Endocrine Abstracts

Background. The endothelial dysfunction prevalent in hypertension and diabetes is associated with an imbalance in the levels of nitric oxide (NO) and superoxide (SO). NAD(P)H oxidase is the predominant source of SO in the vasculature. Objectives. To manipulate levels of SO using the NAD(P)H oxidase inhibitors, apocynin, phenyl arsine oxide (PAO) and 4(2aminoethyl)benzenesulfonyl fluoride (AEBSF) and relate this to NO bioavailability. Methods. NO bioavailability was compared in...

Background and Hypothesis:- A common NOS3 Single nucleotide polymorphisms (SNP) (894 G/T) which encodes a Glu298Asp amino acid substitution in endothelial NO synthase has been associated with cardiovascular disorders in which NO bioactivity is impaired. The gene coding for p22phox, a critical component of the NADH/NAD(P)H oxidase enzyme system, a major source of vascular SO, is CYBA. Among the allelic polymorphisms reported in CYBA is C242T, associated wit...

Increased superoxide(SO) production reduces nitric oxide(NO) bioactivity and increases oxidative stress contributing to endothelial dysfunction in vascular disease. The gene coding for p22phox, a critical component of the NADH/NAD(P)H oxidase enzyme system which produces vascular SO, is CYBA. Among the allelic polymorphisms reported in CYBA is C242T which is associated with progression of coronary atherosclerosis. Radial applanation tonometry with pulse waveform analysis (PWA)...

Objective. The aims of our study were to utilise a combination of high fidelity phenotyping, microarray gene expression profiling and conserved synteny mapping between rodent and human genomes to identify genetic determinants underlying human hypertension.Methods. We used the stroke-prone spontaneously hypertensive rat (SHRSP) and a congenic strain (SP.WKYGla2c*) produced by introgressing a quantitative trait locus responsible for blood pressure regulation on rat chromosom...