All Phenotypes Agtr2<tm1Tin> MGI Mouse

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Phenotypes associated with this allele

Allele Symbol
Allele Name
Allele ID

Agtr2^tm1Tin
targeted mutation 1, Tadashi Inagami
MGI:2178475

Summary

13 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Agtr2^tm1Tin/Agtr2^tm1Tin	involves: 129P2/OlaHsd	MGI:4453876
hm2	Agtr2^tm1Tin/Agtr2^tm1Tin	involves: 129P2/OlaHsd * C57BL/6	MGI:4453872
cn3	Agtr2^tm1Tin/Y Efemp2^tm1.1Hiya/Efemp2^tm1.2Hiya Tg(Tagln-cre)1Her/0	involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * SJL	MGI:5585151
cx4	Agtr1a^tm1Unc/Agtr1a^tm1Unc Agtr1b^tm1Cof/Agtr1b^tm1Cof Agtr2^tm1Tin/Agtr2^tm1Tin	involves: 129P2/OlaHsd * C57BL/6	MGI:4454284
cx5	Agtr1a^tm1Unc/Agtr1a^tm1Unc Agtr1b^tm1Cof/Agtr1b^tm1Cof Agtr2^tm1Tin/Y	involves: 129P2/OlaHsd * C57BL/6	MGI:4454285
cx6	Agtr1b^tm1Cof/Agtr1b^tm1Cof Agtr2^tm1Tin/Y	involves: 129P2/OlaHsd * C57BL/6	MGI:4454287
cx7	Agtr1b^tm1Cof/Agtr1b^tm1Cof Agtr2^tm1Tin/Agtr2^tm1Tin	involves: 129P2/OlaHsd * C57BL/6	MGI:4454288
cx8	Agtr1a^tm1Unc/Agtr1a^tm1Unc Agtr2^tm1Tin/Y	involves: 129P2/OlaHsd * C57BL/6	MGI:4454289
cx9	Agtr1a^tm1Unc/Agtr1a^tm1Unc Agtr2^tm1Tin/Agtr2^tm1Tin	involves: 129P2/OlaHsd * C57BL/6	MGI:4454290
ot10	Agtr2^tm1Tin/Y	B6.129P2-Agtr2^tm1Tin	MGI:4453877
ot11	Agtr2^tm1Tin/Y	involves: 129P2/OlaHsd	MGI:4453871
ot12	Agtr2^tm1Tin/Y	involves: 129P2/OlaHsd * C57BL/6	MGI:2655634
ot13	Agtr2^tm1Tin/Y	SWR.129P2-Agtr2^tm1Tin	MGI:4454268

Allelic Composition	Agtr2^tm1Tin/Agtr2^tm1Tin
Genetic Background	involves: 129P2/OlaHsd

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Agtr2^tm1Tin mutation (0 available); any Agtr2 mutation (11 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

renal/urinary system

decreased renal plasma flow rate ( J:60075 )

• cortical blood flow is lower than in wild-type mice

• at high renal perfusion pressure, renal blood flow is lower than in similarly treated wild-type mice

• as renal perfusion pressure increases, mice fail to exhibit an increase in medullary blood flow unlike in similarly treated wild-type mice

• however, glomerular filtration rate is normal

increased renal vascular resistance ( J:60075 )

• renal vascular resistance is higher than in wild-type mice

abnormal urine homeostasis ( J:60075 )

• at 113 or 118 mm Hg equivalent renal perfusion pressure, diuresis and natriuresis are 3 times lower than in wild-type mice

• as renal perfusion pressure increases, fractional sodium and water excretion curves are shifted rightward compared to in wild-type mice

abnormal urine sodium level ( J:60075 )

• at 113 or 118 mm Hg equivalent renal perfusion pressure, natriuresis is 3 times lower than in wild-type mice

cardiovascular system

decreased renal plasma flow rate ( J:60075 )

• cortical blood flow is lower than in wild-type mice

• at high renal perfusion pressure, renal blood flow is lower than in similarly treated wild-type mice

• as renal perfusion pressure increases, mice fail to exhibit an increase in medullary blood flow unlike in similarly treated wild-type mice

• however, glomerular filtration rate is normal

increased renal vascular resistance ( J:60075 )

• renal vascular resistance is higher than in wild-type mice

homeostasis/metabolism

abnormal urine homeostasis ( J:60075 )

