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PubMed1989

Persistence of retrieval enhancement by amphetamine following scopolamine-induced amnesia.

Little information is available on the permanence of pharmacologically-induced retrieval enhancement following amnesia. This was studied by comparing the rate of forgetting of a memory reactivated by d-amphetamine after amnesia with spontaneous forgetting of undisturbed fear conditioning. Mice were treated with either saline or scopolamine before conditioning and retention was tested three days later. Scopolamine-treated mice received either saline or amphetamine before testing while the saline controls received a second saline injection. The scopolamine-saline group exhibited robust amnesia, whereas both saline-saline and scopolamine-amphetamine groups showed good retention. To test the persistence of these effects mice in the three groups were subdivided and given a second retention test either 1 day, 1 week or 1 month after the first test. Amphetamine was not administered before the second test. The scopolamine-saline mice continued to exhibit amnesia for up to 1 month while the scopolamine-amphetamine and saline-saline groups continued to show strong memory with only a modest decrement in performance by 1 month after the first test. These results show that amphetamine results in a permanent recovery from scopolamine amnesia.

Amnesia↗
PubMed1982

Age-dependent effects of scopolamine on avoidance, locomotor activity, and rearing.

In Experiment 1, 15-, 17-, 21-, 36- and 90-day-old rats were injected with either physiological saline or 0.5, 1.0, 4.0, 8.0, 16.0 or 32.0 mg/kg of scopolamine (an anticholinergic). Immediately after the injection, shuttle crossings during adaptation were recorded for 8 min, and then the rats were given a single session of 100 two-way avoidance trials. In all ages, scopolamine increased two-way avoidance and intertrial responses throughout training and avoidance and intertrial responses were positively correlated, suggesting that increased avoidance was due, in part, to increased locomotor activity. In addition, scopolamine increased locomotor activity at an earlier age in a stressful situation, i.e. during the intertrial interval, than in a less stressful environment, i.e. during adaptation. In Experiment 2, photocell crossings and rearing were examined in 15-, 17-, 21-, 36-, 90- and 275-day-old rats injected with saline or 0.5, 1.0, 4.0, 8.0 or 16.0 mg/kg of scopolamine hydrobromide. Scopolamine increased photocell crossings in rats 21 days of age and older but did not increase rearing until 36 days of age. Scopolamine also had different behavioral effects in the three oldest ages. Thus, cholinergic involvement in these behaviors changes from at least 15 to 275 days of age. Methylscopolamine, which does not cross the blood-brain barrier, did not alter the behaviors examined in Experiments 1 and 2, suggesting that development of cholinergic neurons in the CNS is responsible for the age-dependent behavioral effects of scopolamine.

Acetylcholine↗
PubMed1996

Effects of repeated treatment with methamphetamine plus scopolamine and methamphetamine on behavioral sensitization and conditioning.

This study compared repeated treatment with methamphetamine (4.0 mg/kg, i.p.) plus scopolamine (0.5 mg/kg, i.p.) and methamphetamine alone in behavioral sensitization and drug conditioning with respect to a reciprocal balance between the dopaminergic and cholinergic systems. Repeated methamphetamine plus scopolamine treatment induced a more progressive and enduring enhancement of stereotyped behavior than repeated methamphetamine treatment. Methamphetamine plus scopolamine-induced stereotyped behavior was reproduced by challenge injections of not only methamphetamine plus scopolamine and methamphetamine, but also, to a lesser extent, by scopolamine challenges. The methamphetamine plus scopolamine-sensitized rats were conditioned to a low-frequency tone (300 Hz, 100 dB) as conditioned stimulus associated with the drug state. They responded to pairings of the tone and placebo injections, but not to the tone alone or the placebo alone. The methamphetamine-sensitized rats failed to exhibit conditioning. These results suggest that methamphetamine plus scopolamine-induced pronounced behavioral sensitization may produce an enhanced conditioning. Exteroceptive conditioned stimulus-interoceptive unconditioned stimulus associations may provide an important source for drug conditioning. We concluded that behavioral sensitization may be mediated via a reciprocal balance between the dopaminergic and cholinergic systems, in favor of a dopaminergic dominance. Conditioning to the drug-associated tone may operate via a reciprocal balance between the dopaminergic and cholinergic systems.

