Dependency of hypoxic chemotransduction in cat carotid body on voltage-gated calcium channels

M. Shirahata, Robert S Fitzgerald

Research output: Contribution to journalArticle

Abstract

The hypothesis that the entry of extracellular calcium ions into some compartment, quite possibly the type I cells, through voltage-gated calcium channels (VGCC) is essential for hypoxic chemotransduction in the cat carotid body was tested using an in situ perfusion technique. The neural output of the carotid body of anesthetized, paralyzed, and artificially ventilated cats in response to perfusions with Krebs-Ringer bicarbonate solution (KRB), calcium-free KRB, KRB containing calcium channel blockers, or KRB containing BAY K 8644 was recorded. Selective perfusion of the carotid body with hypoxic calcium-free KRB significantly decreased carotid chemoreceptor activity, suggesting that extracellular calcium is essential for hypoxic chemotransduction. Selective perfusion of the carotid body with hypoxic KRB containing verapamil (10-100 μM), diltiazem (10-100 μM), or nifedipine (10-100 μM) dose dependently attenuated the increase in chemoreceptor activity produced by hypoxia, suggesting that VGCC need to be activated for hypoxic chemotransduction. The carotid body response to hyperoxic KRB containing the calcium channel agonist BAY K 8644 (10 μM) was 267 ± 87% of hyperoxic control KRB, suggesting that an enhanced influx of calcium ions through VGCC stimulates carotid chemoreceptor activity. Selective perfusion of the carotid body with severely hypoxic KRB containing BAY K 8644 did not increase chemoreceptor activity above that produced by severe hypoxia alone. This suggests that severe hypoxia increases intracellular calcium in some compartment of the carotid body to achieve stimulatory maximum response and that further increase in intracellular calcium does not produce further elevation of neural activity. The above results support the hypothesis and suggest a model for hypoxic chemotransduction in the carotid body: hypoxia induces the entry of calcium into the type I cells through VGCC; this triggers the secretion of excitatory transmitter(s) known to exist in the type I cells, producing the action potentials recorded from the carotid sinus nerve chemoreceptor afferents.

Original languageEnglish (US)
Pages (from-to)1062-1069
Number of pages8
JournalJournal of Applied Physiology
Volume71
Issue number3
StatePublished - 1991

Fingerprint

Carotid Body
Calcium Channels
Bicarbonates
Cats
Calcium
Perfusion
Calcium Channel Agonists
Ions
Krebs-Ringer solution
Carotid Sinus
Diltiazem
Calcium Channel Blockers
Nifedipine
Verapamil
Action Potentials
Hypoxia

Keywords

  • calcium channel agonist
  • calcium channel blockers
  • carotid chemoreceptor activity
  • neurotransmitter

ASJC Scopus subject areas

  • Physiology
  • Endocrinology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Dependency of hypoxic chemotransduction in cat carotid body on voltage-gated calcium channels. / Shirahata, M.; Fitzgerald, Robert S.

In: Journal of Applied Physiology, Vol. 71, No. 3, 1991, p. 1062-1069.

Research output: Contribution to journalArticle

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