• at 113 or 118 mm Hg equivalent renal perfusion pressure, diuresis and natriuresis are 3 times lower than in wild-type mice

• as renal perfusion pressure increases, fractional sodium and water excretion curves are shifted rightward compared to in wild-type mice

abnormal urine sodium level ( J:60075 )

• at 113 or 118 mm Hg equivalent renal perfusion pressure, natriuresis is 3 times lower than in wild-type mice

Allelic Composition	Agtr2^tm1Tin/Agtr2^tm1Tin
Genetic Background	involves: 129P2/OlaHsd * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Agtr2^tm1Tin mutation (0 available); any Agtr2 mutation (11 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

renal/urinary system

abnormal renal/urinary system morphology ( J:52542 )

• 23 males and 5 females out of 112 males and 91 females exhibit congenital anomalies of the kidney and urinary tract unlike wild-type mice with greater frequency in male mice and frequent unilaterality

• 23% of affected mice exhibit ureteripelvic junction, 20% hydronephrotic kidney and hydroureter, 13% hypoplastic kidney, 29% multicystic dysplastic kidney, 10% megaureter, and 6% aplastic kidney unlike wild-type mice

• at E18.5, an affected mouse exhibited vesicoureteral junction stenosis or ureterovesical reflux unlike wild-type mice

abnormal kidney morphology ( J:52542 )

• in some affected mice

polycystic kidney ( J:52542 )

• 29% of affected mice display multicystic dysplastic kidney

abnormal kidney development ( J:52542 )

• premature tubules and glomeruli surrounded by undifferentiated mesenchymal cells in some affected mice

hydronephrosis ( J:52542 )

• 20% of affected mice display hydronephrosis and hydroureter, associated with thinning of the renal parenchyma

decreased kidney weight ( J:137944 )

renal hypoplasia ( J:52542 )

• 13% of affected mice show renal hypoplasia

absent kidney ( J:52542 )

• 6% of affected mice show no trace of renal tissue despite the presence of the ureter

ectopic kidney ( J:52542 )

• some affected mice exhibit abnormal rotation or ascent of the kidneys compared with wild-type mice

abnormal ureter development ( J:52542 )

• at E16.5, some affected mice exhibit an increase in the number of undifferentiated mesenchymal cells surrounding the middle portion of the ureter and a lower frequency of apoptotic cells around the ureter compared with wild-type mice

dilated ureter ( J:52542 )

• dilated and tortuous in some affected mice

double ureter ( J:52542 )

• double ureter in an affected mouse at E17.5

hydroureter ( J:52542 )

• 20% of affected mice display hydronephrosis and hydroureter, associated with thinning of the renal parenchyma

large ureter ( J:52542 )

• 10% of affected mice display a megaureter without hydronephrosis, apparent obstruction or atresia of the ureter

ureteropelvic junction atresia ( J:52542 )

• some affected mice exhibit ureteropelvic junction atresia unlike wild-type mice

ureteropelvic junction stenosis ( J:52542 )

• 23% of affected mice exhibit ureteropelvic junction stenosis unlike wild-type mice

ureterovesical junction obstruction ( J:52542 )

• ureterovesical junction stenosis is accompanied by both hydronephrosis and hydroureter

abnormal renal/urinary system physiology ( J:52542 )

• the minimum pressure required to induce backflux of dye from the bladder to the ureter in affected mice is lower than in wild-type mice

• at E16.5, some affected mice exhibit a lower frequency of apoptotic cells around the ureter compared with wild-type mice

• undifferentiated mesenchymal cells from affected mice exhibit reduced Angiotensin 2-induced apoptosis compared with similarly treated wild-type cells

vesicoureteral reflux ( J:52542 )

• VUR is accompanied by both hydronephrosis and hydroureter

homeostasis/metabolism

increased circulating adrenocorticotropin level ( J:102984 )

increased adrenaline level ( J:102984 )

• adrenal epinepherine levels are increased compared to in wild-type mice

increased noradrenaline level ( J:102984 )

• adrenal norepinepherine levels are increased compared to in wild-type mice

abnormal aldosterone level ( J:102984 )

• adrenal aldosterone content is reduced by 70% compared to that in wild-type mice

• however, plasma aldosterone levels are normal

abnormal corticosterone level ( J:102984 )

• adrenal corticosterone levels are slightly reduced compared to in wild-type mice

increased circulating corticosterone level ( J:102984 )

abnormal response/metabolism to endogenous compounds ( J:137944 )

