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PubMed1976

[Effects of diuretics after pretreatment with reserpine and 6-OH-dopamine (author's transl)].

Experiments were performed on groups of 10 rats each with respect to the influence of systemic denervation by 6-OH-dopamine or reserpine on the diuretic effect of furosemide (3 mg/kg). In order to get a measure for the effectiveness of denervation, the tissue content of norepinephrine in kidneys, submaxillary glands, and hearts was determined by fluorimetric analysis. Neurotransmitter content: Chemical sympathectomy with 6-OH-dopamine resulted in a decrease of tissue norepinephrine down to 25% of the initial value in the kidneys, and down to 29 and 17% in submaxillary glands and hearts, respectively. After reserpine pretreatment the kidney norepinephrine was found decreased down to 28% of the initial concentration. Plasma electrolytes: Pretreatment with 6-OH-dopamine increased the plasma magnesium concentration considerably. Further administration of 3 mg/kg of furosemide had no additional effect. Plasma sodium, however, was significantly decreased, whereas potassium and calcium concentrations remained unchanged. After reserpine administration plasma calcium was found decreased. The effect was additionally enhanced by furosemide. Plasma sodium was found decreased, too, after furosemide, whereas potassium and magnesium remained unchanged after both reserpine and furosemide treatment. Fluid and electrolyte excretion: The diuretic effect of furosemide was not significantly influenced by both 6-OH-dopamine and reserpine pretreatment. In the reserpine pretreatment group, however, post furosemide sodium excretion was significantly increased as compared to the controls. In the 6-OH-dopamine pretreated group furosemide did not result in an enhanced natriuresis. In spite of a comparable depletion of intrarenal neurotransmitter after 6-OH-dopamine and reserpine, the kaliuretic effect of furosemide was obviously different in both groups. Reserpine pretreatment resulted in a decrease of the kaliuretic fuorsemide effect, whereas after 6-OH-dopamine this decrease could not be observed. The post furosemide calcium excretion was significantly increased after reserpine and unchanged after 6-OH-dopamine. Basic magnesium excretion was increased by the factor 2 in both groups, as compared to the controls. Administration of furosemide completely abolished this difference.

Animals↗
PubMed1976

The influence of reserpine on the responsiveness to norepinephrine and electrolyte contents of rabbit atria.

This study was designed to investigate the relationships between reserpine-induced supersensitivity and electrolyte levels in isolated rabbit atria. Atria from reserpine-treated (1, 3 or 4 mg/kg 24 hr before) and untreated rabbits were placed in an isolated organ bath for determination of dose-response relationships for norepinephrine, or were used for electrolyte assay. Reserpine-treated atria had greater resting and maximum rates of beat than did untreated atria. However, the ED50 concentrations of norepinephrine producing a rate response were similar. Atria pretreated with 1 or 3 mg/kg reserpine were supersensitive to the inotropic effect of norepinephrine. 4 mg/kg reserpine did not induce inotropic supersensitivity. Atrial sodium contents were significantly increased by 3 mg/kg reserpine. Potassium contents were increased by 1 and 4 mg/kg reserpine. Calcium contents were significantly decreased by 4 mg/kg reserpine, while magnesium contents were increased by 1 and 4 mg/kg. Reserpine induced supersensitivity to the inotropic effects of norepinephrine but did not alter the sensitivity to the chronotropic effect of the drug. This supersensitivity may be linked to alterations in the tissue's homeostatic mechanisms for calcium.

Animals↗
PubMed1976

Association between the increase of cAMP content and the trans-synaptic induction of tyrosine hydroxylase in rat adrenal medulla. Studies with dexamethasone and reserpine.

When dexamethasone 0.25 or 2.5 mumole/kg i.p. was injected 2 h before reserpine (16 mumol/kg i.p.) the time course of the increase in cAMP content of rat adrenal medulla was changed. Reserpine alone caused a monophasic increase lasting between 1-2 h; reserpine after dexamethasone caused a biphasic increase: the immediate response, lasting between 15 and 30 min, was followed by a secondary increase beginning 2-3 h after reserpine and lasting for several hours. The overall increase in cAMP content elicited by reserpine during the 8 h following injection remained unchanged or was even increased, depending on the dose of dexamethasone. Pretreatment with dexamethasone, which delayed the increase in cAMP, also delayed the activation and translocation of protein kinase and the induction of tyrosine hydroxylase caused by reserpine in adrenal medulla. The action of reserpine on the cAMP content of adrenal medulla required an intact innervation and did not appear to be related to increased secretion of ACTH from pituitary. In denervated adrenals reserpine failed to increase the cAMP content of the medulla but not that of the cortex.

