An induced blood pressure rise does not alter upper airway resistance in sleeping humans

Christine R. Wilson, Shalini Manchanda, David Crabtree, James B. Skatrud, Jerome A. Dempsey

Research output: Contribution to journalArticle

15 Scopus citations


Sleep apnea is associated with episodic increases in systemic blood pressure. We investigated whether transient increases in arterial pressure altered upper airway resistance and/or breathing pattern in nine sleeping humans (snorers and nonsnorers). A pressure-tipped catheter was placed below the base of the tongue, and flow was measured from a nose or face mask. During non-rapid-eye-movement sleep, we injected 40- to 200-μg iv boluses of phenylephrine. Parasympathetic blockade was used if bradycardia was excessive. Mean arterial pressure (MAP) rose by 20 ± 5 (mean ± SD) mmHg (range 12-37 mmHg) within 12 s and remained elevated for 105 s. There were no significant changes in inspiratory or expiratory pharyngeal resistance (measured at peak flow, peak pressure, 0.2 1/s or by evaluating the dynamic pressure-flow relationship). At peak MAP, end-tidal CO2 pressure fell by 1.5 Torr and remained low for 20-25 s. At 26 s after peak MAP, tidal volume fell by 19%, consistent with hypocapnic ventilatory inhibition. We conclude that transient increases in MAP of a magnitude commonly observed during non- rapid-eye-movement sleep-disordered breathing do not increase upper airway resistance and, therefore, will not perpetuate subsequent obstructive events.

Original languageEnglish (US)
Pages (from-to)269-276
Number of pages8
JournalJournal of Applied Physiology
Issue number1
StatePublished - Jan 1998


  • Barorecepter
  • Phenylephrine
  • Respiration
  • Sleep apnea

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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