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1 Department of Medicine and 2 White Mountain Research Station, University of California, San Diego, La Jolla, California 92093-0623; and 3 Vollum Institute, Oregon Health Sciences Center, Portland, Oregon 97201
We used genetically
engineered D2 receptor-deficient [D2-(
/)]
and wild-type [D2-(+/+)] mice to test the hypothesis that dopamine D2 receptors modulate the ventilatory response to
acute hypoxia [hypoxic ventilatory response (HVR)] and hypercapnia
[hypercapnic ventilatory response (HCVR)] and time-dependent changes
in ventilation during chronic hypoxia. HVR was independent of gender in
D2-(+/+) mice and significantly greater in
D2-(/) than in D2-(+/+) female mice. HCVR
was significantly greater in female D2-(+/+) mice than in
male D2-(+/+) and was greater in D2-(/)
male mice than in D2-(+/+) male mice. Exposure to hypoxia
for 2-8 days was studied in male mice only. D2-(+/+)
mice showed time-dependent increases in "baseline" ventilation
(inspired PO2 = 214 Torr) and hypoxic stimulated ventilation (inspired PO2 = 70 Torr) after 8 days of acclimatization to hypoxia, but
D2-(/) mice did not. Hence, dopamine D2
receptors modulate the acute HVR and HCVR in mice in a gender-specific
manner and contribute to time-dependent changes in ventilation and the
acute HVR during acclimatization to hypoxia.
hypoxic ventilatory response; hypercapnic ventilatory response; acclimatization to hypoxia; carotid body; transgenic mice
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