Section 41
Chapter 40,175

Frequency-dependence of 3H-noradrenaline release from rabbit pulmonary artery: effect of alpha-adrenoceptor antagonists and inhibitors of transmitter inactivation

Nedergaard, O.A.

Pharmacology and Toxicology 63(5): 317-323


ISSN/ISBN: 0901-9928
PMID: 2907129
DOI: 10.1111/j.1600-0773.1988.tb00961.x
Accession: 040174046

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The aim of this study was to examine the modulating role of presynaptic alpha 2-adrenoceptors on transmitter release from vascular sympathetic neurones. This was done by examining the influence of removal of inactivation pathways on the effect of alpha-adrenoceptor antagonists on the release of transmitter from noradrenergic neurones. The rabbit main pulmonary artery preloaded with 3H-noradrenaline (3H-NA) was used. The artery was stimulated with 300 pulses at various frequencies (1, 3, 10 and 30 Hz). Pargyline (3 x 10(-4) M) increased the stimulation-evoked 3H-overflow at 1 and 3 Hz and decreased it at 30 Hz. U-0521 (3',4'-dihydroxy-2-methylpropiophenone; 3 x 10(-6) M) enhanced the overflow at 1 Hz and had no effect at 3-30 Hz. Corticosterone (4 x 10(-5) M) did not alter the stimulation-evoked 3H-overflow at 1-30 Hz. Cocaine (3 x 10(-6) M) enhanced the 3H-overflow slightly at 1-30 Hz. At 3 x 10(-5) M, cocaine enhanced 3H-overflow at 1 Hz and reduced it at 30 Hz. Neither corticosterone (4 x 10(-5) M) nor propranolol (10(-7) M) modified this effect of cocaine. Propranolol (10(-7) M) alone decreased the 3H-overflow at 30 Hz and had no effect at 1-10 Hz. Phenoxybenzamine (10(-6) M) and chlorpromazine (3 x 10(-6) M) potentiated the stimulation-evoked 3H-overflow at 1-30 Hz.

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