SS <sup>Kcnj16-/-</sup> rats chronically treated with bicarbonate or the carbonic anhydrase inhibitor hydrochlorothiazide had partial restoration of arterial pH, but there was a further reduction in the ventilatory response to hypercapnic acidosis.
Here we recorded from mouse Phox2b+ RTN neurons in brain slices, and found that their response to moderate hypercapnic acidosis (pH 7.4 to ∼7.2) was markedly reduced by antagonists of 5-HT<sub>7</sub> receptors.
This study initially shows both physical and functional interaction between VCL and cardiac sodium channel, and suggests an important role for respiratory acidosis in triggering the fatal arrhythmia underlying SUNDS.
Isocapnic acidosis, hypercapnic acidosis and isohydric hypocapnia evoked inward currents in NBCe1- and CAII-expressing Xenopus laevis oocytes, but not in native oocytes, suggesting that NBCe1 operates in the outwardly directed mode under these conditions consistent with our findings in astrocytes.
Chemogenetic [clozapine<i>-N-</i>oxide (CNO)-hM4Di] perturbation of <i>Tac1-Pet1</i> neuron activity blunted the ventilatory response of the respiratory CO<sub>2</sub> chemoreflex, which normally augments ventilation in response to hypercapnic acidosis to restore normal pH and PCO<sub>2</sub><i>Tac1-Pet1</i> axonal boutons were found localized to brainstem areas implicated in respiratory modulation, with highest density in motor regions.
While the Henderson-Hasselbalch approach identified lactate as main factor responsible for the non-respiratory acidosis, the modified physicochemical approach additionally identified strong ions (i.e. plasma electrolytes, organic acid ions) and non-volatile weak acids (i.e. albumin, phosphate ion species) as important contributors.
Wild-type and mutant SCN5A channels both functioned typically under normal conditions in vitro, but exposure to acidic intracellular pH levels such as those found in respiratory acidosis--a known risk factor for SIDS--produced abnormal gain-of-function late reopenings of S1103Y channels, behavior that is often associated with cardiac arrhythmias.
Following the reduced NF-kappaB activation, HA suppressed the mRNA and protein levels of intercellular adhesion molecule-1 and interleukin-8, resulting in a decrease in both lactate dehydrogenase release into the medium and neutrophil adherence to LPS-activated human pulmonary artery endothelial cells.
Umbilical artery IGFBP-1 levels (mean +/- SEM) from term babies with respiratory acidosis (acute hypoxia), normal babies, and those with mixed respiratory/metabolic acidosis (more profound and prolonged hypoxia) were measured using an immunoradiometric assay.