Smart Baroreceptor Activation Therapy Strikingly Attenuates Blood Pressure Variability in Hypertensive Rats With Impaired Baroreceptor.


Journal

Hypertension (Dallas, Tex. : 1979)
ISSN: 1524-4563
Titre abrégé: Hypertension
Pays: United States
ID NLM: 7906255

Informations de publication

Date de publication:
03 2020
Historique:
pubmed: 31 12 2019
medline: 25 2 2021
entrez: 31 12 2019
Statut: ppublish

Résumé

Increased blood pressure (BP) variability (BPV) is an independent risk factor of cardiovascular events among hypertensive patients. The arterial baroreceptor reflex is a powerful regulator of BP and attenuates BPV via a sympathetic negative feedback control. Conventional baroreceptor activation therapy (cBAT) electrically stimulates the carotid baroreceptors with constant stimulation parameters. While cBAT lowers BP, it does not mount a pressure feedback mechanism. We hypothesized that baroreceptor activation therapy with a pressure feedback system (smart BAT [sBAT]) is able to reduce BPV as well as lower BP. We developed sBAT that electrically stimulated baroreceptors at a frequency proportional to the difference between instantaneous BP and a preset reference pressure, and compared its performance with cBAT. In 14-week-old spontaneously hypertensive rats (n=6), we implanted BP telemeter and created impaired arterial baroreceptors by modified sino-aortic denervation. One week after surgical preparation, we administered sBAT, cBAT or no stimulation (sham) for 15 minutes and compared BP and BPV under freely moving condition. Both cBAT and sBAT significantly lowered mean BP (sham, 141.3±12.8; cBAT, 114.3±11.4; and sBAT, 112.0±7.3 mm Hg). Conventional BAT did not affect BPV at all, while sBAT significantly reduced BPV (sham, 15.4±2.6; cBAT, 16.0±5.2; and sBAT, 9.7±3.3 mm Hg). sBAT also prevented transient excessive BP rise and fall. In conclusion, sBAT was capable of reducing BP and attenuating BPV in hypertensive rats with impaired baroreceptor. sBAT is a novel treatment option for hypertensive patients with increased BPV.

Identifiants

pubmed: 31884856
doi: 10.1161/HYPERTENSIONAHA.119.13673
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

885-892

Auteurs

Takeshi Tohyama (T)

From the Department of Cardiovascular Medicine, Graduate School of Medical Sciences (T.T., K. Saku, Y.O., H.T.), Kyushu University, Fukuoka, Japan.

Kazuya Hosokawa (K)

Department of Cardiovascular Medicine, Kyushu University Hospital, Fukuoka, Japan (K.H., H.T.).

Keita Saku (K)

From the Department of Cardiovascular Medicine, Graduate School of Medical Sciences (T.T., K. Saku, Y.O., H.T.), Kyushu University, Fukuoka, Japan.

Yasuhiro Oga (Y)

From the Department of Cardiovascular Medicine, Graduate School of Medical Sciences (T.T., K. Saku, Y.O., H.T.), Kyushu University, Fukuoka, Japan.

Hiroyuki Tsutsui (H)

From the Department of Cardiovascular Medicine, Graduate School of Medical Sciences (T.T., K. Saku, Y.O., H.T.), Kyushu University, Fukuoka, Japan.
Department of Cardiovascular Medicine, Kyushu University Hospital, Fukuoka, Japan (K.H., H.T.).

Kenji Sunagawa (K)

Department of Therapeutic Regulation of Cardiovascular Homeostasis, Center for Disruptive Cardiovascular Medicine (K. Sunagawa), Kyushu University, Fukuoka, Japan.

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