scholarly journals Kidney function in mice lacking aldosterone

2006 ◽  
Vol 290 (1) ◽  
pp. F61-F69 ◽  
Author(s):  
Natalia Makhanova ◽  
Gene Lee ◽  
Nobuyuki Takahashi ◽  
Maria L. Sequeira Lopez ◽  
R. Ariel Gomez ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Kidney Function ◽  
Plasma Concentrations ◽  
Urine Volume ◽  
Weight Ratio ◽  
Urine Osmolality ◽  
Dietary Salt ◽  
Water Metabolism ◽  
Low Blood Pressure ◽  
Cox 2

To explore the effects of decreased amounts or absence of aldosterone, we have disrupted the gene coding for aldosterone synthase (AS) in mice and investigated blood pressure and kidney function in AS+/+, AS+/−, and AS−/− mice. AS+/− mice have normal blood pressures and show no abnormalities in electrolytes or kidney gene expression, but they have significantly higher than normal urine volume and lower urine osmolality. In contrast, the AS−/− mice have low blood pressure, abnormal electrolyte homeostasis (increased plasma concentrations of K+, Ca2+, and Mg2+ and decreased concentrations of HCO3− and Cl− but no difference in the plasma Na+ level), and disturbances in water metabolism (higher urine output, decreased urine osmolality, and impaired urine concentrating and diluting ability). Absence of aldosterone in the AS−/− mice induced several compensatory changes: an increased food intake-to-body weight ratio, an elevated plasma concentration of glucocorticoids, and strong activation of the renin-angiotensin system. Parallel with the markedly increased synthesis and release of renin, the AS−/− mice showed increased expression of cyclooxygenase-2 (COX-2) in macula densa. On salt supplementation, plasma electrolyte concentrations and kidney renin and COX-2 levels became similar to those of wild-type mice, but the lower blood pressure of the AS−/− mice was not corrected. Thus absence of aldosterone in AS−/− mice results in impairment of Na+ reabsorption in the distal nephron, decreased blood pressure, and strong renin-angiontensin system activation. Our data show the substantial correction of these abnormalities, except the low blood pressure, by high dietary salt does not depend on aldosterone.

Abstract 114: K+ Rich Diet During Angiotensin II Hypertension Reduces Renal Na-Cl Cotransporter and Phosphorylation, but Not Blood Pressure

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Luciana C Veiras ◽  
Jiyang Han ◽  
Donna L Ralph ◽  
Alicia A McDonough
Keyword(s):  
Blood Pressure ◽  
Urine Volume ◽  
Weight Ratio ◽  
Distal Tubule ◽  
Reduce Blood Pressure ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
K Secretion ◽  
Pressure Natriuresis

During Ang II hypertension distal tubule Na-Cl Cotransporter (NCC) abundance and its activating phosphorylation (NCCp), as well as Epithelial Na+ channels (ENaC) abundance and activating cleavage are increased 1.5-3 fold. Fasting plasma [K+] is significantly lower in Ang II hypertension (3.3 ± 0.1 mM) versus controls (4.0 ± 0.1 mM), likely secondary to ENaC stimulation driving K+ secretion. The aim of this study was to test the hypothesis that doubling dietary K+ intake during Ang II infusion will lower NCC and NCCp abundance to increase Na+ delivery to ENaC to drive K+ excretion and reduce blood pressure. Methods: Male Sprague Dawley rats (225-250 g; n= 7-9/group) were treated over 2 weeks: 1) Control 1% K diet fed (C1K); 2) Ang II infused (400 ng/kg/min) 1% K diet fed (A1K); or 3) Ang II infused 2% K diet fed (A2K). Blood pressure (BP) was determined by tail cuff, electrolytes by flame photometry and transporters’ abundance by immunoblot of cortical homogenates. Results: As previously reported, Ang II infusion increased systolic BP (from 132 ± 5 to 197 ± 4 mmHg), urine volume (UV, 2.4 fold), urine Na+ (UNaV, 1.3 fold), heart /body weight ratio (1.23 fold) and clearance of endogenous Li+ (CLi, measures fluid volume leaving the proximal tubule, from 0.26 ± 0.02 to 0.51 ± 0.01 ml/min/kg) all evidence for pressure natriuresis. A2K rats exhibited normal plasma [K+] (4.6 ± 0.1 mM, unfasted), doubled urine K+ (UKV, from 0.20 to 0.44 mmol/hr), and increased CLi (to 0.8 ± 0.1 ml/min/kg) but UV, UNaV, cardiac hypertrophy and BP were unchanged versus the A1K group. As expected, NCC, NCCpS71 and NCCpT53 abundance increased in the A1K group to 1.5 ± 0.1, 2.9 ± 0.5 and 2.8 ± 0.4 fold versus C1K, respectively. As predicted by our hypothesis, when dietary K+ was doubled (A2K), Ang II infusion did not activate NCC, NCCpS71 nor NCCpT53 (0.91 ± 0.04, 1.3 ± 0.1 and 1.6 ± 0.2 fold versus C1K, respectively). ENaC subunit abundance and cleavage increased 1.5 to 3 fold in both A1K and A2K groups; ROMK was unaffected by Ang II or dietary K. In conclusion, evidence is presented that stimulation of NCC during Ang II hypertension is secondary to K+ deficiency driven by ENaC stimulation since doubling dietary K+ prevents the activation. The results also indicate that elevation in BP is independent of NCC activation

