JAX Mice Database - Hypertension

Search Criteria: Research Area is "Cardiovascular Research: Hypertension"

JAX^® Mice Strains

Stock Number	Strain Name Phenotype	Standard Supply
002684	B6.129P2-Nos3^tm1Unc/J	Level 2
	Mice homozygous for the Nos3^tm1Unc targeted mutation are viable and fertile. They have elevated blood pressure that is about 20 mmHg higher than that seen in normal wildtype siblings. They also show a decreased heart rate. Female homozygotes are smaller in body weight than normal wildtype siblings. Hyperglycemic-euglycemic clamp studies demonstrate that homozygotes exhibit insulin resistance at the level of the liver and peripheral tissues.
007175	129S-Cyp4a14^tm1Jhc/J	Repository- Live
	Mice homozygous for this "Cyp 4a14" mutant allele are viable and fertile. Homozygous deficiency of the targeted gene leads to spontaneous hypertension (more severe in males) that is androgen-sensitive. Homozygotes also exhibit other interrelated metabolic and regulatory effects; increased renal vascular resistance, impaired renal hemodynamics, elevated plasma androgens (5a-dihydrotestosterone (DHT) and testosterone), upregulated Cyp4a12 gene expression, and increased formation of prohypertensive 20-HETE. These "Cyp 4a14" mutant mice may be useful studying kidney function and metabolism, cardiovascular physiology, hypertension, and the relationships between blood pressure, sex hormones, and p450 w-hydroxylases.
006860	B6.129-Ins2^Akita Bdkrb2^tm1Jfh/SmiJ	Repository- Live
	Mice homozygous for the targeted mutation and heterozygous for the Akita spontaneous mutation are viable and fertile. Similar to mice only heterozygous for the Akita mutation, the double mutant mice are severely diabetic: their body weights are 70% of wildtype, they consume over 3-fold the normal amount of food, and their urinary output is approximately 20-fold more than that of wildtype mice. Double mutant mice have markedly enlarged kidneys. Urinary albumin excretion in double mutants is almost 4-fold that of either single mutant, and double mutants experience more severe nephropathy than mice that are heterozygous for the Akita mutation alone. Megsin and nephrin expression is markedly increased in double mutant mice when compared to wildtype or to mice with either single mutation alone. By 12 months of age, double mutant mice experience hair loss due to a reduction in hair follicle numbers and thinning of the dermis. Double mutants have essentially no subcutaneo ..... For more information please see the full phenotype on the strain data sheet
007809	B6.129S4-Mc3r^tm1Cone/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable and fertile. Female homozygotes at approximately 50 to 60 days of age exhibit significantly heavier body weight when compared to heterozygotes. No gene product (mRNA) is detected by RT-PCR analysis of hypothalamus tissue. Male homozygotes exhibit an approximately 40% increase in body fat at 15-20 weeks of age when compared to wildtype. Heterozygotes display an intermediate increase in body fat percentage of approximately 36%. Although homozygotes have increased adiposity, there is no increased food intake or weight gain and resting basal or total oxygen consumption is lower in mutant mice when compared to wildtype. High fat diet causes an increased respiratory quotient within 24 hours of the diet change. Homozygotes on a low fat diet have a lower respiratory quotient than wildtype. Male homozygotes exhibit an approximately 50% decrease in wheel running behavior. Mutant mice become hypertensive with increased gamma-melanocyt ..... For more information please see the full phenotype on the strain data sheet
002641	B6;129S7-Bdkrb2^tm1Jfh/J	Repository- Live
	Mice homozygous for the Bdkrb2^tm1Jfh targeted mutation are viable and fertile and display no major defects. Homozygous mutant tissue from the ileum, uterus, and superior cervical ganglia all failed to respond to pharmacological doses of bradykinin. This finding supports the existance of only one type of B2 receptor. B2 deficient mice also display a greater hypertensive response to chronic high sodium intake compared to controls. These mice may be used to study the role of the B2 receptor in hypertension, inflammation, the cardiovascular system, renal function and reproduction.
