PubMed · 13223121
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R E LONG. Save that sphygmomanometer.. https://pubmed.ncbi.nlm.nih.gov/13223121/
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Decreased production of vasodilator substances such as nitric oxide (NO) has been proposed as important in development of pulmonary arterial hypertension (PAH). We hypothesize that NO measured over time serves as a non invasive marker of severity of PAH and response to therapy. We prospectively and serially measured exhaled NO and carbon monoxide (CO), a vasodilator and anti-inflammatory product of heme oxygenases, in 17 PAH patients in conjunction with hemodynamic parameters over 2 years. Although pulmonary artery pressures and NO were similar in all patients at entry to the study, NO increased in the 12 individuals who survived to complete the study, and correlated with change in pulmonary artery pressures. In contrast, CO did not change or correlate with hemodynamic parameters. Investigation of NO-oxidant reaction products in PAH in comparison to controls suggests that NO synthesis is impaired in the lung and that reactive oxygen species may be involved in the pathophysiology of pulmonary hypertension. Endogenous NO is inversely related to pulmonary artery pressure in PAH, with successful therapy of PAH associated with increase in NO.
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BACKGROUND: The serum- and glucocorticoid-regulated kinase (SGK1) gene is an important mediator of aldosterone action, regulating the expression of the renal epithelial Na(+) channel. In renal failure, blood pressure (BP) is markedly salt-dependent and increases with decreasing renal function. Mutations of the SGK1 gene affecting phosphorylation could be responsible for salt-mediated increases in BP and hypertension-related progression to end-stage renal disease (ESRD). METHODS: The SGK1 gene was analysed for mutations in the exons 4, 5, 8 and 10-12, because of potential phosphorylation sites, in 591 subjects, including 311 ESRD patients (either dialysis or transplanted). In addition, an intron 6 single-nucleotide polymorphism (SNP) described previously was also investigated in this study. Genotyping was performed either by using a strategy based on single strand conformation polymorphism analysis of polymerase chain reaction (PCR) products and subsequent direct sequencing of identified gel shift variants or by using high throughput 5' nuclease allelic discrimination assay. RESULTS: Two SNPs in coding regions of SGK1 potentially influencing the phosphorylation of Sgk1 were identified. Both SNPs were synonymous. The prevalence of the first variant, a previously reported SNP at codon 240 in exon 8, did not differ between ESRD patients (16.3%) and controls (15.7%). There was no association between the SNP in exon 8 and either BP within the control population or progression of renal disease in the ESRD population. The second SNP at codon 398 in exon 12 was identified in one patient only. Intron 6 and exon 8 SNPs were in strong linkage disequilibrium, but did not show any association with either BP or renal diseases. CONCLUSIONS: Based on statistical analysis homozygosity for nonconservative mutations in the coding region of the SGK1 gene is estimated at < 1/300 000 when a white Caucasian population is considered, arguing against an important role of mutations of this coding region in hypertension and hypertension-associated progression of renal disease.