Animals↗
PubMed1992

Effects of noradrenergic DSP4 lesion on the effectiveness of pilocarpine in reversing scopolamine-induced amnesia.

We studied the effectiveness of pilocarpine in reversing the scopolamine-induced water maze learning deficit (increase in escape latencies, decrease in spatial bias) in control and DSP4- (a noradrenergic neurotoxin) lesioned rats. The water maze acquisition deficit (escape latency, first spatial bias) induced by scopolamine 0.8 mg/kg was augmented by DSP4 treatment. The water maze performance deficit induced by scopolamine was reversed by pilocarpine 4 mg/kg in both DSP4-lesioned and control rats. A smaller dose of pilocarpine (1 mg/kg) did not reverse scopolamine-induced acquisition deficit in either control or DSP4-lesioned rats. Analysis of the second spatial bias test measured 2 weeks after training revealed that pilocarpine 4 mg/kg reversed scopolamine-induced retention deficit in control and DSP4-lesioned rats. Pilocarpine 1 mg/kg reversed scopolamine-induced retention performance deficit during the second spatial bias test in control but not in DSP4-lesioned rats. The present results suggest that 1) noradrenergic and cholinergic systems may interact in the regulation of spatial acquisition and retention and 2) the effectiveness of cholinergic drugs in reversing scopolamine-induced spatial retention deficit may be affected by noradrenergic lesioning.

Amnesia↗
PubMed1993

Scopolamine increases vagal tone and vagal reflexes in patients after myocardial infarction.

OBJECTIVES: The goal of this study was to assess the hypothesis that transdermal scopolamine would increase vagal activity in patients after myocardial infarction. BACKGROUND: In postmyocardial infarction patients, low heart rate variability and reduced baroreceptor reflex sensitivity are associated with increased mortality. Accordingly, there is an increasing interest in a mechanism for shifting the sympathovagal balance toward vagal dominance. METHODS: The effects of transdermal administration of scopolamine on heart rate variability and baroreceptor reflex sensitivity were assessed in 20 patients (mean age 59 +/- 11 years) by pharmacologic washout 14 +/- 3 days after myocardial infarction. Heart rate variability and baroreceptor reflex sensitivity were measured 24 h after application of the scopolamine patch and compared with the values measured before scopolamine and after application of a placebo patch. The following variables were derived from a 15-min electrocardiographic recording: the mean RR interval and its standard deviation, the mean square successive difference, the percent of intervals differing > 50 ms from the preceding RR interval and the low and high frequency areas resulting from power spectral analysis. RESULTS: The placebo patch had no effect on the variables measured. Scopolamine increased both heart rate variability and baroreceptor reflex sensitivity significantly. Specifically, the mean RR interval and its standard deviation increased by 7.1% (p = 0.01) and 25% (p = 0.004), respectively. The mean square successive difference increased by 38% (p = 0.0003) and the percent of intervals differing > 50 ms from the preceding interval by 100% (p = 0.001). The ratio of low to high frequency areas of the power spectrum decreased by 24% (p = 0.02), and baroreceptor reflex sensitivity increased by 42% (p = 0.0006). These effects were also evident in patients with very low initial values. Side effects were minimal. CONCLUSIONS: Transdermal scopolamine increased measures of heart rate variability and baroreceptor reflex sensitivity in patients with a recent myocardial infarction toward values associated with a better prognosis. Pharmacologic modulation of the autonomic balance by scopolamine or related drugs deserves evaluation as a new and promising approach to reduce risk after myocardial infarction.

