A University of Houston biomedical engineer is expanding his study of electrodes to treat high blood pressure, also known as hypertension.
Mario Romero-Ortega, Cullen Endowed Professor of biomedical engineering, previously reported that deep peroneal nerve stimulation (DPNS) elicits an acute reduction in blood pressure on rats.
His current study, published in Frontiers in Neuroscience, advances that work, focusing on his development of a small implantable wireless neural stimulation system.
He explores different stimulation parameters to achieve a maximum lowered response.
Wireless
Romero-Ortega integrated a sub-millimetre nerve stimulation circuit with a novel nerve attachment microchannel electrode that facilitates implantation into small nerves and allows external power and DPNS modulation control.
Using this implantable device, his team demonstrated that systolic blood pressure can be lowered 10 per cent in one hour and 16 per cent two hours after nerve stimulation.
“Our results indicate that DPNS consistently induces an immediate and reproducible arterial depressor effect in response to electrical stimulation of the deep peroneal nerve,” reported Romero-Ortega.
Hypertension
High blood pressure or hypertension, often called the ‘silent killer’, speaks loudly in statistics.
In the United States, it is the number one cause of death. Globally it is the number one risk factor for death, impacting more than one billion people and is to blame for about half of all stroke and heart related deaths.
The American College of Cardiology/American Heart Association 2018 guidelines classified average systolic blood pressure as greater than 130 mmHg and diastolic BP greater than 80 mmHg, on at least two separate occasions, as hypertension.
While pharmacological treatments are effective, blood pressure remains uncontrolled in 50 to 60 per cent of resistant hypertensive subjects.
And about 12 to 18 per cent of them develop resistant hypertension, defined as blood pressure greater than 140/90 mmHg despite the use of antihypertensive drugs.
“In this study, DPNS induced an initial increase in RSNA during the first two to three seconds, followed by a reduction in renal activity and mean arterial pressure, despite the increase in heart rate,” said Romero-Ortega.
The observed activation of the RSNA during the DPNS was not expected since its activity is associated with hypertension.”
