Insulin resistance in eNOS(-/-) mice was related specifically to impaired NO synthesis, because in equally hypertensive 1-kidney/1-clip mice (a model of renovascular hypertension), insulin-stimulated glucose uptake was normal.
The decreased activity of 11beta-HSD2 increases the intracellular availability of cortisol, which might be relevant for the pathogenesis of hypertension and preeclampsia.
Recently, consistent data showed that hypoglycemic agents targeting PPARγ as well as renin⁻angiotensin system inhibitors and mineralocorticoid receptor blockers may influence pulmonary hemodynamics in different models of pulmonary hypertension.
Here we describe an inducible tissue specific KO protocol used to study the role of PPARγ in smooth muscle cells (SMC) in angiotensin (Ang) II-induced hypertension in adult mice.
The results of the present study support that homozygosity for +G894T (E298D) in NOS3 is a genetic risk factor for the development of LVH in patients with hypertension.
Although endothelial nitric oxide synthase (eNOS) haplotypes have been associated with hypertension, it is unknown whether eNOS genotypes/haplotypes are associated with resistance to antihypertensive therapy.
Our findings demonstrate that the hypertension-susceptibility variants in PLCE1 and ATP2B1 confer a protective effect on risk of developing anthracycline-related cardiotoxicity, and functional analyses suggest that these genes are influenced by exposure to anthracyclines.
Given the vasodilatory role of the eNOS gene product, it is possible that the linkage recently reported for eNOS reflects its relationship with hypertension rather than preeclampsia.
Four loci-ATP2B1 (ATPase, Ca(++) transporting, plasma membrane 1), CSK (c-src tyrosine kinase), CYP17A1 (cytochrome P450 17A1) and PLEKHA7 (pleckstrin homology domain-containing family A member 7)-were associated with blood pressure and hypertension in the Korean population.
It was found that the myocardial infarction combined with hypertension group had a much higher serum ADMA level and relatively low levels of eNOS and NO compared to those of the other three groups; the myocardial infarction group and the hypertension group had a much higher serum ADMA level compared to that of the healthy control group and the two groups had much lower levels of eNOS and NO.
Also, EGb761 inhibited hypertension with hypercholesterolemia-induced decrease in endothelial nitric oxide synthase (eNOS) protein expression and increase in the protein expressions of inducible NO synthase (iNOS), TNF-α, IL-6 and IL-1β in the kidney tissues.
Our findings suggest that PPAR-gamma may be a key regulator of blood-brain barrier permeability and a potential therapeutic target during hypertension.
Reduced eNOS activity could mediate an increased stroke risk through hypertension or independent of hypertension through abnormal vasomotor responses, promoting atherogenesis, or increased platelet adhesion and aggregation.
For detection of polymorphisms all 22 PMCA1 exons from 44 patients with essential hypertension (based on rigorous clinical data in addition to a positive family history) and from 40 normotensives without a family history of hypertension were PCR amplified and subsequently subjected to combined single-strand conformation polymorphism (SSCP) and heteroduplex (HTX) analysis.
The Pro12Ala and the 4a/b polymorphisms of the peroxisome proliferator-activated receptor gamma (PPARgamma) and the endothelial nitric oxide-synthase (eNOS) genes, respectively, have been associated with hypertension in some but not all studies.