Collecting duct-specific knockout of endothelin-1 alters vasopressin regulation of urine osmolality

2005 ◽  
Vol 288 (5) ◽  
pp. F912-F920 ◽  
Author(s):  
Yuqiang Ge ◽  
Dowahn Ahn ◽  
Peter K. Stricklett ◽  
Alisa K. Hughes ◽  
Masashi Yanagisawa ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Urine Volume ◽  
Urine Osmolality ◽  
Water Metabolism ◽  
Urinary Osmolality ◽  
Water Load ◽  
Endothelin 1 ◽  
Normal Water

In vitro studies suggest that endothelin-1 (ET-1) inhibits vasopressin (AVP)-stimulated water permeability in the collecting duct (CD). To evaluate the role of CD-derived ET-1 in regulating renal water metabolism, the ET-1 gene was selectively disrupted in the CD (CD ET-1 KO). During normal water intake, urinary osmolality (Uosm), plasma Na concentration, urine volume, and renal aquaporin-2 (AQP2) levels were unchanged, but plasma AVP concentration was reduced in CD ET-1 KO animals. CD ET-1 KO mice had impaired ability to excrete an acute, but not a chronic, water load, and this was associated with increased CD ET-1 mRNA in control, but not CD ET-1 KO, mice. In response to continuous infusion of 1-desamino-8-d-arginine vasopressin, CD ET-1 KO mice had greater increases in Uosm, V2 and AQP2 mRNA, and phosphorylation of AQP2. CD suspensions from CD ET-1 KO mice had enhanced AVP- and forskolin-stimulated cAMP accumulation. These data indicate that CD ET-1 KO increases renal sensitivity to the urinary concentrating effects of AVP and suggest that ET-1 functions as a physiological autocrine regulator of AVP action in the CD.

Role of prostaglandins in collecting duct-derived endothelin-1 regulation of blood pressure and water excretion

2007 ◽  
Vol 293 (6) ◽  
pp. F1805-F1810 ◽  
Author(s):  
Yuqiang Ge ◽  
Kevin A. Strait ◽  
Peter K. Stricklett ◽  
Tianxin Yang ◽  
Donald E. Kohan
Keyword(s):  
Blood Pressure ◽  
Collecting Duct ◽  
Urine Volume ◽  
Mrna Levels ◽  
Water Excretion ◽  
Salt Loading ◽  
Endothelin 1 ◽  
Cox 2 ◽  
Cox 1