Administration, Cutaneous↗
PubMed2004

Attenuation of scopolamine-induced learning deficits by LVV-hemorphin-7 in rats in the passive avoidance and water maze paradigms.

Central administration of angiotensin IV (Ang IV) analogues attenuates scopolamine-induced amnesia. Ang IV mediates its effects by binding to a high affinity, binding site, AT(4) receptor, that has recently been identified as insulin regulated aminopeptidase (IRAP). The purpose of this study was to examine the effect of the distinct AT(4) ligand, LVV-hemorphin-7 (LVV-H7), on scopolamine-induced learning deficits, one which involves fear-conditioning and the other spatial learning. Rats were pretreated with an intracerebroventricular (ICV) dose of scopolamine hydrobromide followed by treatment with 1 nmol LVV-H7 or artificial cerebrospinal fluid (aCSF). During the acquisition phase of the water maze task, daily ICV infusions of 1 nmol of LVV-H7 25 min after scopolamine treatment produced marked improvement in both the latency and distance swum in order to locate the submerged platform using visual cues compared to animals treated with scopolamine only. In addition, the same dose of LVV-H7 attenuated the learning deficit observed for scopolamine-treated animals in the passive avoidance task. These studies clearly demonstrate that LVV-H7, like Ang IV, is a pharmacologically active AT(4) ligand that attenuates the deleterious effects of scopolamine on learning performance in two different behavioral paradigms.

Aminopeptidases↗
PubMed2005

Microinjection of ritanserin into the CA1 region of hippocampus improves scopolamine-induced amnesia in adult male rats.

The effect of ritanserin (5-HT2 antagonist) on scopolamine (muscarinic cholinergic antagonist)-induced amnesia in Morris water maze (MWM) was investigated. Rats were divided into eight groups and bilaterally cannulated into CA1 region of the hippocampus. One week later, they received repeatedly vehicles (saline, DMSO, saline+DMSO), scopolamine (2 microg/0.5 microl saline/side; 30 min before training), ritanserin (2, 4 and 8 microg/0.5 microl DMSO/side; 20 min before training) and scopolamine (2 microg/0.5 microl; 30 min before ritanserin injection)+ritanserin (4 microg/0.5 microl DMSO) through cannulae each day. Animals were tested for four consecutive days (4 trial/day) in MWM during which the position of hidden platform was unchanged. In the fifth day, the platform was elevated above the water surface in another position to evaluate the function of motor, motivational and visual systems. The results showed a significant increase in escape latencies and traveled distances to find platform in scopolamine-treated group as compared to saline group. Ritanserin-treated rats (4 microg/0.5 microl/side) showed a significant decrease in the mentioned parameters as compared to DMSO-treated group. However, scopolamine and ritanserin co-administration resulted in a significant decrease in escape latencies and traveled distances as compared to the scopolamine-treated rats. Our findings show that microinjection of ritanserin into the CA1 region of the hippocampus improves the scopolamine-induced amnesia.

Amnesia↗
PubMed2005

Delayed rectifier potassium currents and Kv2.1 mRNA increase in hippocampal neurons of scopolamine-induced memory-deficient rats.

To explore the ionic mechanisms of memory deficits induced by cholinergic lesion, whole-cell patch clamp recording techniques in combination with single-cell RT-PCR were used to characterize delayed rectifier potassium currents (IK) in acutely isolated hippocampal pyramidal neurons of scopolamine-induced cognitive impairment rats. Scopolamine could induce deficits in spatial memory of rats. The peak amplitude and current density of IK measured in hippocampal pyramidal neurons were increased from 1.2+/-0.6 nA and 38+/-19 pA/pF of the control group (n=12) to 1.8+/-0.5 nA and 62+/-24 pA/pF (n=48, P<0.01) of the scopolamine-treated group. The steady-state activation curve of IK was shifted about 8 mV (P<0.01) in the direction of hyperpolarization in scopolamine-treated rats. The mRNA level of Kv2.1 was increased (P<0.01) in the scopolamine-treated group, but there was no significant change of Kv1.5 mRNA level. The present study demonstrated for the first time that IK was enhanced significantly in hippocampal pyramidal neurons of scopolamine-induced cognitive impairment rats. The increase of Kv2.1 mRNA expression in hippocampal pyramidal cells might be responsible for the enhancement of IK and could be the ionic basis of the memory deficits induced by scopolamine.

