PMID: 7529004Dec 1, 1994Paper

Dopamine or transmitter release from rat carotid body may not be essential to hypoxic chemoreception

The American Journal of Physiology
M K Sun, D J Reis

Abstract

In anesthetized, paralyzed, and ventilated rats, hypoxia or intracarotid cyanide excited the carotid chemoafferents, whereas intracarotid dopamine and tyramine inhibited the chemoafferent discharges. The inhibition was abolished by chlorpromazine without attenuating the hypoxic excitation. Comparably, the hypoxic excitation was not attenuated by the following: 1) inhibition of nitric oxide synthase with NG-nitro-L-arginine; 2) inhibition of heme oxygenase with zinc protoporphyrin IX; 3) antagonism of ATP receptors with reactive blue 2; 4) antagonism of cholinergic receptors with atropine or trimethaphan; 5) inactivation of adenosine with adenosine deaminase; and 6) blockade of glutamate receptors with kynurenate. Systemic administration of ethylene glycol-bis(beta-aminoethyl ether)-N,N,N'N'-tetraacetic acid, in doses reversibly blocking sympathetic ganglionic transmission, was also without effect. Cyanide microinjection (0.05-0.5 nmol) into the petrosal but not nodose ganglion elicited a rapid dose-dependent elevation of arterial pressure. We conclude that excitation of the chemoreceptor afferents by hypoxia/cyanide cannot be attributed to release of these agents nor to others by Ca(2+)-dependent mechanisms. The results suggest...Continue Reading

Citations

Aug 12, 2006·Journal of Applied Physiology·Edward Vincent S Faustino, David F Donnelly
Oct 23, 2002·Journal of Applied Physiology·Ryan W Bavis, Gordon S Mitchell
Mar 13, 2014·Journal of Applied Physiology·Benjamin GastonStephen J Lewis
Apr 16, 2010·Physiological Reviews·Luc J Teppema, Albert Dahan

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