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  • Title: Release of 3H-noradrenaline from rabbit isolated ear artery.
    Author: Abrahamsen J, Nedergaard OA.
    Journal: Pharmacol Toxicol; 1990 Oct; 67(4):288-94. PubMed ID: 2077519.
    Abstract:
    The stimulation-evoked 3H-overflow from rabbit isolated ear arteries preincubated with 3H-noradrenaline was studied. Three strips were derived from each central artery. The strips were incubated (30 min.) with 3H-noradrenaline (10(-7) M) and the spontaneous 3H-outflow and stimulation-evoked 3H-overflow were followed by fractional collection. After a wash-out period (75 min.), the strips were stimulated (225 mA; 150 monophasic pulses; 3 Hz; 0.5 msec.) several times. The initial stimulation-evoked 3H-overflow (S1) was about 5-fold higher than the subsequent five 3H-overflows (S2-S6) which remained almost constant. Bretylium (10(-5) M), tetrodotoxin (10(-6) M), and omission of Ca2+ from the physiological salt solution reduced the stimulation-evoked 3H-overflow by maximally 52%, 77% and 62%, respectively. An increase in stimulation current from 50 to 225 mA caused a continuous rise in stimulation-evoked 3H-overflow, which tended to be Ca2(+)-sensitive. The stimulation-evoked 3H-overflow was frequency-dependent: at 1-4 Hz, the 3H-overflows were the same; at 8 and 16 Hz, they increased. Cocaine (3 x 10(-5) M) plus corticosterone (4 x 10(-5) M) enhanced the stimulation-evoked 3H-overflow at 1-8 Hz, while it had no effect at 16 Hz. Propranolol (3 x 10(-7) M) did not antagonize this enhancement. An increase in number of pulses from 10 to 1000 in the stimulus caused a corresponding rise in the evoked 3H-overflow. This was also the case when cocaine plus corticosterone were present.(ABSTRACT TRUNCATED AT 250 WORDS)
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