• Et-1-treated mice exhibit a positive chronotropic effect unlike wild-type mice

increased physiological sensitivity to xenobiotic ( J:146326 )

• mice exposed to repeated treatments with cerulein to induce pancreatitis exhibit a greater decrease in pancreas weight, more severe alterations in pancreas morphology with replacement of acinar cell architecture with fibrous stromal tubular structures, and increased fibrosis compared to in similarly treated wild-type mice

cardiovascular system

decreased heart weight ( J:137944 )

abnormal heart rate ( J:137944 )

• Et-1-treated mice exhibit a positive chronotropic effect unlike wild-type mice

increased mean systemic arterial blood pressure ( J:137944 )

endocrine/exocrine glands

abnormal pancreas morphology ( J:146326 )

• mice exposed to repeated treatments with cerulein to induce pancreatitis exhibit a more severe alterations in pancreas morphology than similarly treated wild-type mice with replacement of acinar cell architecture with fibrous stromal tubular structures

pancreatic acinar cell atrophy ( J:146326 )

• mice exposed to repeated treatments with cerulein to induce pancreatitis exhibit replacement of acinar cell architecture with fibrous stromal tubular structures unlike similarly treated wild-type mice

decreased pancreas weight ( J:146326 )

• mice exposed to repeated treatments with cerulein to induce pancreatitis exhibit a greater decrease in pancreas weight than similarly treated wild-type mice

pancreas fibrosis ( J:146326 )

• following repetitive cerulein treatment

digestive/alimentary system

pancreatic acinar cell atrophy ( J:146326 )

growth/size/body

polycystic kidney ( J:52542 )

• 29% of affected mice display multicystic dysplastic kidney

Allelic Composition	Agtr2^tm1Tin/Y Efemp2^tm1.1Hiya/Efemp2^tm1.2Hiya Tg(Tagln-cre)1Her/0
Genetic Background	involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Agtr2^tm1Tin mutation (0 available); any Agtr2 mutation (11 available)
Efemp2^tm1.1Hiya mutation (0 available); any Efemp2 mutation (26 available)
Efemp2^tm1.2Hiya mutation (0 available); any Efemp2 mutation (26 available)
Tg(Tagln-cre)1Her mutation (2 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cardiovascular system

abnormal aorta smooth muscle morphology ( J:213282 )

• hyperproliferation and disarray of aorta smooth muscle cells at 3 months of age

increased aorta wall thickness ( J:213282 )

• the medium of the aortic wall is thicker than in single Agtr2 mutants, with hyperproliferation and disarray of smooth muscle cells at 3 months of age

ascending aorta aneurysm ( J:213282 )

• mice develop aneurysms

• treatment with losartan completely prevents aneurysms

muscle

abnormal aorta smooth muscle morphology ( J:213282 )

• hyperproliferation and disarray of aorta smooth muscle cells at 3 months of age

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
aortic aneurysm		DOID:3627		J:213282

Allelic Composition	Agtr1a^tm1Unc/Agtr1a^tm1Unc Agtr1b^tm1Cof/Agtr1b^tm1Cof Agtr2^tm1Tin/Agtr2^tm1Tin
Genetic Background	involves: 129P2/OlaHsd * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Agtr1a^tm1Unc mutation (1 available); any Agtr1a mutation (40 available)
Agtr1b^tm1Cof mutation (0 available); any Agtr1b mutation (18 available)
Agtr2^tm1Tin mutation (0 available); any Agtr2 mutation (11 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

postnatal lethality, incomplete penetrance ( J:137944 )

• fewer than expected mice are present at weaning

cardiovascular system

decreased heart weight ( J:137944 )

abnormal heart rate ( J:137944 )

• compared with wild-type mice and Agtr1a^tm1Unc homozygotes

decreased heart rate ( J:137944 )

• compared with wild-type mice and Agtr1a^tm1Unc homozygotes

abnormal systemic arterial blood pressure ( J:137944 )

• Ang II-treated mice exhibit an almost completely blunted increase in mean arterial blood pressure (MAP) and heart rate with a shortened time to peak MAP and an increased time to normalization of MAP compared with similarly treated wild-type mice

• PE-treated mice exhibit a smaller increase in MAP compared with similarly treated wild-type mice

decreased mean systemic arterial blood pressure ( J:137944 )