Collecting duct (CD)-derived endothelin-1 (ET-1) exerts natriuretic, diuretic, and hypotensive effects. In vitro studies have implicated cyclooxygenase (COX) metabolites, and particularly PGE2, as important mediators of CD ET-1 effects. However, it is unknown whether PGE2 mediates CD-derived ET-1 actions in vivo. To test this, CD ET-1 knockout (KO) and control mice were studied. During normal salt and water intake, urinary PGE2 excretion was unexpectedly increased in CD ET-1 KO mice compared with controls. Salt loading markedly increased urinary PGE2 excretion in both groups of mice; however, the levels remained relatively higher in KO animals. Acutely isolated inner medullary collecting duct (IMCD) from KO mice also had increased PGE2 production. The increased IMCD PGE2 was COX-2 dependent, since NS-398 blocked all PGE2 production. However, increased CD ET-1 KO COX-2 protein or mRNA could not be detected in inner medulla or IMCD, respectively. Inner medullary COX-1 mRNA and protein levels and IMCD COX-1 mRNA levels were unaffected by Na intake or CD ET-1 KO. KO mice on a normal or high-Na diet had elevated blood pressure compared with controls; this difference was not altered by indomethacin or NS-398 treatment. However, indomethacin or NS-398 did increase urine osmolality and reduce urine volume in KO, but not control, animals. In summary, IMCD COX-2-dependent PGE2 production is increased in CD ET-1 KO mice, indicating that CD-derived ET-1 is not a primary regulator of IMCD PGE2. Furthermore, the increased PGE2 in CD ET-1 KO mice partly compensates for loss of ET-1 with respect to maintaining urinary water excretion, but not in blood pressure control.

Abstract 308: Nephron Specific Deletion Of Angiotensinogen Modulates Blood Pressure

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Nirupama Ramkumar ◽  
Deborah Stuart ◽  
Matias Calquin ◽  
Shuping Wang ◽  
Fumio Niimura ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Proximal Tubule ◽  
Urine Volume ◽  
Plasma Renin ◽  
Urine Osmolality ◽  
Metabolic Balance ◽  
Salt Diet ◽  
Plasma Renin Concentration ◽  
Specific Deletion

It is unknown if intrarenal generation of angiotensinogen (AGT) is important in blood pressure (BP) regulation. Previous studies showed that proximal tubule-specific overexpression of AGT increases BP, while proximal tubule-specific deletion of AGT using the KAP promoter-Cre transgene did not alter BP. The latter study may not have completely eliminated nephron AGT production; in addition, BP was only assessed on a normal salt diet. To evaluate this issue in greater detail, we developed mice with inducible nephron-wide AGT deletion. Mice were generated which were hemizygous for the Pax8-rtTA and LC-1 transgenes and homozygous for loxP flanked AGT alleles to achieve nephron-specific AGT disruption after doxycycline induction. Adult Pax8-rtTA/LC-1/floxed AGT mice at 3 months of age were treated with doxycycline 2 mg/ml in drinking water for 11 days and studied 4 weeks after treatment. Blood pressure (recorded via telemetry) and metabolic balance studies were determined during 5 days of normal, high and low Na diets. Compared to controls, AGT knockout (KO) mice demonstrated significantly lower systolic, diastolic, and mean BPs on all three diets (N=4 each group). The BP reduction was most evident on a low Na diet (mean BP 107 ± 2 mmHg in controls and 88 ± 13 mmHg in AGT KO). Plasma renin concentration was higher in the AGT KO mice as compared to controls on all three diets. There were no detectable differences in weight, urine volume, urine osmolality or urine Na excretion between the controls and KO mice on all three diets, however due to variability, small differences in these parameters may not have been detected. Taken together, these data suggest that nephron AGT may contribute to BP regulation and this is most evident during low Na intake.

Abstract 42: AT1 Angiotensin Receptors in Principal Cells of the Collecting Duct Have Minimal Impact on Blood Pressure and the Development of Hypertension.