003005	BPH/2J	Repository- Live
	The hypertensive BPH/2 mice have elevated systolic blood pressures at five weeks and by 150 days differ from the BPL/1 by 60 mmHg. The BPH/2 strain has a higher heart rate, larger hearts and kidneys, and higher hematocrits than the BPL/1. It also has lower renin, aldosterone and angiotensin I levels compared to the BPL/1 and BPN/3. The original HBP (high blood pressure) and LBP (low blood pressure) selected lines showed a number of biochemical and physiological differences which have not been reexamined in the inbred strains. These include differences in brain catecholamines, calmodulin concentrations, heat sensitivity, alcohol preference, and longevity. The differences in longevity were striking. The hypotensive selected lines lived two to three hundred days longer, on average, than the hypertensive selected line. Biometrical genetic analysis suggested that three to five genes are responsible for the difference in blood pressure between the BPH/2 and BPL/1. A recent genome scan of an ..... For more information please see the full phenotype on the strain data sheet
003004	BPN/3J	Repository- Live
	The normotensive BPN/3 inbred strain serves as a control for the high blood pressure (BPH/2, Stock No. 003005) and low blood pressure (BPL/1, Stock No. 003006) inbred strains BPH/2 mice have elevated systolic blood pressures at five weeks and by 150 days differ from the BPL/1 by 60 mmHg. The BPH/2 strain has a higher heart rate, larger hearts and kidneys, and higher hematocrits than the BPL/1. It also has lower renin, aldosterone and angiotensin I levels compared to the BPL/1 and BPN/3. The original HBP (high blood pressure) and LBP (low blood pressure) selected lines showed a number of biochemical and physiological differences which have not been reexamined in the inbred strains. These include differences in brain catecholamines, calmodulin concentrations, heat sensitivity, alcohol preference, and longevity. The differences in longevity were striking. The hypotensive selected lines lived two to three hundred days longer, on average, than the hypertensive selected line. Biometrical ge ..... For more information please see the full phenotype on the strain data sheet
005564	FVB(Cg)-Tg(Ins2-CALM1)26Ove Tg(Cryaa-TAg)1Ove/PneJ	Repository- Live
	Transgenic mice are viable, display small eyes with cataracts and are hyperglycemic within 24 hours of age. S1 Nuclease protection assays indicate expression of calmodulin in the pancreas of 40-60 day old transgenic mice. Immunofluorescence analysis of the pancreas indicates increased levels of camodulin in B-cells of the pancreas. Camodulin fluorescing cells were not detected in the pancreatic acinar cells or any other tissue. Digital image scanning indicates the concentration of camodulin in transgenic B-cells is 5-fold higher than in wild type controls. Pancreatic insulin is 28% of control levels by 15 days of age. Insulin mRNA levels were also reduced in the transgenic animals. Transgenic mice experience hypoalbuminemia, elevated blood pressure, impaired cardiomyocytes and late stage diabetic nephropathy. Although transgenic mice are hyperglycemic within 24 hours of age, they are able to survive over a year without insulin treatment. This stock is useful for studying systemic c ..... For more information please see the full phenotype on the strain data sheet
004374	129-Npr1^tm1Gar/J	Repository-Cryopreserved
	Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) was detected. Homozygous mutant mice have elevated systolic, diastolic and mean blood pressure when compared to wildtype. Heterozygous mutant mice display systolic, diastolic and mean blood pressure that are slightly elevated above wildtype levels. Blood pressure in mutant mice remains elevated independent of salt content in diet. Infusion treatment of atrial natriuretic peptide in mutant mice does not result in the increased urine output or sodium excretion response seen in wildtype mice. Plasma volume expansion to release natriuretic/diuretic factors from the heart fails to induce increased urine output, sodium excretion and cyclic GMP excretion in the mutant. The same plasma volume expansion in wildtype mice results in a 12-fold increase in urine output, a 6-fold increase in sodium excretion and a 4-fold increase in c ..... For more information please see the full phenotype on the strain data sheet
004376	B6.129-Ptger2^tm1Brey/J	Repository-Cryopreserved
	Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Reduced fertility in homozygous females is due to a pre-implantation defect. Fewer eggs are released during ovulation, of which fewer are fertilized and implanted when compared to wildtype controls, resulting in smaller litters (3 pups/litter). Mutant mice display slightly elevated baseline systolic blood pressure. Prostaglandin 2 infusion or high salt diet causes systolic hypertension in homozygous mice. This mutant mouse strain represents a model that may be useful in studies of salt sensitive hypertension and infertility.