• compared with wild-type mice and Agtr1a^tm1Unc homozygotes

homeostasis/metabolism

abnormal response/metabolism to endogenous compounds ( J:137944 )

• angiotensin II (Ang II)-treated mice exhibit an almost completely blunted increase in mean arterial blood pressure (MAP) and heart rate with a shortened time to peak MAP and an increased time to normalization of MAP compared with similarly treated wild-type mice

• endothelin 1 (Et-1)-treated mice exhibit a positive chronotropic effect unlike wild-type mice

abnormal physiological response to xenobiotic ( J:137944 )

• phenylephrine (PE)-treated mice exhibit a smaller increase in MAP and fail to exhibit any chronotropic response compared with similarly treated wild-type mice

renal/urinary system

hydronephrosis ( J:137944 )

• in some mice

decreased kidney weight ( J:137944 )

• compared with wild type mice and Agtr1a^tm1Unc Agtr1b^tm1Cof double homozygotes

growth/size/body

decreased body weight ( J:137944 )

• compared with wild-type mice that is not as severe as in Agtr1a^tm1Unc Agtr1b^tm1Cof double homozygotes

Allelic Composition	Agtr1a^tm1Unc/Agtr1a^tm1Unc Agtr1b^tm1Cof/Agtr1b^tm1Cof Agtr2^tm1Tin/Y
Genetic Background	involves: 129P2/OlaHsd * C57BL/6

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

postnatal lethality, incomplete penetrance ( J:137944 )

• fewer than expected mice are present at weaning

cardiovascular system

decreased heart weight ( J:137944 )

abnormal heart rate ( J:137944 )

• compared with wild-type mice and Agtr1a^tm1Unc homozygotes

decreased heart rate ( J:137944 )

• compared with wild-type mice and Agtr1a^tm1Unc homozygotes

abnormal systemic arterial blood pressure ( J:137944 )

• PE-treated mice exhibit a smaller increase in MAP compared with similarly treated wild-type mice

decreased mean systemic arterial blood pressure ( J:137944 )

• compared with wild-type mice and Agtr1a^tm1Unc homozygotes

homeostasis/metabolism

abnormal response/metabolism to endogenous compounds ( J:137944 )

• endothelin 1 (Et-1)-treated mice exhibit a positive chronotropic effect unlike wild-type mice

abnormal physiological response to xenobiotic ( J:137944 )

• phenylephrine (PE)-treated mice exhibit a smaller increase in MAP and fail to exhibit any chronotropic response compared with similarly treated wild-type mice

renal/urinary system

hydronephrosis ( J:137944 )

• in some mice

decreased kidney weight ( J:137944 )

• compared with wild type mice and Agtr1a^tm1Unc Agtr1b^tm1Cof double homozygotes

growth/size/body

decreased body weight ( J:137944 )

• compared with wild-type mice that is not as severe as in Agtr1a^tm1Unc Agtr1b^tm1Cof double homozygotes

Allelic Composition	Agtr1b^tm1Cof/Agtr1b^tm1Cof Agtr2^tm1Tin/Y
Genetic Background	involves: 129P2/OlaHsd * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Agtr1b^tm1Cof mutation (0 available); any Agtr1b mutation (18 available)
Agtr2^tm1Tin mutation (0 available); any Agtr2 mutation (11 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

renal/urinary system

abnormal renal glomerulus morphology ( J:137944 )

• mice exhibit hyperemic capillary loops unlike wild-type mice

• however, glomeruli are well perfused with distinct basal membranes

decreased kidney weight ( J:137944 )

cardiovascular system

increased mean systemic arterial blood pressure ( J:137944 )

growth/size/body

decreased body weight ( J:137944 )

Allelic Composition	Agtr1b^tm1Cof/Agtr1b^tm1Cof Agtr2^tm1Tin/Agtr2^tm1Tin
Genetic Background	involves: 129P2/OlaHsd * C57BL/6

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

renal/urinary system

abnormal renal glomerulus morphology ( J:137944 )

• mice exhibit hyperemic capillary loops unlike wild-type mice

• however, glomeruli are well perfused with distinct basal membranes

decreased kidney weight ( J:137944 )

cardiovascular system

increased mean systemic arterial blood pressure ( J:137944 )

growth/size/body

decreased body weight ( J:137944 )

