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Renal Denervation Reduces Monocyte Activation and Monocyte-Platelet Aggregate Formation: An Anti-Inflammatory Effect Relevant for Cardiovascular Risk.

Zaldivia MTRivera JHering DMarusic PSata YLim BEikelis NLee RLambert GWEsler MDHtun NMDuval JHammond LEisenhardt SUFlierl USchlaich MPPeter K.

Hypertension. 2017 Feb;69(2):323-331.

https://www.ncbi.nlm.nih.gov/m/pubmed/27956575/

Maria Zaldivia (Australia)



 

1) Summarize your work in one sentence.

Our study investigated the link between inflammation and sympathetic activity. We used renal denervation as a unique opportunity allowing to modulate the sympathetic activation status and then assess how this influences monocyte activation as well as other inflammatory markers in hypertensive patients.


2) Summarize your findings in one sentence.

We found renal denervation-induced inhibition of sympathetic activity is associated with an improved blood pressure control and attenuates monocyte activation and systemic inflammation in hypertensive patients.


3) Which were the more important methods you used in this work? If it is not a traditional method you can briefly explain the concept of that methodology.

We used three important methods in this study:

  • Firstly, the renal denervation procedure was performed in hypertensive patients using a radiofrequency ablation catheter, which was shown to lower blood pressure by reducing sympathetic activity.
  • Secondly, we assessed the sympathetic outflow to the periphery by recording multiunit muscle sympathetic nerve activity from post-ganglionic sympathetic nerves using microneurography to measure real-time sympathetic nerve activity.
  • Lastly, using a single-chain antibody MAN-1 which was generated by our laboratory, we measure the activation status of monocytes. The single-chain antibody specifically detects monocyte activation by binding to the activated conformation of integrin MAC-1 (macrophage-1 antigen; αMβ2; CD11b/CD18) during monocyte activation. Using this diagnostic tool together with the measurement of monocyte– platelet aggregates and other inflammatory markers, we measured monocyte activation and systemic inflammation at baseline, 3 months, and 6 months after renal denervation in patients with high blood pressure.

 4) What did you learn from this paper, what was your take-home message?

Modulation of sympathetic activation via renal denervation is associated with improved blood pressure and importantly also attenuates the monocyte activation status, thereby targeting 2 mechanisms relevant for cardiovascular risk. Our findings demonstrate an intricate link between the sympathetic nervous and immune system that can be targeted therapeutically and is likely to confer cardiovascular risk reduction.

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