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Cardiovasc Res. 2019 Feb 4. doi: 10.1093/cvr/cvz033. [Epub ahead of print]

Successful Renal Denervation Decreases the Platelet Activation Status in Hypertensive Patients.

Author information

Atherothrombosis and Vascular Biology, Baker Heart and Diabetes Institute, Melbourne.
Department of Medicine, Monash University, Melbourne.
Neurovascular Hypertension and Kidney Disease, Baker Heart and Diabetes Institute, Melbourne.
Dobney Hypertension Centre, School of Medicine, Royal Perth Hospital Unit, University of Western Australia, Perth.
Heart Centre, Alfred Hospital, Melbourne.
Department of Physiology, Anatomy and Microbiology, School of Life Sciences, La Trobe University, Bundoora.
ACRF Department of Cancer Biology and Therapeutics, John Curtin School of Medical Research, Australian National University, Canberra.
Australian Centre for Blood Diseases, Monash University, Melbourne.



To determine whether renal denervation (RDN) in hypertensive patients affects the platelet activation status.

Methods and Results:

We investigated the effect of RDN on the platelet activation status in 41 hypertensive patients undergoing RDN. Ambulatory blood pressure (BP), plasma sympathetic neurotransmitter Neuropeptide Y, and platelet activation markers were measured at baseline, at 3 months, and 6 months after RDN. RDN significantly decreased BP at 3 months (150.6±11.3/80.9±11.4 mmHg to 144.7 ± 12.0/77.1 ±11.1 mm Hg; P < 0.01) and at 6 months (144.3±13.8/78.3±11.1 mmHg; P < 0.01). Plasma levels of the sympathetic neurotransmitter Neuropeptide Y, an indicator of sympathetic nerve activity, were significantly decreased at 3 months (0.29 ± 0.11 ng/mL to 0.23 ± 0.11 ng/mL; P < 0.0001) and at 6 months (0.22 ± 0.12 ng/mL; P < 0.001) after RDN. This was associated with a reduction in platelet membrane P-selectin expression (3 months, P < 0.05; 6 months, P < 0.05), soluble P-Selectin (6 months, P < 0.05), circulating numbers of platelet-derived extracellular vesicles (3 months, P < 0.001; 6 months, P < 0.01) and phosphatidylserine expressing extracellular vesicles (3 months, P < 0.001; 6 months, P < 0.0001), indicative of a reduction in platelet activation status and procoagulant activity. Only patients who responded to RDN with a BP reduction showed inhibition of P-selectin expression at 3 months (P < 0.05) and 6 months (P < 0.05) as well as reduction of GPIIb/IIIa activation at 3 months (P < 0.05). Notably, 13 patients who took aspirin did not show significant reduction in platelet P-selectin expression following RDN.


Our results imply a connection between the sympathetic nervous system and the platelet activation status and provide a potential mechanistic explanation by which RDN can have favourable effects towards reducing cardiovascular complications.


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