Action Potentials↗
PubMed1998

The influence of ondansetron and m-chlorophenylpiperazine on scopolamine-induced cognitive, behavioral, and physiological responses in young healthy controls.

BACKGROUND: There is evidence from animal and human experiments that learning and memory come under the separate influence of both cholinergic and serotonergic pathways. We were interested in learning whether serotonergic drugs could attenuate or exacerbate the memory-impairing effects of anticholinergic blockade in humans. METHODS: The selective serotonin 5-HT3 receptor antagonist ondansetron (0.15 mg/kg i.v.) and the serotonergic agent m-chlorophenylpiperazine (m-CPP; 0.08 mg/kg i.v.) were administered in combination with the anticholinergic agent scopolamine (0.4 mg PO) and compared to scopolamine alone in 10 young, healthy volunteers. Testing occurred on three separate days. RESULTS: As expected, i.v. administration of scopolamine induced significant impairments in episodic memory and processing speed; however, these scopolamine-induced cognitive deficits were not attenuated by pretreatment with i.v. ondansetron (0.15 mg/kg), nor were they exacerbated by administration of i.v. m-CPP (0.8 mg/kg) in addition to scopolamine; however, administration of i.v. m-CPP was followed by a significant increase of self-rated functional impairment, altered self-reality, and dysphoria ratings, and scopolamine's effect on pupil size was potentiated. CONCLUSIONS: Together, these results suggest that in young, healthy volunteers scopolamine-induced changes of cognitive performance are only minimally modulated by the serotonergic effects on ondansetron and m-CPP. Further studies with older controls are needed to test whether these findings may be influenced by age.

Adult↗
PubMed1998

Involvement of dopamine receptors in beneficial effects of tachykinins on scopolamine-induced impairment of alternation performance in mice.

The involvement of dopamine receptors in the beneficial effects of intracerebroventricular injection of substance P, neurokinin A and senktide on the scopolamine-induced impairment of spontaneous alternation performance was investigated in mice. Scopolamine (1 mg/kg) significantly impaired spontaneous alternation performance, while substance P (0.1 microg), neurokinin A (0.3 microg), senktide (0.003 microg) and S(-)-sulpiride (10 mg/kg), a dopamine D2 receptor antagonist, improved the scopolamine (1 mg/kg)-induced disturbance of spontaneous alternation performance. However, the dopamine D1 receptor antagonist SCH23390 (7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine maleate) did not influence the scopolamine-induced disturbance of spontaneous alternation performance. The dopamine D2 receptor agonist RU24213 (N-n-propyl-N-phenylethyl-p-(3-hydroxyphenyl)-ethylamine hydrochloride) (1 mg/kg) but not the dopamine D1 receptor agonist SKF38393 (2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1 H-3-benzazepine hydrochloride) (3 and 10 mg/kg) reversed the beneficial effects of substance P (0.1 microg) and neurokinin A (0.3 microg) on the scopolamine (1 mg/kg)-induced impairment of spontaneous alternation performance. In contrast, neither SKF38393 (3 and 10 mg/kg) nor RU24213 (0.3 and 1 mg/kg) significantly affected the beneficial effects of senktide (0.003 microg) on the scopolamine (1 mg/kg)-induced impairment of spontaneous alternation performance. Although RU24213 (1 mg/kg) and SCH23390 (0.03 mg/kg) markedly decreased total arm entries, SKF38393 (10 mg/kg), RU24213 (1 mg/kg), SCH23390 (0.03 mg/kg) or S(-)-sulpiride (10 mg/kg) had no significant effects on spontaneous alternation performance. These results suggest that stimulation of dopamine D2 but not D1 receptors reverses the ameliorative effects of substance P and neurokinin A, whereas neither dopamine D1 nor D2 receptors play an important role in the beneficial effects of senktide on the scopolamine-induced impairment of spontaneous alternation performance associated with spatial working memory.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2003

Role of cholinergic receptors in locomotion induced by scopolamine and oxotremorine-M.

