Maxi-K+ Channel 1 Expression in Sleep Apnea Patients and Its Modulation by CPAP Treatment | Zendy

Javier Navarro-Antolı́n | Zendy; Carmen Carmona-Bernal | Zendy; V. Rivero-Valdenebro | Zendy; José R. Villar | Zendy; F. Capote | Zendy; José LópezBarneo | Zendy

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Maxi-K+ Channel 1 Expression in Sleep Apnea Patients and Its Modulation by CPAP Treatment

Author(s) -

Javier Navarro-Antolı́n,

Carmen Carmona-Bernal,

V. Rivero-Valdenebro,

José R. Villar,

F. Capote,

José LópezBarneo

Publication year - 2008

Publication title -

american journal of hypertension

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.009

H-Index - 136

eISSN - 1941-7225

pISSN - 0895-7061

DOI - 10.1038/ajh.2008.342

Subject(s) - medicine , blood pressure , hypoxemia , cardiology , apnea , polysomnography , ambulatory blood pressure , continuous positive airway pressure , hypoxia (environmental) , obstructive sleep apnea , anesthesia , endocrinology , chemistry , organic chemistry , oxygen

Maxi-K(+) channels play a major vasodilator role in the regulation of arterial tone. Hypoxia downregulates the expression of the maxi-K(+) channel beta1-subunit in rat and human arterial myocytes, thus facilitating vasoconstriction. We have investigated the relationships among hypoxemia, arterial pressure, and the expression of the beta1-subunit in patients with severe obstructive sleep apnea-hypopnea syndrome (SAHS), a highly prevalent condition that predisposes to hypertension.

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