Mitochondrial cytochrome redox states and respiration in acute pulmonary oxygen sensing.

Hypoxic pulmonary vasoconstriction (HPV) is an essential mechanism to optimise lung gas exchange. We aimed to decipher the proposed oxygen sensing mechanism of mitochondria in HPV. Cytochrome redox state was assessed by remission spectrophotometry in intact lungs and isolated pulmonary artery smooth muscle cells (PASMC).

Unusual cytochrome a592 with low PO2 affinity correlates as putative oxygen sensor with rat carotid body chemoreceptor discharge.

Light-absorption spectra and afferent chemoreceptor discharge were simultaneously recorded on superfused rat carotid bodies (CBs) under the influence of cytochrome a3-CuB ligands (O2, CN-, CO) in order to identify the primary mitochondrial cytochrome c oxidase (CCO) oxygen sensor. Spectra could be described on the basis of weighted light-absorption spectra of cytochrome b558 of the NAD(P)H oxidase and mitochondrial cytochromes b and c, CCO, cytochrome a3, and an unusual cytochrome a peaking at 592 nm. Discharge signals were deconvoluted into phasic and tonic activity for comparing different CB responses.

Cardiovascular and renal effects of systemic hypoxia in chronically instrumented conscious WKY and SHR rats.

The effects of systemic hypoxia upon cardiovascular and renal function in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) are controversial. We examined the effects of systemic normobaric hypoxia (12.5% O2 in N2 for 4 hours) on arterial blood gases (pO2, pCO2, pH), mean arterial pressure (MAP), heart rate (HR), effective renal blood flow (ERBF), glomerular filtration rate (GFR), urine flow (UMV) and renal sodium excretion (U Na V) in conscious unilaterally nephrectomized WKY (n = 12) and SHR (n = 14) chronically instrumented with an arterial, venous and ureter cannula.