002681	B6.129P2-Agt^tm1Unc/J	Repository-Cryopreserved
	Newborn homozygotes for the targeted disruption of Agt have no obvious pathological defects although only a few survive to adulthood. There are pathological changes in adult kidney and blood vessels. The effect of gene copy number was examined using these mice and C57BL/6J-TgH(Agtdup)1Unc (002690). Plasma angiotensinogen levels increase progressively, although not linearly, from zero in zero-copy (Agt^tm1Unc/Agt^tm1Unc) mice to 145% of normal in four-copy (Agt^dup/Agt^dup) mice. Mice of all genotypes are normal at birth, but most zero-copy animals show pathological changes as adults, the kidneys are normal in the other genotypes. The blood pressures of the one-copy through four-copy animals show significant and almost linear increases of approximately 8mmHg per gene copy despite their normal compensatory mechanisms being intact.
002690	B6.129P2-Agt^tm2Unc/J	Repository-Cryopreserved
	The entire agiotensinogen gene (Agt) was duplicated by homologous recombination allowing the examination of the effects of gene copy number on normal AGT function. Homozygous mice (Agtdup/Agtdup) are viable and fertile. They show blood pressure levels ~16 mmHg higher than normal wildtype siblings (two copies of Agt gene). Hemizygous mice (Agtdup/+) show blood pressure levels ~8 mmHg higher than normal wildtype siblings. This transgenic demonstrates the causality between genotypes at the angiotensinogen locus and blood pressures. Blood pressures of one-copy (Agt^tm1Unc/+) through four-copy (Agtdup/Agtdup) animals show significant and almost linear increases of approximately 8mmHg per gene copy despite their normal compensatory mechanisms being intact.
002685	B6.129P2-Nppa^tm1Unc/J	Repository-Cryopreserved
	Homozygotes are viable and fertile. Homozygotes show elevated blood pressure on both high and low salt diets. Heterozygous mice show normal blood pressure on a low salt diet but elevated blood pressue on a high salt diet.
002958	B6.129S4-Drd3^tm1Dac/J	Repository-Cryopreserved
	Mice homozygous for the Drd3^tm1Dac mutation are viable and fertile. They show no gross anatomical or morphological changes. Dopamine antagonist binding studies indicate the absence of D3 receptors in homozygotes and a greatly reduced number in heterozygotes. Behavioral analysis of both homozygous and heterozygous mice reveals hyperactivity, increased locomotor activity and rearing behavior. Behavioral alterations were less pronounced in heterozygotes. D3 receptors are expressed in renal proximal tubules and juxtaglomerular cells and may be responsible for the dopamine-mediated decrease in renin secretion in these cells. Both systolic and diastolic blood pressures were approximately 20 mmHg higher in heterozygotes and homozygotes compared to wild-type mice.
002425	B6;129S4-Drd3^tm1Dac/J	Repository-Cryopreserved
	Mice homozygous for the Drd3^tm1Dac mutation are viable and fertile. They show no gross anatomical or morphological changes. Dopamine antagonist binding studies indicate the absence of D3 receptors in homozygotes and a greatly reduced number in heterozygotes. Behavioral analysis of both homozygous and heterozygous mice reveals hyperactivity, increased locomotor activity and rearing behavior. Behavioral alterations were less pronounced in heterozygotes. D3 receptors are expressed in renal proximal tubules and juxtaglomerular cells and may be responsible for the dopamine-mediated decrease in renin secretion in these cells. Both systolic and diastolic blood pressures were approximately 20 mmHg higher in heterozygotes and homozygotes compared to wild-type mice.
