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H Wirtz

Publications and source records attributed to H Wirtz.

6 recordsLinked to original sources

Ventilation and secretion of pulmonary surfactant.

Various factors are involved in the regulation of surfactant secretion: chemical agonist; local environmental factors such as mediators, locally produced hormones, and possibly pH; and finally, mechanical stress occurring during lung inflation. Here we suggest a model of regulation which is grouped into three levels: a basal autoregulatory mechanism with local factors being superimposed and a systemic level acting through hormones reaching the lung via the bloodstream. Depending on the situation, the different levels may vary in their importance. For the normal situation, in the absence of stress factors, we suggest the autoregulation of stretch-induced secretion and SP-A inhibition as indicated by in vitro experiments to be the prominent regulatory mechanism for surfactant secretion. From this model, mechanisms can be derived which indicate involvement of the surfactant system in, for example, obstructive lung disease. Support from the literature for this hypothesis is reviewed. Because quantitative measurement of the amount of surfactant-associated phospholipids cannot be done adequately at this time, we suggest testing the relatively risk-free application of exogenous surfactant in a pilot phase based on indications for its involvement and usefulness derived from animal and in vitro experiments.

Animals

Stretch-dependent regulation of atrial peptide synthesis and secretion in cultured atrial cardiocytes.

We have developed a novel system to study stretch-dependent secretion of atrial natriuretic peptide (ANP) using cultured neonatal rat atriocytes in vitro. Application of tension (i.e., 2 sequential stretches) to cells grown on a flexible culture surface effected a dose-dependent increase in immunoreactive (ir) ANP release into the medium. Analysis of atriocyte cytoplasmic RNA 24 h poststretch revealed an increase in ANP mRNA levels of about ninefold relative to the unstretched controls. Medium ATP levels, measured as an index of cellular damage, were similar in control and stretched cells. Furthermore, cooling the cultures to 0 degrees C suppressed both basal as well as stretch-stimulated release. These findings argue against cellular damage and nonspecific release of irANP as an explanation for the increase in medium immunoreactivity. Stretch was incapable of amplifying the secretory response to prostaglandin F2 alpha, suggesting possible overlap in the pathways whereby these stimuli effect release of the peptide. The calcium channel blocker verapamil had no effect on stretch-dependent irANP release, whereas calmidzolium, a calmodulin inhibitor, suppressed basal as well as stretch-dependent secretion, implying a potentially important relationship between intracellular calcium metabolism and irANP release.

1-Methyl-3-isobutylxanthine