Cutaneous and renal vasodilatory response to local pressure application: A comparative study in mice

• Published in: Microvascular research 2018-01, Vol.115, p.44-51
• Main Authors: Begey, Anne-Laure, Liu, Kiao Ling, Lo, Ming, Josset-Lamaugarny, Audrey, Picard, Nicolas, Gauthier, Catherine, Fromy, Berengere, Sigaudo-Roussel, Dominique, Dubourg, Laurence
• Format: Article
• Language: English
• Subjects: Adaptation, Physiological; Animals; Blood Flow Velocity; Calcitonin Gene-Related Peptide - metabolism; Endothelium dysfunction; Endothelium, Vascular - metabolism; Endothelium, Vascular - physiology; Kidney - blood supply; Laser Doppler flux; Laser-Doppler Flowmetry; Life Sciences; Male; Mice, Inbred C57BL; Microcirculation; Microvessels - metabolism; Microvessels - physiology; Nitric Oxide - metabolism; Pressure; Pressure-induced vasodilation; Prostaglandins - metabolism; Regional Blood Flow; Renal Circulation; Skin - blood supply; Sodium Chloride, Dietary - administration & dosage; Time Factors; Transient receptor potential vanilloid type 1; TRPV Cation Channels - metabolism; Vasodilation
• ISSN: 0026-2862; 1095-9319
• DOI: 10.1016/j.mvr.2017.08.007

We have reported a novel relationship involving mechanical stimulation and vasodilation in rodent and human skin, referred to as pressure-induced vasodilation (PIV). It is unknown whether this mechanism exists in kidney and reflects the microcirculation in deep organs. Therefore, we compared the skin and kidney PIV to determine whether their changes were similar. In anesthetized mice fed a normal salt-diet, laser Doppler flux (LDF) signals were measured when an increase in local pressure was applied to the surface of the head skin with the rate of 2.2Pa/s (1mmHg/min) and to the left kidney with a rate of 4.4Pa/s (2mmHg/min). The mechanism underlying renal PIV was also investigated. The skin and kidney PIV were also compared during salt load (4% NaCl diet). The kidney had higher baseline LDF and vascular conductance compared to those of the skin. Pressure application increased the LDF in the kidney as well as in the skin with a comparable maximal magnitude (about 25% from baseline value), despite different kinetics of PIV evolution. As we previously reported in the skin, the kidney PIV response was mediated by the activation of transient receptor potential vanilloid type 1 channels, the release of calcitonin gene-related peptide, and the participation of prostaglandins and nitric oxide. In the absence of hypertension, high salt intake abolished the cutaneous PIV response and markedly impaired the renal one. PIV response in the mouse kidney results from a neuro-vascular interaction. Despite some differences between the skin and the kidney PIV, the similarities in their response and signaling mechanisms suggest that the cutaneous microcirculation could reflect, in part, the microcirculation of the renal cortex.