Respiration during acute hypoxia: angiotensin- and vasopressin-receptor blocks.

Published

Journal Article

In normoxic conscious dogs, increased angiotensin II (ANG II), or activation (disinhibition) of the renin-angiotensin system by vasopressin (AVP) V1-receptor block, increases ventilation and decreases arterial PCO2. Both hormones can be increased during hypoxia and might modulate ventilatory drive. Six conscious dogs were studied before and during hypocapnic, isocapnic, and hypercapnic hypoxia. To study potential hormonal effects during hypocapnic hypoxia, experiment 1 included three protocols in which 12.8% O2 was breathed for 60 min: protocol 1, control studies without block; protocol 2, AVP V1 receptors were blocked at the onset of hypoxia; and protocol 3, ANG II receptors were blocked 20 min before hypoxia. To study potential effects of acid-base changes during acute hypoxia, experiment 2 included two protocols (with and without AVP V1-receptor block). A 40-min period of hypocapnic hypoxia was followed by two successive 20-min periods with hypoxia maintained but inspired CO2 progressively increased. Neither hormonal block affected respiration during the hypoxic conditions. Unlike normoxia in conscious dogs, during acute hypoxia, respiratory control by ANG II is not modulated by AVP and acid-base effects on receptors do not account for this difference.

Full Text

Duke Authors

Cited Authors

  • Overgaard, CB; Walker, JK; Jennings, DB

Published Date

  • March 1996

Published In

Volume / Issue

  • 80 / 3

Start / End Page

  • 810 - 817

PubMed ID

  • 8964741

Pubmed Central ID

  • 8964741

Electronic International Standard Serial Number (EISSN)

  • 1522-1601

International Standard Serial Number (ISSN)

  • 8750-7587

Digital Object Identifier (DOI)

  • 10.1152/jappl.1996.80.3.810

Language

  • eng