| Description: |
Tropacocaine has cardiovascular effects.Tropacocaine inhibits norepinephrine uptake at the concentration of 30 microM. Tropacocaine has antimuscarinic activity, it can attenuate the oxotremorine-induced inhibition of the release of acetylcholine, it can inhibit the spontaneous and veratridine-induced release of newly synthesized acetylcholine, but not via activation of presynaptic muscarinic receptors. |
| Targets: |
5-HT Receptor | AChR |
| In vitro: |
| J Pharmacol Exp Ther. 1990 Aug;254(2):584-90. | | Effects of benzoyltropine and tropacocaine on several cholinergic processes in the rat brain.[Pubmed: 1974643] | Benzoyltropine and Tropacocaine are two contaminants of street-cocaine reported to have parasympatholytic activity. These studies used rat cerebral cortical synaptosomes, except for the receptor-binding studies, which used whole brain plasma membranes.
METHODS AND RESULTS:
Benzoyltropine and Tropacocaine each inhibited sodium-dependent choline uptake and acetylcholine synthesis in a dose-related manner that was competitive with extracellular choline. Benzoyltropine was 4 to 5 times more potent in both actions than Tropacocaine. Sodium-independent choline uptake was not affected by either compound. Benzoyltropine (30 microM) had no effect on the sodium-dependent uptake of norepinephrine, gamma-amino-butyric acid, glutamate or serotonin; Tropacocaine (30 microM) inhibited only norepinephrine uptake at this concentration. Benzoyltropine and Tropacocaine each inhibited the spontaneous and veratridine-induced release of newly synthesized acetylcholine, but not via activation of presynaptic muscarinic receptors. Instead, each compound was able to attenuate the oxotremorine-induced inhibition of the release of acetylcholine, suggesting antimuscarinic activity.
CONCLUSIONS:
Binding experiments showed that benzoyltropine and Tropacocaine were, respectively, about 1,000- and 10,000-fold less potent than scopolamine as receptor antagonists. |
|
| In vivo: |
| Neurotoxicology. 1995 Spring;16(1):145-51. | | Cardiovascular effects of tropacocaine in conscious and anesthetized rabbits: lack of evidence for neuro-cardiac interactions and acute neurotoxicity.[Pubmed: 7603635] |
The cardiovascular effects of Tropacocaine, a structural analog of cocaine, were investigated in both conscious and anesthetized New Zealand white rabbits to determine if such effects were mediated through the CNS as had been demonstrated with cocaine, i.e., did a neuro-cardiac pathway exist?
METHODS AND RESULTS:
To facilitate the requisite cardiovascular measurements in both urethane- and pentobarbital-anesthetized animals, the right femoral artery and vein were cannulated for the measurement of arterial blood pressure and subsequent delivery of drugs, respectively. In addition, urethane-anesthetized animals had a branch of the left renal nerve isolated and multiunit renal nerve activity was monitored to obtain measures of sympathetic nerve activity originating from the CNS. Animals utilized in conscious experiments were surgically prepared 3 days prior to drug administration by placing canulae in the femoral artery and vein that were tunneled subcutaneously to the back between the scapulae. ECG and respiratory activity were also monitored in each animal. Doses of 0.3, 1, 3, and 10 mg/kg of Tropacocaine were administered in both an ascending and descending fashion at 15 min intervals to 5 animals in each group, i.e., conscious, urethane-, and pentobarbital-anesthetized.
CONCLUSIONS:
In urethane-anesthetized animals a comparison was made between sympathetic renal nerve activity, systolic and diastolic blood pressure, respiratory rate, and heart rate. No pressor effects were observed and the changes in renal nerve activity could not be assigned as the cause of the observed depressor effects at the higher doses. |
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