Allelic Composition	Agtr1a^tm1Unc/Agtr1a^tm1Unc Agtr2^tm1Tin/Y
Genetic Background	involves: 129P2/OlaHsd * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Agtr1a^tm1Unc mutation (1 available); any Agtr1a mutation (40 available)
Agtr2^tm1Tin mutation (0 available); any Agtr2 mutation (11 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cardiovascular system

decreased heart weight ( J:137944 )

abnormal heart rate ( J:137944 )

• Ang II-treated mice exhibit less of an increase in mean arterial blood pressure and heart rate compared with similarly treated wild-type mice

decreased heart rate ( J:137944 )

abnormal systemic arterial blood pressure ( J:137944 )

• Ang II-treated mice exhibit less of an increase in mean arterial blood pressure and heart rate compared with similarly treated wild-type mice

decreased mean systemic arterial blood pressure ( J:137944 )

homeostasis/metabolism

abnormal circulating protein level ( J:137944 )

• serum levels of Ang II are increased compared to in wild-type mice

abnormal response/metabolism to endogenous compounds ( J:137944 )

• angeotensin II (Ang II)-treated mice exhibit less of an increase in mean arterial blood pressure and heart rate compared with similarly treated wild-type mice

renal/urinary system

increased glomerular capsule space ( J:137944 )

• mice exhibit cystic dilated Bowman's space unlike wild-type mice

renal glomerulus atrophy ( J:137944 )

• mice exhibit multifocal glomeruli atrophy unlike wild-type mice

decreased kidney weight ( J:137944 )

Allelic Composition	Agtr1a^tm1Unc/Agtr1a^tm1Unc Agtr2^tm1Tin/Agtr2^tm1Tin
Genetic Background	involves: 129P2/OlaHsd * C57BL/6

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cardiovascular system

decreased heart weight ( J:137944 )

abnormal heart rate ( J:137944 )

• Ang II-treated mice exhibit less of an increase in mean arterial blood pressure and heart rate compared with similarly treated wild-type mice

decreased heart rate ( J:137944 )

abnormal systemic arterial blood pressure ( J:137944 )

• Ang II-treated mice exhibit less of an increase in mean arterial blood pressure and heart rate compared with similarly treated wild-type mice

decreased mean systemic arterial blood pressure ( J:137944 )

homeostasis/metabolism

abnormal circulating protein level ( J:137944 )

• serum levels of Ang II are increased compared to in wild-type mice

abnormal response/metabolism to endogenous compounds ( J:137944 )

• angeotensin II (Ang II)-treated mice exhibit less of an increase in mean arterial blood pressure and heart rate compared with similarly treated wild-type mice

renal/urinary system

increased glomerular capsule space ( J:137944 )

• mice exhibit cystic dilated Bowman's space unlike wild-type mice

renal glomerulus atrophy ( J:137944 )

• mice exhibit multifocal glomeruli atrophy unlike wild-type mice

decreased kidney weight ( J:137944 )

Allelic Composition	Agtr2^tm1Tin/Y
Genetic Background	B6.129P2-Agtr2^tm1Tin

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Agtr2^tm1Tin mutation (0 available); any Agtr2 mutation (11 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:146723 )

• one week after myocardial infarction, more mice exhibit death due to cardiac rupture compared with similarly treated wild-type mice

• however, 6 week survival following myocardial infarction is normal

cardiovascular system

abnormal myocardial fiber morphology ( J:63751 )

• following aorta banding, cardiomyocyte cross-sectional area does not increase as much as in similarly treated wild-type mice

thin interventricular septum ( J:63751 )

• the intraventricular septum is thinner than in wild-type mice

abnormal heart left ventricle morphology ( J:146723 )

• after myocardial infarction, the increase in left ventricular internal diameter at end diastole and end systole is less than similarly treated wild-type mice

decreased heart left ventricle weight ( J:146723 )

• prior to and after myocardial infarction

decreased heart left ventricle posterior wall thickness ( J:63751 )

• the left ventricular posterior wall is thinner than in wild-type mice

cardiac fibrosis ( J:63751 , J:146723 )

• following aorta banding, mice exhibit less left ventricular and interstitial fibrosis compared with similarly treated wild-type mice (J:63751)

• after myocardial infarction cardiac fibrosis are reduced compared to in similarly treated wild-type mice (J:146723)

decreased response of heart to induced stress ( J:63751 )