Mesopontine cholinergic neurons activate dopamine neurons important for reward-seeking and locomotor activity. The present studies tested whether cholinergic receptor blockade in the ventral tegmental area (VTA) altered locomotion induced by scopolamine (3 mg/kg i.p.) or by oxotremorine-M (0.1 microg bilaterally in the VTA). It was predicted that cholinergic blockers in the VTA would attenuate these cholinergic-induced locomotor increases. Locomotor activity was increased by scopolamine and oxotremorine-M administration in all treatments. When dihydro-beta-erythroidine (DHBE), a nicotinic receptor antagonist, was applied in VTA prior to oxotremorine-M, locomotion was reduced to slightly above saline baseline levels, but atropine, a muscarinic antagonist, had no effect. This suggests that the locomotor effect of oxotremorine-M at this dose was mediated mainly via nicotinic, not muscarinic, receptors. Intra-VTA injections of DHBE, however, did not attenuate scopolamine-induced locomotion indicating that scopolamine-induced locomotion is not mediated mainly via VTA cholinergic receptors. In mutant mice with a deletion in the M5 muscarinic receptor gene, scopolamine-induced locomotion was increased versus wild type mice after scopolamine injection. This suggests that the M5 receptor has an inhibitory effect on scopolamine-induced locomotion.

Animals↗
PubMed1988

Strength of scopolamine-induced amnesia as a function of time between training and testing.

Variations in the strength of scopolamine-induced amnesia as a function of age of the habit were studied in Swiss Webster mice. Animals were trained in an active avoidance task to a criterion of 9/10 avoidances and immediately following training injected with scopolamine hydrochloride (1.0 mg/kg) or saline. Retention of the avoidance learning was evaluated by testing different groups of animals 1, 3, 7, 10, 14, and 28 days following training. The retention test consisted of five trials in which the CS but not the UCS was presented. Results indicated that saline-treated mice exhibited near-perfect retention up to 14 days post-training with forgetting beginning to be apparent at 28 days. Scopolamine treatment produced strong amnesia in animals tested 1 and 3 days post-training but normal retention in animals tested 7 and 10 days after learning. The amnesia abruptly reappeared at 14 days after which time it remained stable. The marked similarity of the scopolamine retention curve to changes in the strength of memory of discrimination learning in undertrained rats reported by Deutsch suggested that scopolamine resulted in the storage of a weak memory of the avoidance response. To explore this idea further we trained mice to a criterion (4/5) which would result in a weak avoidance response and tested different groups 1, 3, 10, 14, and 28 days following learning. Results showed that strength of the memory of avoidance learning increased up to 10 days and then decreased abruptly at 14 days thus replicating the general shape of the retention curve produced by injecting scopolamine following strong training. These data suggest that scopolamine disrupts processes essential for the formation of durable memories.

Animals↗
PubMed1996

Bioavailability of intranasal scopolamine in normal subjects.

