Cardiovascular effects of cocaine in anesthetized and conscious rats
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Cited by (87)
The Critical Role of Peripheral Targets in Triggering Rapid Neural Effects of Intravenous Cocaine
2020, NeuroscienceCitation Excerpt :Furthermore, this rapid hypertensive effect is resistant to DA receptor blockade (Kiritsy-Roy et al., 1990; Poon and van den Buuse, 1998) and is mimicked by a BBB-impermeable cocaine-methiodide (Dickerson et al., 1999). While the initial, transient rise in arterial blood pressure was the most prominent effect of iv cocaine, it was followed by weaker and more prolonged pressure increase (Pitts et al., 1987), which was blocked by DA antagonists (Tella and Goldberg, 1998). Therefore, the effect of iv cocaine on arterial blood pressure appears to be biphasic, with the initial, peripherally triggered and subsequent centrally mediated components.
Ventral tegmental area neurons are either excited or inhibited by cocaine's actions in the peripheral nervous system
2012, NeuroscienceCitation Excerpt :However, under this scenario, cocaine should have fast access to sympathetic afferents that are located in the adventitia of blood vessels. Diffusion from the inside of the vessel to the adventitia takes approximately 60 s, as measured by physiological responses to cocaine on aortic baroreceptor activity (Andresen et al., 1990), which is more than the time of onset of the cocaine-induced rise in blood pressure, which is about 10–15 s (Pitts et al., 1987; Poon and van den Buuse, 1998). Other evidence against this view is that cocaine inhibits, but not activates, baroreceptors by an adrenoreceptor-independent mechanism (Andresen et al., 1990).
Effects of a long-acting mutant bacterial cocaine esterase on acute cocaine toxicity in rats
2011, Drug and Alcohol DependenceCitation Excerpt :In addition to demonstrating the power of DM CocE to protect against the convulsant and lethal effects of cocaine, the current studies also evaluated the capacity of DM CocE to affect the cardiovascular effects of 5.6 mg/kg; IV cocaine. Consistent with previous reports (Chen et al., 1995; Kiritsy-Roy et al., 1990; Mactutus et al., 2000; Pitts et al., 1987; Tella et al., 1992b), this relatively low dose of 5.6 mg/kg; IV cocaine increased MAP, decreased HR, and induced convulsion in approximately 80% of rats. Pretreatment with a low dose of DM CocE (0.32 mg/kg) not only effectively blunted the cocaine-induced changes in MAP and HR, but also completely prevented the onset of convulsion; effects that are similar to those observed with a 3 mg/kg dose of the mutant BChE, Albu-CocH (Brimijoin et al., 2008).
Electrophysiological evaluation of the time-course of dopamine uptake inhibition induced by intravenous cocaine at a reinforcing dose
2008, NeuroscienceCitation Excerpt :This peripheral trigger may also be activated by procaine, a local anesthetic structurally similar to cocaine but with minimal effects on DA uptake (Ritz et al., 1987). Procaine with rapid i.v. administration is able to mimic cardiovascular effects of cocaine (Pitts et al., 1987) and induce powerful limbic activation as well as sensory and emotional effects in humans (Servan-Shreiber et al., 1998). Despite the lack of primary reinforcing properties, procaine also mimics cocaine-induced euphoria in human cocaine abusers (Fischman and Schuster, 1983; Adinoff et al., 1998) and maintains drug-taking behavior in cocaine-trained animals (Johanson, 1980; Kiyatkin and Stein, 1995).
I.v. cocaine induces rapid, transient excitation of striatal neurons via its action on peripheral neural elements: Single-cell, iontophoretic study in awake and anesthetized rats
2007, NeuroscienceCitation Excerpt :Although procaine has only one-hundredth the affinity that COC has for the DA transporter (Ritz et al., 1987), in experienced users its i.v. administration fully mimics the initial subjective effects of i.v. COC (Fischman and Schuster, 1983; Adinoff et al., 1998). In addition to sensory and affective actions, i.v. procaine also induces an acute, transient hypertensive response (Pitts et al., 1987) associated with peripheral vasoconstriction (Brown and Kiyatkin, 2006), although acting topically it has an opposite, weak vasodilative action (Lindoft, 1979; Willatts and Reynolds, 1985). By affecting various central neurons involved in the processing of somato-sensory information and organization of brain activational processes, this rapid and brief “indirect” action of COC can modulate its slow and prolonged “direct” actions on monoamine uptake.