Adrenal Cortex↗
PubMed1976

Serum glucose, serum free fatty acids and adipose tissue lipids after fatal hypothermia of cold acclimatized, reserpine or propranolol treated guinea-pigs.

Surviving ability in frost (-20 degree C) was studied in cold acclimatized guinea-pigs given either reserpine, propranolol or saline. Survival time, rectal temperature at death, serum glucose, serum FFA and triglycerides in the interscapular adipose tissue were determined. Rectal temperature was highest in the reserpine group, in the same animals that endured the frost the shortest time. The survival time had decreased by about a half of that in the controls. Propranolol treatment decreased the living time only slightly. The fact that serum glucose remained high in the reserpine treated animals was obviously related to the short survival time. In the propranolol group glucose values were somewhat higher than in the control group (saline-animals). Reserpine seemed to have inhibited the release of FFA in the warm-acclimatized animals as interpreted from the low serum values. On the other hand, FFA were rather high in the cold-acclimatized reserpine animals. The blocking effect of reserpine reflected also in the higher contents of triglycerides in the adipose tissue both in cold-acclimatized and warm-acclimatized animals. Propranolol prevented slightly the depletion of the triglycerides. Amount of total lipids in the adipose tissue was lower in the cold-acclimatized animals than in the warm-acclimatized ones because of the change of the type of the adipocytes from unilocular to multilocular. The results corroborated the importance of FFA for longer survival in severe cold. Sensitization to reserpine seems to develop during cold-acclimatization. It calls attention to a possible hazard of reserpine treatment in cold environment.

Acclimatization↗
PubMed1994

Dose-dependent differences in the development of reserpine-induced oral dyskinesia in rats: support for a model of tardive dyskinesia.

Rats treated with reserpine develop spontaneous orofacial dyskinesia that has features similar to tardive dyskinesia (TD) in humans. In contrast to TD, however, reserpine-induced oral dyskinesia develops rapidly reaching a maximal level within 3 days at a dose of 1 mg/kg per day. The present study examined whether rats administered lower doses of reserpine would develop the oral dyskinesia at a slower rate, similar to the protracted development of TD. Rats were administered 0, 0.01, 0.05, 0.1, or 1.0 mg/kg reserpine subcutaneously every other day for 100 days. Oral dyskinesia was measured by recording the incidence of tongue protrusions for 30 min on days 1, 4, 10, 20, 40, 60, and 100. The time course of the development of reserpine-induced oral dyskinesia varied dose-dependently. The response was evident within 4 days at 1 mg/kg, within 20 days at 0.1 mg/kg, within 60 days at 0.05 mg/kg, and was not evident at 0.01 mg/kg at any time during the 100 days of treatment. The protracted development of reserpine-induced oral dyskinesia at the lower doses is consistent with TD. Doses of reserpine that produced an increase in tongue protrusions also produced a 90-95% depletion of dopamine and an increase in the ratio of dopamine metabolites to dopamine in the caudate-putamen. The disruption of dopamine neurotransmission may be involved in development of the oral dyskinesia. Furthermore, it is suggested that the 1 mg/kg dose of reserpine may induce neurochemical changes similar to that produced by long-term neuroleptic treatment, but at an accelerated rate, thereby providing a new efficient model of TD.

Animals↗
PubMed1994

Antiparkinsonian action of MK-801 on the reserpine-induced rigidity: a mechanomyographic analysis.

MK-801, a non-competitive antagonist of NMDA receptors, is known to exhibit a beneficial action in many animal models of Parkinson's disease. The aim of this study was to examine the influence of MK-801 on the reserpine-induced muscle rigidity. The rigidity was estimated by a direct mechanomyographic method. This method consists in successive bending and straightening of a rat's hind foot in the ankle joint and measuring the resistance of the foot to passive movements. Reserpine in doses of 5-10 mg/kg ip, given alone or in combination with alpha-methyl-p-tyrosine (alpha MT, 250 mg/kg ip), induced rigidity. The strongest muscle rigidity was induced by 10 mg/kg of reserpine 1 hour after administration. MK-801 (0.32-1.28 mg/kg sc) injected 70 min after reserpine (10 mg/kg ip) decreased the rigidity induced by the latter compound. Similarly, MK-801 (1.28 mg/kg sc), administered 27 h 40' after joint treatment with reserpine (10 mg/kg ip) and alpha MT (250 mg/kg ip), strongly inhibited the reserpine-induced muscle rigidity. The obtained results show that the glutamatergic hyperactivity plays a significant role in the reserpine-induced rigidity. As the reserpine-induced motor disturbances are commonly accepted to be an animal model of parkinsonian symptoms, it may be assumed that the NMDA receptor blocking component may contribute substantially to the therapeutic action of antiparkinsonian drugs.

Animals↗
PubMed1983

Differential interactions of phencyclidine with tetrabenazine and reserpine affecting intraneuronal dopamine.