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Daian Chen ◽  
Johannes Stegbauer ◽  
Matthew A. Sparks ◽  
Donald Kohan ◽  
Susan B. Gurley ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Collecting Duct ◽  
Weight Ratio ◽  
Angiotensin Receptors ◽  
Mrna Levels ◽  
Ang Ii ◽  
Mouse Line ◽  
Dietary Salt ◽  
Transgenic Mouse Line

The main actions of the renin angiotensin system to control blood pressure (BP) are mediated by the angiotensin type 1 receptors (AT 1 R). The major murine AT 1 R isoform, AT 1A is highly expressed in epithelial cells throughout the nephron, including the collecting duct (CD). The CD consists of two cell types, principal (PC) and intercalated cells (IC) with distinct functions. Activation of AT 1 R in PC stimulates solute reabsorption in the CD by increasing the activity of epithelial sodium channels. To examine the role of the AT 1A R in the PC to BP regulation and the development of hypertension in vivo , we generated inbred 129SvEv mice with cell-specific deletion of AT 1A R in PC (PC-KO, n=6). AQP2-Cre transgenic mouse line was used to excise the floxed Agtr1a allele in PC. mTmG reporter mouse line was used to confirm specific expression of AQP2-Cre transgene in PC, and found the pattern of expression to be predominantly in medullary CD. Using RT-PCR, mRNA levels for AT 1A R were reduced by ≈50% in the inner medulla of PC-KO mice ( P <0.05), but unaffected in cortex. Baseline BP measured by radiotelemetry was similar between PC-KO (122±1.6 mm Hg) and controls (122±1.6 mm Hg). During one week of feeding a low salt (<0.002% NaCl) diet, MAP fell significantly (P<0.05) and to a similar extent in both groups, (PC-KO: 116±1 mm Hg; Controls: 117±2 mm Hg). High salt (6% NaCl) diet increased BP (P<0.01), but was not different between groups (PC-KO: 129±2 mm Hg; Controls: 131±2 mm Hg). Finally, we induced hypertension with chronic infusion of Ang II (1000 ng/kg/min) by osmotic mini-pumps. During the initial phase (days 1-8), there was a modest but significant attenuation of hypertension in PC-KO (167±7 mm Hg) compared to controls (178±3 mm Hg, P<0.001). However, by day 9 levels of BP were indistinguishable between groups and there was no difference in BP in the later phase (days 9-14) of hypertension (PC-KO: 175±12 mm Hg; Controls: 177±7 mm Hg). Heart to body weight ratio after Ang II infusion was not different between groups. In summary, AT 1A R in PC of the medullary CD have little influence on BP, adaptation to changes in dietary salt intake or development of hypertension. We suggest that other mediators, such as aldosterone, may have a more important role to influence sodium handling in this nephron segment.

Effect of Saralasin and Serum in Myohaemoglobinuric Acute Renal Failure of Rats

1978 ◽  
Vol 54 (5) ◽  
pp. 555-560
Author(s):  
K. Bauereiss ◽  
K. G. Hofbauer ◽  
A. Konrads ◽  
F. Gross
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Plasma Concentrations ◽  
Urine Volume ◽  
Plasma Renin ◽  
Urine Osmolality ◽  
Rat Serum ◽  
Renin Substrate ◽  
Plasma Urea ◽  
Solute Excretion

1. In rats deprived of food and water for 24 h acute renal failure was produced by the intramuscular injection of glycerol. Eight hours later plasma urea concentration had increased threefold despite a small rise in urine volume. Plasma concentrations of renin and renin substrate were elevated. 2. When saralasin, a competitive antagonist of angiotensin II, was infused for 8 h after glycerol injection, urine volume and plasma urea were similar to values in rats that had received an infusion of saline. 3. Administration of rat serum (4·5 ml h−1 kg−1) for 4 h suppressed plasma renin concentrations, but plasma urea increased to the same extent as in rats without serum. 4. When saralasin and serum were infused at the same time, urine volume, urine osmolality and solute excretion increased and the rise of plasma urea was diminished. 5. Saralasin has a protective effect against glycerol-induced acute renal failure only when volume is replaced concomitantly.

scholarly journals Long-term aldosterone treatment induces decreased apical but increased basolateral expression of AQP2 in CCD of rat kidney

2007 ◽  
Vol 293 (1) ◽  
pp. F87-F99 ◽  
Author(s):  
Sophie de Seigneux ◽  
Jakob Nielsen ◽  
Emma T. B. Olesen ◽  
Henrik Dimke ◽  
Tae-Hwan Kwon ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Rat Kidney ◽  
Urine Volume ◽  
Urine Osmolality ◽  
Sodium Reabsorption ◽  
Urinary Concentration ◽  
High Dose ◽  
Free Access ◽  
Cortical Collecting Duct ◽  
Water Metabolism

