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At least 811 records · Page 45Linked to original sources
PubMed1985

Effects of carotid sinus nerve stimulation on respiratory sinus arrhythmia and respiratory blood pressure waves of the dog.

The effect on the amplitudes of RSA and RBPW of the time of the stimulus in the cardiac cycle, and also of continuous stimulation were studied. When the stimulus train was applied near peak systole the amplitudes of RSA and RBPW decreased. Stimulation in late systole increased both RSA and RBPW. Continuous stimulation did not exert any effects on RSA and RBPW.

Animals↗
PubMed1999

[Ion transport in nasal and paranasal sinus mucosa in mucoviscidosis and chronic sinusitis].

Cystic fibrosis (CF) is the most commonly inherited disease in Caucasians and is caused by a mutation in the gene encoding a membrane transport protein. This cystic fibrosis transmembrane conductance regulator (CFTR) is thought to be an apical Cl- channel activated by intracellular cAMP. Most recent findings suggest that CFTR is more than a pure Cl- channel and might be involved in the regulation of other transport systems. In the present study we show that CFTR as a Cl- channel plays only a minor role in primary cultured human nasal epithelium derived from non-CF and CF patients. These findings are especially of interest for non-CF human nasal epithelia in which CFTR is correctly inserted. In both tissues Cl- secretion is negligible as compared with Na+ absorption. We confirm and expand our previous observations that Na+ absorption in human nasal epithelium is the dominant ion transport process and that Cl- secretion is detectable in both CF and non-CF tissue. Moreover, we show that cAMP and ATP were not able to stimulate any silent Cl- channels in CF or non-CF human nasal epithelial cells. We further give evidence that in human nasal CF and non-CF epithelium Na+ absorption is mediated by epithelial Na+ channels (ENaC) that are either different from those of other epithelia or which exhibit altered regulation. These differences between Na+ channels of human nasal epithelium and "classical" epithelial Na+ channels include lack of activation by the intracellular second messenger cAMP and the steroid hormone aldosterone. We show further that human nasal Na+ channels are inhibited by Cl- channel blockers and exhibit a different pharmacology towards common Na+ channel blockers.

Chloride Channels↗