Systemic inhibition of the Na(+)/H (+) exchanger type 3 in intact rats activates brainstem respiratory regions.

Selective inhibition of the Na(+)/H(+) exchanger type 3 (NHE3) increases the firing rate of brainstem ventrolateral CO(2)/H(+) sensitive neurons, resembling the responses evoked by hypercapnic stimuli. In anesthetized animals, NHE3 inhibition has also been shown to stimulate the central chemosensitive drive. We aimed to analyze the respiratory-related brainstem regions affected by NHE3 inhibition in anaesthetized spontaneously-breathing rats with intact peripheral afferents.

Respiratory response to systemic inhibition of the Na+/H+ exchanger type 3 in intact rats.

The Na+/H+ exchangers (NHEs) are a family of antiporters involved in the maintenance of neural steady-state intracellular pH. The NHE3 seems to be the predominant subtype in central chemosensitive cells. We aimed to analyze the effect of a selective NHE3 inhibition on the respiratory pattern in spontaneously breathing rats with intact vagi.

Enhanced c-Fos expression in the rostral ventral respiratory complex and rostral parapyramidal region by inhibition of the Na+/H+ exchanger type 3.

Previous studies have shown that selective inhibition of Na+/H+ exchanger type 3 (NHE3) induces intracellular acidification and activates CO2/H+-sensitive medullary neurons, mimicking the responses evoked by hypercapnic stimuli. In addition, NHE3 blockers administration decreases the duration of apnoea induced by laryngeal stimulation, presumably by means of central chemoreceptor activation. To test the hypothesis that the central chemoreceptor network may be affected by NHE3 inhibition, brainstem c-Fos immunoreactive cell counting was performed after systemic administration of the NHE3 blocker AVE1599 (Aventis Pharma Deutschland GmbH) (2 mg/kg).

Characterization of efferent projections of chemosensitive neurons in the caudal parapyramidal area of the rat brain.

The caudal parapyramidal area of the rat brain contains a population of neurons that are highly sensitive to an increase in the extracellular hydrogen ion concentration ([H+]o). Some of them fire synchronously with respiration when [H+]o is increased. These chemosensitive neurons are located in the caudal ventrolateral medulla in a medial region, closest to the pyramidal tract, and a lateral region, beneath the lateral reticular nucleus.

[Central chemoreceptors and sudden infant death syndrome].

Introduction: Carbon dioxide partial pressure and pH in the extracellular compartment are the most powerful signals regulating respiration. Central chemoreceptors (QC) undergo the stimulating effect of CO2 and pH upon respiration.

Aims: This review tries to provide an actual envision of the progress in the knowledgement on central chemoreception.