003266	B6;129S7-Epas1^tm1Rus/J	Repository-Cryopreserved
	Mice homozygous for the Epas1^tm1Rus targeted mutation develop normally until embryonic day 11.5. Beginning at embryonic day 12.5 the ratio of homozygous embryos begins to decline and by day 16.5 there are no viable mutant embryos. Overall morphological development, including the circulatory system, is normal. Of particular interest however, is a pronounced bradycardia in homozygous mutant mice. Catecholamine levels in homozygous mutant mice are also significantly lower than wildtype controls. Administration of the catecholamine precursor DOPS to pregnant females rescues approximately 40% of mutant embryos. Embryos that survive to birth appear runted, fail to nurse, and die within 24 hours of birth. These results suggest a pivotal role of EPAS1 in catecholamine homeostasis. Heterozygous mice from this strain contain a modified lacZ gene in the targeting construct. This characteristic makes this strain useful as a marker for endothelial cells.
002749	C57BL/6-Tg(hAGT)2041Sig/J	Repository-Cryopreserved
	This strain carries a human angiotensinogen transgene whose expression results in angiotensinogen plasma concentrations 150X that normally found in human plasma. These mice are normotensive but become transiently hypertensive when injected with a bolus of purified renin. A chronically hypertensive mouse can by created by breeding this strain with a strain carrying the human renin transgene (C57BL/6-TgN(hREN)9Sig; 002750). The mean arterial pressure of the double transgenic is ~155 mmHg (controls ~111 mmHg). Both systolic and diastolic blood pressures are elevated.
002750	C57BL/6-Tg(hREN)9Sig/J	Repository-Cryopreserved
	Mice carrying the human renin transgene have high levels of expression in the kidney, adrenal gland, ovary, testis, lung and adipose. No expression is evident in the liver or brain. Active renin is released into the plasma of the transgenic mice. These mice are normotensive but a chronically hypertensive mouse can be created by breeding this strain with a strain carrying the human angiotensinogen transgene (C57BL/6-TgN(hAGT)2041Sig; 002749). The mean arterial pressure of the double transgenic is ~155 mmHg (controls ~111 mmHg). Both systolic and diastolic blood pressures are elevated.
008411	C57BL/6J-Hlb426/J	Repository-Cryopreserved
	For information on Hlb426 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
004530	C57BL/6J-hlb15/J	Repository-Cryopreserved
	For information on hlb15 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
005863	C57BL/6J-Tg(ACTB-DDAH1)1Jpck/J	Repository-Cryopreserved
	Hemizygous mice are viable and fertile with no anatomic abnormalities. Transgene expression is observed in aorta, heart, and brain. Transgenic dimethylarginine dimethylaminohydrolase (DDAH) activity is reflected in a reduction of plasma asymmetric dimethylarginine (ADMA). Nitric oxide synthase (NOS) activity is significantly increased in transgenic skeletal and cardiac muscle. Transgenic mice have lower blood pressure and higher heart rate. Transgenic mice may be useful in studies of atherosclerosis, hypertension, hyperlipidemia, hypercholesterolemia, hyperhomocystinemia, diabetes mellitus, stroke, renal failure, preeclampsia, and other conditions associated with vascular pathophysiology and/or cardiovascular disease.
