Abstract
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The provocative data for this hypothesis link salt-dependent, macrophage-derived VEGF-C effects to lymphatic capillary density, 1 but little attention has been directed to the role of the lymphatic collecting system in this salt-dependent response.
In the current issue of the Journal, Mizuno et al. explicate modulating effect of high salt diet upon the mechanical activity of afferent and efferent collecting lymphatics in murine iliac lymph nodes. 2 In their investigation, they have observed and contrasted the effects of normal and high-salt diet (HSD) upon changes in the mechanical activity of isolated murine afferent and efferent lymphatics in response to increases in intraluminal pressures, as measured using video-microscopy. They observed that the increased salt intake suppressed the amplitude, ejection fraction, and stroke volume of afferent lymphatics, leading to marked reductions in pumping activity. In contrast, the pumping activities of efferent lymphatics were resistant to a HSD and were preserved by enhancing the contraction frequency within these vessels.
These elegant observations complement and enhance the prior observations that relate lymphatic capillary responses to salt intake, strengthening the inference that an important link might exist between hypertensive pathology and the inherent function of the lymphatic vascular network.
The authors correctly conclude that further investigation should clarify the role of the collecting lymphatics in hypertensive patients and expand upon the mechanisms through which salt load can differentially modulate the mechanical activity of afferent and efferent lymphatics.