This study has examined the effects on synaptosomal (P2) dopamine of interactions of phencyclidine and some other stimulants with tetrabenazine and reserpine. Tetrabenazine and reserpine both enhanced the spontaneous synaptosomal release of [14C]dopamine and inhibited its formation from [14C]phenylalanine. The [14C]dopamine formation increases induced by phencyclidine and amfonelic acid, however, were affected differentially by coadditions of tetrabenazine and reserpine. At the lower concentrations, tetrabenazine either did not affect or augmented the dopamine formation enhancements by the stimulants. Reserpine at all levels blocked the synthesis enhancements and revealed inhibitory effects of phencyclidine and amfonelic acid upon dopamine formation; only at the highest concentration did the action of tetrabenazine mimick that of reserpine. Amphetamine stimulation of dopamine formation was affected by tetrabenazine and reserpine alike; the stimulation was either maintained or enhanced. Ketamine did not affect dopamine formation either by itself, with tetrabenazine, or with reserpine. In summary, tetrabenazine and reserpine affected synaptosomal dopamine formation and release in a comparable manner, but intraneuronal dopaminergic actions of phencyclidine and also of amfonelic acid may be influenced differentially by these two releasing agents.

Animals↗
PubMed1992

Acute reserpine treatment induces down regulation of D-1 dopamine receptor associated adenylyl cyclase activity in rat striatum.

Behavioural studies suggest a functional interaction between D-1 and D-2 systems in normal rat striatum to alter motor behaviour and which is disrupted by dopamine depletion induced by acute reserpine treatment. Consequently, we have investigated the effect of acute reserpine treatment on the biochemical interaction between D-1 and D-2 receptors present in rat striatal slices. Twenty-four hours following the administration of reserpine (5 mg/kg i.p.), striatal dopamine content was depleted by more than 73%; the density (B(max)) of D-1 receptor sites measured by the in vitro binding of [3H]SCH 23390 to striatal membranes was increased while the binding of [3H]spiperone to D-2 receptor sites was unaltered. Reserpine treatment had no effect on the affinity (Kd) of [3H]SCH 23390 or [3H]spiperone for D-1 and D-2 sites. Basal levels of cyclic AMP accumulation in striatal slices prepared from reserpine-treated rats were lower than those observed in control slices. In striatal slices prepared from normal rats, dopamine (10-320 microM) and the D-1 agonist SKF 38393 (0.1-3.2 microM) induced concentration-dependent increases in cyclic AMP accumulation. The D-1 antagonist SCH 23390 (10 microM) abolished the accumulation of cyclic AMP produced by dopamine or SKF 38393. The D-2 antagonist (+/-)-sulpiride (50 microM) enhanced the response to dopamine (10-320 microM) while the D-2 agonist quinpirole (10 microM) abolished the response to SKF 38393 (0.1-3.2 microM). However, 24 hr after reserpine treatment the ability of dopamine (10-320 microM) and SKF 38393 (0.1-3.2 microM) to elicit an increase in cyclic AMP accumulation was markedly reduced in striatal slices. SCH 23390 (10 microM) did not enhance the trend for an increase in cyclic AMP accumulation produced by dopamine. Also, quinpirole (10 microM) did not affect the response to SKF 38393 (0.1-3.2 microM) in striatal slices from reserpine pretreated rats. The data confirm the positive linkage between D-1 receptors and adenylyl cyclase and the inhibitory coupling to D-2 sites in striatal slices from normal, rats. Acute reserpine treatment appears to cause an uncoupling of D-1 receptors associated with adenylyl cyclase.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1983

Reserpine inhibits rat anterior pituitary hormone secretion in vitro: effects on prolactin and ACTH and ultrastructural observations.

We measured [3H]prolactin ([3H]Prl) synthesis and secretion in female rat anterior hemipituitary glands incubated in vitro, and immunoassayable Prl secretion from dispersed anterior pituitary cells in a perfused column. Anterior pituitary glands which were incubated in 9 microM reserpine showed a marked inhibition of [3H]Prl secretion but no change in hormone synthesis, thus causing [3H]Prl accumulation within the gland. The same concentration of reserpine produced a similar effect in pituitary glands taken from rats depleted of dopamine with alpha-methyl-p-tyrosine. Reserpine inhibited Prl secretion from dispersed anterior pituitary cells with a gradual onset and prolonged duration. Thyrotropin-releasing hormone (TRH), but not dibutyryl cyclic AMP (dbcAMP), the calcium ionophore A23187 or excess Ca2+, stimulated both [3H]Prl and Prl secretion in the presence of reserpine. In contrast, neither basal nor vasopressin-stimulated ACTH (bio- and immunoassayable) secretion was inhibited by 9 microM reserpine. Ultrastructurally, pituitary glands incubated in reserpine had an increased content of Prl secretory granules. Reserpine thus selectively inhibited Prl secretion, secondarily causing accumulation of both measurable hormone and Prl secretory granules within the pituitary gland. We hypothesize that reserpine interrupted calcium-dependent mechanisms in the stimulus-secretion coupling process to inhibit Prl release.