003507	D2;B6-Npr3^lgj-2J/J	Repository-Cryopreserved
	Homozygous mutants are identifiable as young as six days of age by their elongated bodies and digits and a conical extension of the body at the base of the tail. Older mice are extremely thin and exhibit arachnodactyly, thoracic kyphosis and, often, kinks in the tail and/or sacrum. Upon necropsy, mice are found to lack normal body fat deposits. No significant craniofacial defects have been observed. Skeletal analysis demonstrated delayed endochondrial ossification, most obvious in the hind- and forepaws but affecting the entire skeleton. Retarded ossification was apparent in neonates and presumably occurs in utero.Both male and female Npr3^lgj-2J/Npr3^lgj-2Jmice are fertile and can breed. An earlier mutation at this locus, Npr3^lgj, in the BALB/cJ inbred strain (stock number 003206) produces a similar phenotype. However, homozygous males of this stock number 003206 cannot reproduce because their more extreme spinal defect prevents ..... For more information please see the full phenotype on the strain data sheet

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New Strains Under Development

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Stock Number	Strain Name Phenotype	Standard Supply
007853	129S/SvEv-Tg(Alb1-Ren)1Unc/CofJ	Under Development for Production
Mice heterozygous for the RenTgMK transgene are viable and fertile. The RenTgMK transgene contains a liver-specific albumin promoter/enhancer controlling the expression of a synthetic renin gene (engineered to allow efficient cleavage and secretion of the prorenin transgene product by the liver). This, and because the transgene was targeted to the apolipoprotein locus on Chromosome 9, results in active renin secretion from the liver independently of renal or other homeostatic cardiovascular control mechanisms (i.e. genetically clamped). RenTgMK heterozygotes have high ectopic levels of active mouse renin in the liver and elevated plasma levels of prorenin and active renin. Heterozygous mice display significantly elevated blood pressure, enhanced thirst, high urine output, proteinuria, and kidney damage. Because active renin overexpression results in increased circulating levels of angiotensin II (Ang II), heterozygotes also exhibit cardiac hypertrophy and 50% male mortality between 6-8 ..... For more information please see the full phenotype on the strain data sheet
008101	B6.129S6(FVB)-Ptgs2^tm1.1Fun/J	Under Development for Production
Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Female homozygotes are not fertile. The protein gene product does not have cyclooxygenase activity while the peroxidase activity is normal as measured by LPS induction of macrophages derived from mutant mice. Mutant mice are more sensitive to collagen treatment resulting in reduction of platelet numbers (indicating enhanced thrombogenesis) and exhibit a higher frequency of sudden death due to thromboxane receptor agonist treatment. No prolonged bleeding time from LPS administration is observed. Prostaglandin E metabolite levels are diminished in urine. Three month old mutant mice have elevated systolic blood pressure (measured by the tail cuff method). Homozygotes exhibit undersize, pale kidneys with atrophic cortices, interstitial inflammation, hypoplastic glomeruli and glomerulosclerosis. This mutant mouse strain may be useful in studi ..... For more information please see the full phenotype on the strain data sheet
008082	B6;SJL-Tg(Tagln-tTA)1Mrab Tg(tetO-Mcpt1)1Mrab/J	Under Development for Production
Hemizygous tTA+/RVCH+ (or SM22a-tTA/TRE-RVCH-HA) mice are viable and fertile, harboring two transgenes using the Tet-Off system. The SM22a-tTA transgene has the 3 kb SM22alpha promoter directing expression of the tetracycline transactivator gene (tTA) to vascular smooth muscle cells (SMCs). The TRE-RVCH-HA transgene has the tetracycline-responsive element (TRE; also called tet-operator or tetO) controlling expression of a rat vascular chymase-hemagglutinin tag (RVCH-HA) fusion gene. In the absence of tetracycline (or its analog doxycycline (dox)), the SM22alpha promoter limits RVCH-HA fusion protein expression to vascular SMCs. This RVCH overexpression results in hypertension. Because this binary transgenic system also allows for a second level of control, i.e. addition of dox, expression of the RVCH-HA fusion protein can be completely abolished; reversing the hypertension phenotype. These SM22a-tTA/TRE-RVCH-HA bi-transgenic mice allow targeted overexpression or Tet-Off conditional exp ..... For more information please see the full phenotype on the strain data sheet

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The Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
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