Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 9085514

Vascular function in OSA.

J Hedner
View original source ↗Export metadata ↓

Abstract

A number of pathophysiological phenomena linked to sleep disordered breathing are likely to affect vascular function. This report briefly reviews current knowledge regarding neurogenic vascular tone and a number of circulating hormones with vascular actions in obstructive sleep apnea (OSA). New evidence suggesting a role of the vascular endothelium in the development of vascular disease in OSA is also presented.

Explore related subjects

AldosteroneAngiotensin IIArginineAtrial Natriuretic FactorEndotheliumHumansHypertensionSleep Apnea SyndromesSnoringSympathetic Nervous SystemJournal ArticleResearch Support, Non-U.S. Gov'tReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J Hedner. 1996. Vascular function in OSA.. https://doi.org/10.1093/sleep%2F19.suppl_10.s213

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2001

Epithelial sodium channel and the mineralocorticoid receptor in cultured rat Müller glial cells.

Müller glial cells are the major non-neuronal cells of the retina. They are involved in retinal function and exert a profound influence on the function of retinal neurons. We present an in vitro study of the localization of the mineralocorticoid receptor (MCR) and of the epithelial sodium channel (ENaC) in rat Müller glial cells isolated from rat retina, using respectively, a polyclonal antiserum raised against the rat purified MCR, and a rabbit polyclonal antibody against the 14-amino acid (aa) peptide QGLGKGDKREEQGL, which corresponds to the N-terminal region (44-58aa) of the alpha-subunit of the ENaC. In an immunocytochemical study using anti-MCR and anti-ENaC antibodies, the MCR was detected as a protein present in the cytoplasm and in the nucleus, whereas ENaC was detected as a membrane-bound protein. Reverse transcription-polymerase chain reaction (RT-PCR) analysis using specific primers, 5'-CTGCCTTTATGGATGATGGT-3' (sense), 5'-GTTCAGCTCGAAGAAGA-3' (antisense) for ENaC and 5'-AGGCTACCACAGTCTCCCTG-3' (sense) and 5'-GCAGTGTAAAATCTCCAGTC-3' (antisense) for MCR, showed expression of the ENaC and MCR genes in Müller cells. The presence of ENaC and MCR was detected as the predicted bands of 520 bp and 843 bp, respectively. In both cases, 100% identity was observed between the sequences of rat Müller cell (RMC) PCR products and rat kidney. Interestingly, the basal levels of ENaC were increased in vitro by the MCR-specific hormone, aldosterone. Thus, our results strongly suggest that the Müller glial cells may play a role in the regulation of extracellular Na+ concentration, which could be regulated by steroid-mediated sodium uptake.

Aldosterone↗
PubMed2001

Endothelins stimulate aldosterone secretion from dispersed rat adrenal zona glomerulosa cells, acting through ETB receptors coupled with the phospholipase C-dependent signaling pathway.

Compelling evidence indicates that endothelins (ETs) stimulates aldosterone secretion from rat zona glomerulosa (ZG) cells, acting through the ETB receptor subtype. We have investigated the mechanisms transducing the aldosterone secretagogue signal elicited by the pure activation of ETB receptors. Aldosterone response of dispersed rat ZG cells to the selective ETB-receptor agonist BQ-3020 was not affected by inhibitors of adenylate cyclase/protein kinase (PK)A, tyrosine kinase-, mitogen-activated PK-, cyclooxygenase- and lipoxygenase-dependent pathways. In contrast, the inhibitor of phospholipase C (PLC) U-73122 abrogated, and the inhibitors of PKC, phosphatidylinositol trisphosphate (IP(3))-kinase and calmodulin (calphostin-C, wortmannin and W-7, respectively) partially prevented aldosterone response to BQ-3020. When added together, calphostin-C and wortmannin or W-7 abolished the secretagogue effect of BQ-3020. BQ-3020 elicited a marked increase in the intracellular Ca2+ concentration ([Ca2+]i) in dispersed rat ZG cells, and the effect was abolished by the Ca(2+)-release inhibitor dantrolene. The Ca2+ channel blocker nifedipine affected neither aldosterone nor Ca2+ response to BQ-3020. Collectively, our findings suggest that (1) ETs stimulate aldosterone secretion from rat ZG cells through the activation of PLC-coupled ETB receptors; (2) PLC stimulation leads to the activation of PKC and to the rise in [Ca2+]i with the ensuing activation of calmodulin; and (3) the increase in [Ca2+] is exclusively dependent on the stimulation of IP(3)-dependent Ca2+ release from intracellular stores.

Aldosterone↗
PubMed2001

Aldosterone in renal disease.

Blockade of the renin-angiotensin-aldosterone system has proved effective in retarding the progression of renal disease in the remnant kidney model, as well as other experimental diseases, and most importantly, in a range of progressive human renal diseases. Attention has focused on the role of angiotensin II in propagating progression both by its hemodynamic and non-hemodynamic actions. Recent evidence, predominantly in the remnant kidney model, indicates that the drugs used to block this hormone system, angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, also lower aldosterone levels. Aldosterone as well as angiotensin II thus appears to be instrumental in sustaining the hypertension and fibroproliferative destruction of the residual kidney.

Aldosterone↗