The bioavailability of scopolamine in three dosage forms was compared in 12 healthy nonsmoking male volunteers. Subjects received 0.4-mg doses of scopolamine bromide in intravenous (i.v.), intranasal (i.n.), or oral (p.o.) dosage forms on three occasions, with at least 2 weeks separating the doses. Scopolamine concentrations in plasma were determined with a combined reverse-phase liquid chromatographic-radioreceptor binding assay. Saliva volume and flow rate and percent suppression of control flow rate were determined from each sample. Absorption after i.n. and po scopolamine administration was rapid; plasma concentrations [1680 (i.n.) and 164 pg/mL (p.o.)] peaked within 1 h of dosing [0.37 (i.n.) and 0.78 h (p.o.)], respectively. i.n. and i.v. scopolamine suppressed salivary flow rate to similar extents (95% and 99.7%), respectively. Times to reach maximum effect were 1.05 and 0.27 h after i.n. and i.v. dosage, respectively. Absolute intranasal bioavailability, calculated from the area under the drug concentration vs time curve, was found to be significantly greater than that of p.o. scopolamine (83% vs 3.7%, p < 0.05). The i.n. route may provide a noninvasive, reliable, fast, and effective route for administering scopolamine.

Administration, Intranasal↗
PubMed2004

Winter cherry bugs feed on plant tropane alkaloids and de-epoxidize scopolamine to atropine.

The winter cherry bug colonizes the Duboisia leichhardtii tree, which is a rich source of scopolamine. It consumes the tropane alkaloids atropine and scopolamine. Quantitative analysis revealed that the ratio of scopolamine to atropine in the winter cherry bug (0.46) was far from that found in the leaves of the host plant (7.20). To elucidate whether the winter cherry bugs selectively excrete or decompose scopolamine, they were fed scopolamine and/or atropine together with sucrose. They took up scopolamine as well as atropine, and converted scopolamine into atropine.

Alkaloids↗
PubMed1999

S 15535, a benzodioxopiperazine acting as presynaptic agonist and postsynaptic 5-HT1A receptor antagonist, prevents the impairment of spatial learning caused by intrahippocampal scopolamine.

1 The effect of S 15535 (4-benzodioxan-5-yl)1-(indan-2-yl)piperazine), an agonist at presynaptic and antagonist at postsynaptic 5-HT1A receptors, on the impairment of spatial learning caused by intrahippocampal scopolamine in a two-platform spatial discrimination task was studied. 2 Scopolamine (4.0 microg microl-1), injected bilaterally into the CA1 region of the dorsal hippocampus 10 min before each training session, impaired choice accuracy with no effect on choice latency and errors of omission. 3 Administered subcutaneously 30 min before each training session, S 15535 1.0 (but not 0.3) mg kg-1 did not modify choice accuracy but prevented its impairment by intrahippocampal scopolamine. 4 WAY 100635, a 5-HT1A receptor antagonist, injected into the dorsal raphe at 1.0 microg 0.5 microl-1 5 min before scopolamine, had no effect on choice accuracy and latency or errors of omission and did not modify the effect of scopolamine but completely antagonized the effect of S 15535 (1.0 mg kg-1) on scopolamine-induced impairment of choice accuracy. 5 The results confirm a previous report (Carli et al., 1998) that stimulation of presynaptic 5-HT1A receptors in the dorsal raphe counteracts the deficit caused by intrahippocampal scopolamine, probably by facilitating the transfer of facilitatory information from the entorhinal cortex to the hippocampus. 6 Drugs that stimulate action on presynaptic 5-HT1A receptors, such as S 15535 and other partial 5-HT1A receptors agonists, may be useful in the symptomatic treatment of human memory disturbances associated with loss of cholinergic innervation to the hippocampus.

Animals↗
PubMed1998

Stimulation of 5-HT1A receptors in the dorsal raphe reverses the impairment of spatial learning caused by intrahippocampal scopolamine in rats.

