Toxic doses ofrac-, (?)-(S)- and (+)-(R)-propranolol in rats and rabbits

Toet, Arthur E.; Kuil, A. van de; Vleeming, W.; Wemer, J.; Bode, W.; Meulenbelt, Jan; Wildt, Dick J. De

doi:10.1002/(sici)1520-636x(1996)8:6<411::aid-chir1>3.0.co;2-f

Cited by 6 publications

(3 citation statements)

References 19 publications

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“…In fact, in spontaneously breathing rats, propranolol administered at 30 mg/kg i.v. decreases heart rate and mean arterial blood pressure and causes hypoventilation, serious hypoxaemia, respiratory acidosis, and death by respiratory arrest (Toet et al 1996).…”

Section: Discussionmentioning

confidence: 99%

Limited efficacy of propranolol on the reconsolidation of fear memories

Muravieva¹,

Alberini²

2010

Learn. Mem.

120

113

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Previous studies suggested that the b-adrenergic receptor antagonist propranolol might be a novel, potential treatment for post-traumatic stress disorder (PTSD). This hypothesis stemmed mainly from rodent studies showing that propranolol interferes with the reconsolidation of Pavlovian fear conditioning (FC). However, subsequent investigations in humans have produced controversial evidence about the effect of propranolol on fear memories and an effect on PTSD symptomatology has yet to be reported. Thus, it remains to be established whether propranolol interferes with the reconsolidation of fear memories at large. To address this question, we tested the effect of systemic injections of propranolol administered before or after the retrieval of an inhibitory avoidance (IA) memory elicited with different footshock intensities. In parallel, the same treatment was tested on the reconsolidation of Pavlovian FC. Propranolol showed no effect on the reconsolidation of IA, although the pre-retrieval administration resulted in a significant retrieval impairment. This impairment was transient, and memory returned to control levels at later times. In agreement with previous studies, we found that systemic administration of propranolol disrupts the reconsolidation of Pavlovian FC and that its injection following a retrieval elicited by cue exposure also interferes with the reconsolidation of contextual FC. Hence, propranolol disrupts the reconsolidation of Pavlovian FC, but has no effect on the reconsolidation of IA. The results indicate that the efficacy of systemic administration of propranol in disrupting the reconsolidation of fear memories is limited.

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Section: Discussionmentioning

confidence: 99%

Limited efficacy of propranolol on the reconsolidation of fear memories

Muravieva¹,

Alberini²

2010

Learn. Mem.

120

113

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“…it took 14 days to fully develop). Because systemic administration of propranolol is toxic in rats (Toet et al ., 1996), we chronically administered the selective β 2 ‐adrenergic receptor antagonist ICI 118,551 (Bilski et al ., 1983).…”

Section: Methodsmentioning

confidence: 99%

Vagal modulation of nociception is mediated by adrenomedullary epinephrine in the rat

Khasar

Green

Miao

et al. 2003

Eur J of Neuroscience

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Vagal afferent activity modulates mechanical nociceptive threshold and inflammatory mediator-induced hyperalgesia, effects that are mediated by the adrenal medulla. To evaluate the role of epinephrine, the major hormone released from the adrenal medulla, the beta2-adrenergic receptor antagonist ICI 118,551 was chronically administered to vagotomized rats and epinephrine to normal rats. In vagotomized rats, chronic administration of ICI 118,551 markedly attenuated vagotomy-induced enhancement of bradykinin hyperalgesia but had no effect on nociceptive threshold. In normal rats, chronic epinephrine had the opposite effect, enhancing bradykinin hyperalgesia. Like vagotomy-, epinephrine-induced enhancement of hyperalgesia developed slowly, taking 14 days to reach its peak. Vagotomy induced a chronic elevation in plasma concentrations of epinephrine. We suggest that ongoing activity in vagal afferents inhibits the release of epinephrine from the adrenal medulla. Chronically elevated levels of epinephrine, occurring after vagotomy, desensitize peripheral beta2-adrenergic receptors and lead to enhancement of bradykinin hyperalgesia. The ability of prolonged elevated plasma levels of epinephrine to sensitize bradykinin receptors could contribute to chronic generalized pain syndromes.

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“…The enantiospecific effects of propranolol on Daphnia magna heart Recently, it was shown that racemic propranolol exhibits higher toxicity in rat than both its pure enantiomers. This increase in toxicity can be at least partially based on pharmacokinetic interactions [66,67].…”

Section: Propranololmentioning

confidence: 99%

Survey of Pharmacological Activity and Pharmacokinetics of Selected β-Adrenergic Blockers in Regard to Their Stereochemistry

et al. 2019

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The present survey concentrates on pharmacodynamics and pharmacokinetics of selected β-adrenergic blockers from the point of view of their stereochemistry. It could be shown that the activity in the arylaminoethanol and aryloxyaminopropanol group of β-blockers is higher in their (–)-enantiomers as compared with the (+)-enantiomers. The stereoisomers differ also in other types of bioactivity as well as in toxicity. The particular pharmacokinetic stages such as resorption, distribution, and metabolism are discussed in regard to their stereochemistry.

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Toxic doses ofrac-, (?)-(S)- and (+)-(R)-propranolol in rats and rabbits

Cited by 6 publications

References 19 publications

Limited efficacy of propranolol on the reconsolidation of fear memories

Limited efficacy of propranolol on the reconsolidation of fear memories

Vagal modulation of nociception is mediated by adrenomedullary epinephrine in the rat

Survey of Pharmacological Activity and Pharmacokinetics of Selected β-Adrenergic Blockers in Regard to Their Stereochemistry

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