma ◽  
Kaushik P. Patel
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Left Ventricle ◽  
Cardiac Function ◽  
Renal Denervation ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Sprague Dawley ◽  
Cardiac Damage ◽  
Sprague Dawley Rats

Chronic activation of the sympathetic drive contributes to cardiac remodeling and dysfunction during chronic heart failure (HF). The present study was undertaken to assess whether renal denervation (RDN) would abrogate the sympathoexcitation in HF and ameliorate the adrenergic dysfunction and cardiac damage. Ligation of the left coronary artery was used to induce HF in Sprague-Dawley rats. Four weeks after surgery, RDN was performed, 1 wk before the final measurements. At the end of the protocol, cardiac function was assessed by measuring ventricular hemodynamics. Rats with HF had an average infarct area >30% of the left ventricle and left ventricular end-diastolic pressure (LVEDP) >20 mmHg. β1- and β2-adrenoceptor proteins in the left ventricle were reduced by 37 and 49%, respectively, in the rats with HF. RDN lowered elevated levels of urinary excretion of norepinephrine and brain natriuretic peptide levels in the hearts of rats with HF. RDN also decreased LVEDP to 10 mmHg and improved basal dP/d t to within the normal range in rats with HF. RDN blunted loss of β1-adrenoceptor (by 47%) and β2-adrenoceptor (by 100%) protein expression and improved isoproterenol (0.5 μg/kg)-induced increase in +dP/d t (by 71%) and −dP/d t (by 62%) in rats with HF. RDN also attenuated the increase in collagen 1 expression in the left ventricles of rats with HF. These findings demonstrate that RDN initiated in chronic HF condition improves cardiac function mediated by adrenergic agonist and blunts β-adrenoceptor expression loss, providing mechanistic insights for RDN-induced improvements in cardiac function in the HF condition.

Cardiovascular dysfunction in Zucker obese and Zucker diabetic fatty rats: role of hydronephrosis

2007 ◽  
Vol 293 (1) ◽  
pp. H292-H298 ◽  
Author(s):  
Susan A. Marsh ◽  
Pamela C. Powell ◽  
Anupam Agarwal ◽  
Louis J. Dell'Italia ◽  
John C. Chatham
Keyword(s):  
Renal Dysfunction ◽  
Wall Stress ◽  
Left Ventricular ◽  
Zucker Rats ◽  
Sprague Dawley ◽  
Zdf Rat ◽  
Sd Rats ◽  
Kidney Morphology ◽  
Zucker Diabetic Fatty Rats ◽  
Systolic Wall Stress

Recent studies in our laboratory using the Zucker obese (ZO) and Zucker diabetic fatty (ZDF) rat models resulted in unexpectedly high mortality rates in all genotypes including healthy homozygous lean Zucker rats, possibly because of renal dysfunction. Therefore, we evaluated left ventricular (LV) and kidney morphology and function in young ZO, Zucker diabetic fatty obese (ZDFO), homozygous Zucker/ZDF lean (ZL), and Sprague-Dawley (SD) rats. Hydronephrosis was evident in ZL, ZO, and ZDFO but not SD kidneys. ZDFO rats exhibited impaired LV shortening and relaxation with increased arterial stiffness. LV wall thickness was lower and LV end-systolic wall stress was higher in ZDFO compared with SD rats. Plasma ANG II was lower in ZO and ZDFO rats, which may be a result of reduced renal parenchyma with hydronephrosis; norepinephrine was higher in ZDFO rats than SD controls. Covariate analysis indicated that LV end-systolic wall stress was associated with renal dysfunction. The presence of hydronephrosis and its association with LV dysfunction potentially limits the ZDF model for study of the effects of diabetes on renal and cardiovascular function.

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