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THE EFFECT OF COCAINE AND DESIPRAMINE ON NEURONAL UPTAKE OF [ 3 H]‐NORADRENALINE AND SENSITIVITY TO NORADRENALINE OF RAT MESENTERIC RESISTANCE ARTERIES
Author(s) -
Byg Anne M.,
Bund Stuart,
Mulvany Michael J.,
Aalkjær Christian
Publication year - 1994
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1994.tb02563.x
Subject(s) - desipramine , mesenteric arteries , norepinephrine , medicine , sensitivity (control systems) , chemistry , endocrinology , dopamine , artery , electronic engineering , engineering , hippocampus , antidepressant
SUMMARY 1. The effects of cocaine and desipramine (DMI) on neuronal uptake (uptake 1 ) of [ 3 H]‐noradrenaline (NA) and isometric tension development to exogenous NA were assessed in mesenteric resistance arteries of Wistar rats. 2. Both drugs concentration‐dependently inhibited [ 3 H]‐NA uptake 1 , DMI being more potent than cocaine. The maximum inhibition produced by each drug was the same as that produced by denervation with 6‐hydroxydopamine. In denervated vessels there was no effect of cocaine on [ 3 H]‐NA uptakel. 3. Cocaine, in the same concentration range which caused inhibition of uptakel, increased the sensitivity to NA, while DMI, in a concentration range which inhibited uptake 1 , did not increase the sensitivity to NA and at high concentrations reduced the sensitivity and maximal response to NA. Since DMI affected responses to NA but not responses to vasopressin and potassium its effect is probably related to blockade of α 1 ‐adrenoceptors. 4. We conclude that the effect of cocaine on the sensitivity to NA reflects inhibition of uptakel in rat resistance arteries, while DMI cannot be used to assess the functional effect of uptakel in this preparation.