HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 288/5/L910    most recent 00414.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Carroll, J. L. Articles by Sterni, L. M. Search for Related Content PubMed PubMed Citation Articles by Carroll, J. L. Articles by Sterni, L. M.

Dopamine D2 receptor modulation of carotid body type 1 cell intracellular calcium in developing rats

¹University of Arkansas for Medical Sciences, College of Medicine, Department of Pediatrics, and ²Arkansas Children's Hospital, Little Rock, Arkansas; and ³Johns Hopkins University School of Medicine, Johns Hopkins Children's Center, Baltimore, Maryland

Submitted 26 November 2003 ; accepted in final form 27 December 2004

Carotid chemoreceptor type 1 cells release dopamine, which inhibits carotid chemoreceptor activity via dopamine D2 autoreceptors on type 1 cells. Postnatal changes in dopaminergic modulation may be involved in postnatal chemoreceptor development. The present study explores dopaminergic modulation of the intracellular calcium ([Ca²⁺]_i) response to hypoxia in type 1 cells from 1, 3, and 11- to 16-day-old rats. Using fura-2, we studied the effects of quinpirole, a D2 receptor agonist, on type 1 cell [Ca²⁺]_i response to 90-s hypoxia challenges (PO₂ 1–2 mmHg). Cells were sequentially exposed to the following challenges: 1) hypoxia control, 2) hypoxia plus quinpirole, and 3) hypoxia plus quinpirole plus sulpiride (D2 receptor antagonist). In the 11- to 16-day-old group, type 1 cell [Ca²⁺]_i increased 3 to 4-fold over resting [Ca²⁺]_i in response to hypoxia. Quinpirole (10 µM) significantly blunted the peak [Ca²⁺]_i response to hypoxia. Repeat challenge with hypoxia plus 10 µM quinpirole in the presence of 10 µM sulpiride partially restored the hypoxia [Ca²⁺]_i response. In sharp contrast to the older aged group, 10 µM quinpirole had minimal effect on hypoxia response of type 1 cells from 1-day-olds and a small but significant effect at 3 days of age. We conclude that stimulation of dopamine D2 receptors inhibits type 1 cell [Ca²⁺]_i response to hypoxia, consistent with an inhibitory autoreceptor role. These findings suggest dopamine-mediated inhibition and oxygen sensitivity increase with age on a similar time course and do not support a role for dopamine as a major mediator of carotid chemoreceptor resetting.

dopamine receptors; hypoxia; development; chemoreceptor