The purpose of the present studies was to determine the effects of high-dose aldosterone and dDAVP treatment on renal aquaporin-2 (AQP2) regulation and urinary concentration. Rats were treated for 6 days with either vehicle (CON; n = 8), dDAVP (0.5 ng/h, dDAVP, n = 10), aldosterone (Aldo, 150 μg/day, n = 10) or combined dDAVP and aldosterone treatment (dDAVP+Aldo, n = 10) and had free access to water with a fixed food intake. Aldosterone treatment induced hypokalemia, decreased urine osmolality, and increased the urine volume and water intake in ALDO compared with CON and dDAVP+Aldo compared with dDAVP. Immunohistochemistry and semiquantitative laser confocal microscopy revealed a distinct increase in basolateral domain AQP2 labeling in cortical collecting duct (CCD) principal cells and a reduction in apical domain labeling in Aldo compared with CON rats. Given the presence of hypokalemia in aldosterone-treated rats, we studied dietary-induced hypokalemia in rats, which also reduced apical AQP2 expression in the CCD but did not induce any increase in basolateral AQP2 expression in the CCD as observed with aldosterone treatment. The aldosterone-induced basolateral AQP2 expression in the CCD was thus independent of hypokalemia but was dependent on the presence of sodium and aldosterone. This redistribution was clearly blocked by mineralocorticoid receptor blockade. The increased basolateral expression of AQP2 induced by aldosterone may play a significant role in water metabolism in conditions with increased sodium reabsorption in the CCD.

Correlation of Cigarette-Induced Increase in Serum Nicotine Levels with Arginine Vasopressin Concentrations in the Syndrome of Self-Induced Water Intoxication and Psychosis (SIWIP)

1986 ◽  
Vol 31 (2) ◽  
pp. 108-111 ◽  
Author(s):  
W.V.R. Vieweg ◽  
J.J. David ◽  
W.T. Rowe ◽  
M.J. Peach ◽  
J.D. Veldhuis ◽  
...  
Keyword(s):  
Arginine Vasopressin ◽  
Urine Volume ◽  
Urine Osmolality ◽  
Depressive Illness ◽  
Water Intoxication ◽  
Manic Depressive Illness ◽  
Water Metabolism ◽  
Water Drinking ◽  
Manic Depressive ◽  
Plasma Arginine

Ten patients [9 men and 1 woman; mean age 42.4 ± 8.5 (± SD) years] who were smokers and who suffered the complications of self-induced water intoxication and psychosis (SIWIP) (8 patients with schizophrenic disorders, 1 patient with manic-depressive illness, 1 patient with dementia) are reported. Each patient underwent serial determinations of parameters of water metabolism including plasma and urine osmolality and plasma arginine vasopressin (AVP). The syndrome of inappropriate antidiuresis (SIAD) was found in each patient. Because of the reported effect that cigarette smoking has on anti-diuresis, we correlated serum nicotine (NIC) levels with plasma and urine osmolality, AVP, and 24-hour urine volume (24°-UV). We found no relationship between NIC and plasma or urine osmolality, AVP, or 24°-UV. In the presence of SIWIP and SIAD, we infer the limbic-hypothalamic neurotransmitters in these psychotic patients are sufficiently powerful in stimulating both compulsive water drinking and inappropriate release of AVP so as to overshadow any effects that NIC may have on water metabolism.

