Search Criteria: Research Area is "Cardiovascular Research: Hypotension"
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 002682 | B6.129P2-Agtr1atm1Unc/J | Repository- Live |
| Mice homozygous mice for the targeted mutation are viable and fertile. Pressor responses to angiotensin II infusions are absent and blood pressure levels are ~24 mmHg lower than normal wildtype siblings. Heterozygous mice have blood pressure levels ~12 mmHg lower than normal wildtype siblings and show qualitatively altered responses to angiotensin II infusions. | ||
| 003006 | BPL/1J | Repository- Live |
| The hypertensive BPH/2 mice (Stock No. 003005) 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 (Stock No. 003004). The original HBP (high blood pressures) 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
..... 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 | ||
| 004367 | B6.129-Adra2atm1Bkk/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. Expression of the receptor in the brain was significantly reduced as assessed by antagonist binding, which indicated a 90% reduction. The antagonist binding assay is not entirely specific for the receptor, as the residual 10% binding was attributable to a different subtype of receptor. Mutant mice exhibit a resting tachycardia of more than 180 beats/min greater than normal. Although mutant mice do not have elevated blood pressure, administration of the hypotensive agonist, dexmedetomidine, does not reduce blood pressure. Electrical stimulation of isolated heart atria at frequencies mimicking physiological sympathetic nerve activity results in increased release of noradrenaline at high frequencies and inhibited release at low frequencies. Noradrenaline release from isolated wildtype atria is higher at high frequencies than at low frequencies. I
..... For more information please see the full phenotype on the strain data sheet | ||
| 002679 | B6.129P2-Acetm1Unc/J | Repository-Cryopreserved |
| Mice homozygous for the Acetm1Unc targeted mutation lack both the somatic and testicular isozyme forms of the Ace gene. They show reduced viability prior to weaning. Surviving homozygotes are hypotensive with blood pressures ~35 mmHg lower than normal wildtype silbings. Heterozygous male mice have blood pressures 15-20 mmHg below wildtype siblings. Fertility of homozygous males is greatly impaired. Ten to twelve month old female homoygotes exhibit abnormal renal vessels and tubules, increased renin synthesis accompanied by an abnormal expression pattern. | ||
| 004159 | B6.129P2-Adra1btm1Cta/J | Repository-Cryopreserved |
| Mice that are homozygous null for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Adra1b transcripts are detected. The amount of alpha 1 adrenergic recptor binding activity as measured by radioligand assays is dramatically decreased in homozygous liver, heart and cerebral cortex. The blood pressure response induced by increasing doses of phenylephrine is reduced by 45% in comparison to wild type mice. Similarly, phenylephrine-induced contraction of aortic tissue is diminished 25%. This mutant mouse strain represents a model that may be useful in studies related to blood pressure regulation. | ||
| 002777 | B6.129S2-Adra2atm1Lel/J | Repository-Cryopreserved |
| Mice homozygous for this mutation are viable and fertile. They exhibit loss of physiological functions evoked by alpha1-adrenergic receptor agonists and display increased susceptibility to kindling-induced seizures. | ||
| 004165 | B6.129X-Ephx2tm1Gonz/J | Repository-Cryopreserved |
| Mice homozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Ephx2 gene product (mRNA or protein) is detected. Systolic blood pressure is minimally effected in homozygous females but males exhibit markedly lower blood pressure. Both sexes also display an altered arachidonic acid metabolism; renal formation of dihydroxyeicosatrienoic acid is significantly diminished. This mutant mouse strain represents a model that may be useful in studies related to blood pressure regulation. | ||
| 005039 | B6.129X1-Adra1atm1Pcs/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR or RNase protection assay analysis. Total alpha-1 adrenergic receptor binding is reduced by 50% in brain and kidney, and by approximately 30% in heart. Expression of the beta-galactosidase reporter gene under the control of the endogenous gene promoter, is detected in embryonic day 12.5 aged embryos and in adult tissues closely mimicking the endogenous gene expression pattern. The resistance arteries, abdominal aorta, celiac, renal, mesenteric, hepatic, splenic, gastric, testicular, ovarian, iliac, femoral and tail arteries, as well as dermal arterioles, are positive for beta-galactosidase staining. Homozygotes are hypotensive with an 8-12% reduction from wildtype control blood pressure levels, as measured in conscious animals at rest. Administration of an alpha-1 adrenergic receptor specif
..... For more information please see the full phenotype on the strain data sheet | ||
| 003266 | B6;129S7-Epas1tm1Rus/J | Repository-Cryopreserved |
| Mice homozygous for the Epas1tm1Rus 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. | ||
| 002637 | B6SJL-Tg(CAMalpha1b)7Wjk/J | Repository-Cryopreserved |
| Mice carrying the CAMalpha1b transgene display stable myocardial specific hypertrophy with ensuing markers of hypertrophy being elevated. In addition, alpha 1 adrenergic receptor signaling through the Gq-phospholipase C-protein kinase C signaling pathway is enhanced. | ||
| 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. | ||
| 003256 | STOCK Fgf2tm1Doe/J | Repository-Cryopreserved |
| Mice homozygous for the Fgf2tm1Doe targeted-mutant allele have low blood pressure, presumably resulting from low vascular tone, increased megakaryocyte colony stimulation activity-induced megakaryocyte colony formation; increased platelet counts, and decreased IL3-induced colony formation. Vessel layer hypertrophy following vessel injury is not altered in the absence of FGF2. Cardiac hypertrophic response to induced high blood pressure is severely blunted in the absence of FGF2. Both sexes of the mutant exhibit no discernible morphologic or behavioral defects and have a normal life span. Both sexes are fertile and fecundity is normal. | ||
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