• following aorta banding, mice fail to exhibit as much left ventricle hypertrophy, cardiomyocyte cross-sectional area increase, and left ventricular and interstitial fibrosis as in similarly treated wild-type mice

• however, left ventricular function following aorta banding is the same as in similarly treated wild-type mice

abnormal response to cardiac infarction ( J:146723 )

• one week after myocardial infarction, more mice exhibit death due to cardiac rupture compared with similarly treated wild-type mice

• after myocardial infarction, the increase in left ventricular internal diameter at end diastole and end systole is less than similarly treated wild-type mice

• after myocardial infarction, percent infarct area and cardiac fibrosis are reduced compared to in similarly treated wild-type mice

• however, 6 week survival following myocardial infarction is normal

homeostasis/metabolism

decreased response of heart to induced stress ( J:63751 )

• however, left ventricular function following aorta banding is the same as in similarly treated wild-type mice

abnormal response to cardiac infarction ( J:146723 )

• one week after myocardial infarction, more mice exhibit death due to cardiac rupture compared with similarly treated wild-type mice

• after myocardial infarction, the increase in left ventricular internal diameter at end diastole and end systole is less than similarly treated wild-type mice

• after myocardial infarction, percent infarct area and cardiac fibrosis are reduced compared to in similarly treated wild-type mice

• however, 6 week survival following myocardial infarction is normal

muscle

abnormal myocardial fiber morphology ( J:63751 )

• following aorta banding, cardiomyocyte cross-sectional area does not increase as much as in similarly treated wild-type mice

Allelic Composition	Agtr2^tm1Tin/Y
Genetic Background	involves: 129P2/OlaHsd

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Agtr2^tm1Tin mutation (0 available); any Agtr2 mutation (11 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

homeostasis/metabolism

abnormal circulating leptin level ( J:105210 )

• unlike wild-type mice fed a high fat diet, similarly treated wild-type mice fail to exhibit hyperleptinemia

increased energy expenditure ( J:105210 )

• when fed a high fat diet

decreased susceptibility to diet-induced obesity ( J:105210 )

• when fed standard chow or a high fat diet

abnormal respiratory quotient ( J:105210 )

• during the light phase when fed standard chow

• during the dark phase when fed a high fat diet

abnormal glucose homeostasis ( J:105210 )

• unlike in wild-type mice, glucose oxidation and glucose conversion into lipids is not stimulated by Ang II with or without angiotensin II receptor, type 1a, antagonists

• when fed a high fat diet, glucose clearance is increased compared to in similarly treated wild-type mice

abnormal circulating insulin level ( J:105210 )

• unlike wild-type mice fed a high fat diet, mice fail to exhibit an increase in plasma insulin levels

increased insulin sensitivity ( J:105210 )

• when fed standard chow or a high fat diet

abnormal lipid homeostasis ( J:105210 )

• lipid oxidation is increased 30% compared to in wild-type mice

• when fed a high fat diet, mice exhibit increased lipid oxidation compared to in similarly treated wild-type mice

abnormal skeletal muscle triglyceride level ( J:105210 )

• when fed a high fat diet, mice fail to exhibit as much of an increase in muscle triglyceride content as in similarly treated wild-type mice

abnormal urine homeostasis ( J:60075 )

• at 113 or 118 mm Hg equivalent renal perfusion pressure, diuresis and natriuresis are 3 times lower than in wild-type mice

• as renal perfusion pressure increases, fractional sodium and water excretion curves are shifted rightward compared to in wild-type mice

abnormal urine sodium level ( J:60075 )

• at 113 or 118 mm Hg equivalent renal perfusion pressure, natriuresis is 3 times lower than in wild-type mice

abnormal response/metabolism to endogenous compounds ( J:105210 )

• unlike in wild-type mice, glucose oxidation and glucose conversion into lipids is not stimulated by Ang II with or without angiotensin II receptor, type 1a, antagonists

increased physiological sensitivity to xenobiotic ( J:103144 )

• L-NAME-treated mice exhibit a greater increase in blood pressure and reduced heart rate variability compared with similarly treated wild-type mice

muscle

abnormal skeletal muscle triglyceride level ( J:105210 )

• when fed a high fat diet, mice fail to exhibit as much of an increase in muscle triglyceride content as in similarly treated wild-type mice

nervous system

abnormal habenula morphology ( J:102774 )

• the number of cells in the medial habenula is increased compared to in wild-type mice