Abstract P023: Relationship Between TNF-α And SBP In The Baseline Cohort Of The Dietary Approaches To Stop Hypertension (DASH)-Sodium Trial

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Khalid Farhan ◽  
Elizabeth D Drugge ◽  
Hong Zhou ◽  
Lesley Graham ◽  
Shoujin Hao ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Control Diet ◽  
Secondary Analysis ◽  
Urine Volume ◽  
Urinary Sodium ◽  
Dietary Salt ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Urinary Potassium ◽  
Sodium And Potassium

Hypertension (HTN) is a leading global noncommunicable cause of mortality and dietary salt is the most common modifiable risk factor for HTN. Evidence suggests that tumor necrosis factor alpha (TNF-α) modulates mechanisms that may contribute to salt-sensitive hypertension (SSHT). We conducted a secondary analysis of the baseline cohort of the DASH-Sodium trial, to explore the relationship between TNF-α and systolic blood pressure (SBP) in subjects categorized by race, sex, and baseline blood pressure. Urinary TNF-α levels adjusted for creatinine (pg/mg) were measured in (91%) (374 of 412) subjects ingesting high salt (150 mmol) and control diet for 2 weeks prior to randomization. Descriptive analyses were used to determine the sample prevalence of demographic, laboratory, and outcome variables, and bivariate analyses were used to check for highly correlated variables. Robust multiple linear regression was used to evaluate the association of TNF-α and SBP with and without covariates, p < 0.05. SBP, urinary sodium and potassium adjusted for creatinine, and 24-hour urine volume were positively associated with TNF-α, whereas African American, male, and increasing waist circumference exhibited negative associations with TNF-α, p < 0.05. Predicted TNF-α increased from 22.7 (19.3,26.8) to 33.2 (26.9,41.0) pg/mg with increasing SBP (100 to 180 mm Hg). TNF-α was 25.4 (23.7, 27.1) pg/mg for AA vs. 28.9 (27.2, 30.8) pg/mg for non-AA, and 24.2 (22.6, 25.9) for males vs. (27.3, 30.7) pg/mg for females, respectively. TNF-α increased from 22.3 (20.3, 24.5) to 46.8 (36.1, 60.7) pg/mg as urinary potassium increased from 10 to 100 mg/g, and from 22.7 (20.3, 25.5) to 33.1 (29.0, 37.8) pg/mg as urinary sodium increased from 10 to 250 mg/g. There was a statistically significant interaction between urinary sodium and potassium: TNFα increased to a greater extent with increasing urinary potassium at a lower level of urinary sodium (-1 SD),16.7 (14.0, 20.2) to 38.1 (31.3, 47.3) pg/mg compared to that at higher urinary sodium levels (+1SD), 24.4 (21.0, 28.4) to 35.2 (30.9, 40.1) pg/mg. These results suggest that TNF-α may regulate ion transport mechanisms that contribute to differences in potassium handling and changes in sodium and potassium excretion observed in SSHT.

The hypertrophic heart rat: a new normotensive model of genetic cardiac and cardiomyocyte hypertrophy

2002 ◽  
Vol 9 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Stephen B. Harrap ◽  
Vennetia R. Danes ◽  
Justine A. Ellis ◽  
Cory D. Griffiths ◽  
Elizabeth F. Jones ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Ventricular Hypertrophy ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Cardiomyocyte Hypertrophy ◽  
Spontaneously Hypertensive ◽  
Fischer 344 ◽  
Lv Mass ◽  
Low Blood Pressure

We describe a new line of rats with inherited cardiomyocyte and ventricular hypertrophy. From a second-generation cross of spontaneously hypertensive and Fischer 344 rats, we selected for low blood pressure and either high or low echocardiographic left ventricular (LV) mass over four generations to establish the hypertrophic heart rat (HHR) and normal heart rat (NHR) lines, respectively. After 13 generations of inbreeding, HHR had significantly greater ( P < 0.0001) LV mass-to-body weight ratio (2.68 g/kg, SE 0.14) than NHR matched for age (1.94 g/kg, SE 0.02) or body weight (2.13 g/kg, SE 0.03). The isolated cardiomyocytes of HHR were significantly ( P < 0.0001) longer and wider (161 μm, SE 0.83; 35.6 μm, SE 2.9) than NHR (132 μm, SE 1.2; 29.5 μm, SE 0.35). Telemetric 24-h recordings of mean arterial pressure revealed no significant differences between HHR and NHR. The HHR offers a new model of primary cardiomyocyte hypertrophy with normal blood pressure in which to examine genotypic causes and pathogenetic mechanisms of hypertrophy and its complications.

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