This study investigated the effect of stimulating 5-HT1A receptors in the dorsal raphe on the impairment of learning caused by 4 microg/microL scopolamine injected in the CA1 region of the dorsal hippocampus in rats performing a two-platform spatial discrimination task. At 1 (but not 0.2) microg/0.5 microL administered in the dorsal raphe on each acquisition training day 5 min before bilateral intrahippocampal injection of 4 microg/microL scopolamine, 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT), a 5-HT1A receptor agonist, had no effect on choice accuracy and latency or errors of omission but completely antagonized the impairment of choice accuracy by intrahippocampal scopolamine. Administered into the dorsal raphe at 0.2 and 1 microg/0.5 microL, WAY 100635, a 5-HT1A receptor antagonist, had no effect on rats' performance or on the impairment caused by intrahippocampal scopolamine but dose-dependently antagonized the effect of 1 microg/0.5 microL 8-OH-DPAT on the scopolamine-induced deficit. The results show that stimulation of presynaptic 5-HT1A receptors in the dorsal raphe reverses the deficit caused by intrahippocampal scopolamine, probably by facilitating the transfer of facilitatory information from the entorhinal cortex to the hippocampus. Together with a previous study showing that blockade of postsynaptic hippocampal 5-HT1A receptors antagonized the effect of intrahippocampal scopolamine in the two-platform spatial discrimination task (Carli et al., 1995b), the results suggest that drugs with presynaptic stimulatory and postsynaptic blocking actions on 5-HT1A receptors, such as partial agonists at these receptors, may be useful in the symptomatic treatment of human memory disturbances associated with loss of cholinergic innervation to the hippocampus.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1999

Attenuation of morphine tolerance and dependence in scopolamine-treated rats.

Morphine tolerance and dependence were investigated in scopolamine-treated rats. The results showed that scopolamine treatment (up to 2 mg/kg) did not affect basal line or morphine-induced latency in the tail-flick test but significantly increased the escape latency in the Morris water-maze task. Co-administration of scopolamine could considerably attenuate development of morphine tolerance and naloxone-precipitated withdrawal syndrome. Pretreatment of scopolamine for 7 days prior to morphine administration also significantly reduced the tolerance and withdrawal symptoms. Scopolamine treatment was further shown to attenuate morphine-induced conditioned place preference, an indicator of morphine psychological dependence. The present study demonstrated the attenuation of morphine tolerance and dependence in scopolamine-treated animals, probably related to scopolamine-produced learning and memory impairment.

Analgesics, Opioid↗
PubMed1998

Low-dose transdermal scopolamine decreases blood pressure in mild essential hypertension.

BACKGROUND: Increasing cardiovascular parasympathetic nervous activity could have antihypertensive effects. Low-dose transdermal scopolamine increases vagal-cardiac modulation of sinus node and baroreflex sensitivity in healthy subjects and in cardiac patients. OBJECTIVE: To study the short-term effects of transdermal scopolamine on blood pressure and cardiovascular autonomic control in patients with mild essential hypertension. DESIGN: A randomized, double-blind, placebo-controlled crossover trial with 12 untreated middle-aged [aged 39+/-5 years (mean+/-SD)] patients with mild essential hypertension. METHODS: We recorded the electrocardiogram, auscultatory sphygmomanometric and continuous photoplethysmographic finger arterial pressure, and spirometry signals with patients supine and 70 degrees tilted during controlled (0.25 Hz) breathing. Cardiovascular autonomic regulation was analyzed with power spectrum analysis of R-R interval and arterial pressure variability and a spontaneous sequence method for baroreflex sensitivity. In addition, a deep-breathing test was performed to assess maximal breathing-related sinus arrhythmia. RESULTS: Transdermal scopolamine treatment significantly decreased blood pressure both when patients lay supine and when they were in the 70 degrees tilted position. Scopolamine also slowed heart rate and increased baroreflex sensitivity and R-R interval high-frequency variability for both body positionings. In addition, scopolamine accentuated respiratory sinus arrhythmia during deep breathing and blunted the tilt-induced increase in heart rate. Scopolamine did not affect blood pressure variability. CONCLUSIONS: Transdermal scopolamine decreases arterial pressure, increases baroreflex sensitivity and accentuates vagal-cardiac modulation of sinus node in patients with mild hypertension. Our study supports the hypothesis that increasing cardiovascular parasympathetic activity could have antihypertensive effects in essential hypertension.

Administration, Cutaneous↗