BIOMAT Database Logo BIOMAT Database Logo

Elevated blood pressures in mice lacking endothelial nitric oxide synthase. 1996

E G Shesely, and N Maeda, and H S Kim, and K M Desai, and J H Krege, and V E Laubach, and P A Sherman, and W C Sessa, and O Smithies
Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill 27599, USA.

Nitric oxide produced in endothelial cells affects vascular tone. To investigate the role of endothelial nitric oxide synthase (eNOS) in blood pressure regulation, we have generated mice heterozygous (+/-) or homozygous (-/-) for disruption of the eNOS gene. Immunohistochemical staining with anti-eNOS antibodies showed reduced amounts of eNOS protein in +/- mice and absence of eNOS protein in -/- mutant mice. Male or female mice of all three eNOS genotypes were indistinguishable in general appearance and histology, except that -/- mice had lower body weights than +/+ or +/- mice. Blood pressures tended to be increased (by approximately 4 mmHg) in +/- mice compared with +/+, while -/- mice had a significant increase in pressure compared with +/+ mice (approximately 18 mmHg) or +/- mice (approximately 14 mmHg). Plasma renin concentration in the -/- mice was nearly twice that of +/+ mice, although kidney renin mRNA was modestly decreased in the -/- mice. Heart rates in the -/- mice were significantly lower than in +/- or +/+ mice. Appropriate genetic controls show that these phenotypes in F2 mice are due to the eNOS mutation and are not due to sequences that might differ between the two parental strains (129 and C57BL/6J) and are linked either to the eNOS locus or to an unlinked chromosomal region containing the renin locus. Thus eNOS is essential for maintenance of normal blood pressures and heart rates. Comparisons between the current eNOS mutant mice and previously generated inducible nitric oxide synthase mutants showed that homozygous mutants for the latter differ in having unaltered blood pressures and heart rates; both are susceptible to lipopolysaccharide-induced death.

UI MeSH Term Description Entries
D006973 Hypertension Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more. Blood Pressure, High,Blood Pressures, High,High Blood Pressure,High Blood Pressures
D007527 Isoenzymes Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics. Alloenzyme,Allozyme,Isoenzyme,Isozyme,Isozymes,Alloenzymes,Allozymes
D007668 Kidney Body organ that filters blood for the secretion of URINE and that regulates ion concentrations. Kidneys
D008070 Lipopolysaccharides Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed) Lipopolysaccharide,Lipoglycans
D008297 Male Males
D008810 Mice, Inbred C57BL One of the first INBRED MOUSE STRAINS to be sequenced. This strain is commonly used as genetic background for transgenic mouse models. Refractory to many tumors, this strain is also preferred model for studying role of genetic variations in development of diseases. Mice, C57BL,Mouse, C57BL,Mouse, Inbred C57BL,C57BL Mice,C57BL Mice, Inbred,C57BL Mouse,C57BL Mouse, Inbred,Inbred C57BL Mice,Inbred C57BL Mouse
D012083 Renin A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC 3.4.99.19. Angiotensin-Forming Enzyme,Angiotensinogenase,Big Renin,Cryorenin,Inactive Renin,Pre-Prorenin,Preprorenin,Prorenin,Angiotensin Forming Enzyme,Pre Prorenin,Renin, Big,Renin, Inactive
D001794 Blood Pressure PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS. Systolic Pressure,Diastolic Pressure,Pulse Pressure,Pressure, Blood,Pressure, Diastolic,Pressure, Pulse,Pressure, Systolic,Pressures, Systolic
D002417 Cattle Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor. Beef Cow,Bos grunniens,Bos indicus,Bos indicus Cattle,Bos taurus,Cow,Cow, Domestic,Dairy Cow,Holstein Cow,Indicine Cattle,Taurine Cattle,Taurus Cattle,Yak,Zebu,Beef Cows,Bos indicus Cattles,Cattle, Bos indicus,Cattle, Indicine,Cattle, Taurine,Cattle, Taurus,Cattles, Bos indicus,Cattles, Indicine,Cattles, Taurine,Cattles, Taurus,Cow, Beef,Cow, Dairy,Cow, Holstein,Cows,Dairy Cows,Domestic Cow,Domestic Cows,Indicine Cattles,Taurine Cattles,Taurus Cattles,Yaks,Zebus
D002678 Chimera An individual that contains cell populations derived from different zygotes. Hybrids,Chimeras,Hybrid

Related Publications

E G Shesely, and N Maeda, and H S Kim, and K M Desai, and J H Krege, and V E Laubach, and P A Sherman, and W C Sessa, and O Smithies
Hypertension in mice lacking the gene for endothelial nitric oxide synthase.
September 1995, Nature,
E G Shesely, and N Maeda, and H S Kim, and K M Desai, and J H Krege, and V E Laubach, and P A Sherman, and W C Sessa, and O Smithies
Abnormal aortic valve development in mice lacking endothelial nitric oxide synthase.
May 2000, Circulation,
E G Shesely, and N Maeda, and H S Kim, and K M Desai, and J H Krege, and V E Laubach, and P A Sherman, and W C Sessa, and O Smithies
Potassium- and acetylcholine-induced vasorelaxation in mice lacking endothelial nitric oxide synthase.
March 2000, British journal of pharmacology,
E G Shesely, and N Maeda, and H S Kim, and K M Desai, and J H Krege, and V E Laubach, and P A Sherman, and W C Sessa, and O Smithies
Insulin resistance, hyperlipidemia, and hypertension in mice lacking endothelial nitric oxide synthase.
July 2001, Circulation,
E G Shesely, and N Maeda, and H S Kim, and K M Desai, and J H Krege, and V E Laubach, and P A Sherman, and W C Sessa, and O Smithies
Elimination of aggressive behavior in male mice lacking endothelial nitric oxide synthase.
October 1999, The Journal of neuroscience : the official journal of the Society for Neuroscience,
E G Shesely, and N Maeda, and H S Kim, and K M Desai, and J H Krege, and V E Laubach, and P A Sherman, and W C Sessa, and O Smithies
Noncholinergic penile erection in mice lacking the gene for endothelial nitric oxide synthase.
January 2002, Journal of andrology,
E G Shesely, and N Maeda, and H S Kim, and K M Desai, and J H Krege, and V E Laubach, and P A Sherman, and W C Sessa, and O Smithies
Paradoxical reduction of fatty streak formation in mice lacking endothelial nitric oxide synthase.
April 2002, Circulation,
E G Shesely, and N Maeda, and H S Kim, and K M Desai, and J H Krege, and V E Laubach, and P A Sherman, and W C Sessa, and O Smithies
Fetal origins of adult vascular dysfunction in mice lacking endothelial nitric oxide synthase.
May 2005, American journal of physiology. Regulatory, integrative and comparative physiology,
E G Shesely, and N Maeda, and H S Kim, and K M Desai, and J H Krege, and V E Laubach, and P A Sherman, and W C Sessa, and O Smithies
Retinal arteriole reactivity in mice lacking the endothelial nitric oxide synthase (eNOS) gene.
April 2019, Experimental eye research,
E G Shesely, and N Maeda, and H S Kim, and K M Desai, and J H Krege, and V E Laubach, and P A Sherman, and W C Sessa, and O Smithies
Ejaculatory abnormalities in mice lacking the gene for endothelial nitric oxide synthase (eNOS-/-).
October 1999, Physiology & behavior,
Copied contents to your clipboard!