Adrenocorticotropic Hormone↗
PubMed1993

Repeated reserpine treatment alters firing pattern and responses of substantia nigral dopamine neurons.

Repeated reserpine treatment (1 mg/kg x 6 days) increased the number of spontaneously active substantia nigra pars compacta (SNC) dopamine (DA) cells and altered the firing pattern to a more irregular one in locally anesthetized rats. The selective DA D1 receptor agonist, SKF 38393, although having little effect on SNC DA cells in normal rats, profoundly inhibited the firing rate of SNC DA cells in reserpinized rats. On the contrary, the DA D2 receptor agonist, N-0437, significantly inhibited the firing rate of SNC DA cells in control rats, however, the inhibition was not significantly altered by reserpine. The inhibitory effect of the mixed DA receptor agonist, apomorphine, was significantly enhanced after reserpine treatment. In addition, the inhibition of SNC DA cell firing produced by D1 and D2 receptor agonists in reserpinized rats was reversed only by their own subtype antagonists. These results suggest that repeated reserpine treatment renders SNC DA cells responsive to D1 receptor stimulation, and that D1 receptors play a more important role than D2 receptors in the supersensitivity of SNC DA cells induced by repeated reserpine treatment. The results also indicate that D1 and D2 receptor agonists inhibit SNC DA cell firing separately and synergically in reserpinized rats.

Animals↗
PubMed1985

Molecular and physiological properties of tyrosine hydroxylase induced by reserpine in rat adrenal gland.

Newly synthesized tyrosine hydroxylase (TH) induced by reserpine was compared with the enzyme in control rats in terms of the molecular and physiological properties. When repeated doses of reserpine were given at daily intervals for three days, the enzyme activity measured in homogenates of the adrenal glands was increased 3-fold. Furthermore, when TH in the adrenal glands from both control and reserpine-treated rats was purified, both total activity of the enzyme and the enzyme protein content purified from reserpine-treated rats were also about 3-fold higher than those of the control rats. The two purified enzymes revealed similar properties; a single subunit with a Mr of 60,000 was observed by SDS polyacrylamide gel electrophoresis, and the Km value for a pterin cofactor, 6-methyl-tetrahydropterin was about 300 microM. In contrast, in situ TH activity measured under physiological conditions at pH 7.2 in adrenal tissue slices was elevated 6-fold by reserpine pretreatment for 3 days, and was stimulated by carbachol (0.1 mM) and elevated K+ (52 mM) in a roughly proportional rather than additive way relative to slices from untreated rats. These results indicate that newly synthesized TH induced by reserpine in rat adrenal gland had similar properties as the enzyme in control rats and that reserpine increased not only the amount of TH molecules but also the in situ activity of TH. Since reserpine also increases the biosynthesis of tetrahydrobiopterin as demonstrated by Viveros and co-workers, this 6-fold increase in in situ TH activity may depend both upon the 3-fold increase in the amount of enzyme molecules and upon the increase of the physiologically available tetrahydrobiopterin in the adrenal gland.

Adrenal Glands↗
PubMed1981

Tetrahydrocannabinol potentiates reserpine-induced hypokinesia.

Delta-9-tetrahydrocannabinol (THC), a substance in marihuana, was found to produce a profound potentiation of reserpine-induced hypokinesia in rats as measured with a bar test. In these experiments, THC had no hypokinetic effect by itself but produced a more than 20-fold increase in the hypokinesia produced by reserpine. Reserpine-induced hypokinesia has been viewed as animal model of Parkinson's Disease. THC potentiation of reserpine-induced hypokinesia was observed to be both time- and dose-dependent (1 to 10 mg/kg THC). When administered by gavage to reserpine-pretreated subjects (7.5 mg/kg IP, 24 hours before), THC produced a potentiation of hypokinesia that developed fully within 1 hour, lasted at least 5 hours, and was absent by 12 hours after THC administration. This THC effect was slightly increased by physostigmine, a cholinesterase inhibitor, relatively unaffected by scopolamine, a muscarinic antagonist, and almost completely blocked by ethopropazine, an anticholinergic antiparkinson drug. The effect was completely unaffected by naloxone. Insofar as reserpine has been used with some clinical efficacy in hyperkinetic movement disorders such as Huntington's disease and tardive dyskinesia, it may be that potentiation of reserpine's hypokinetic effect by a drug such as THC could greatly increase the clinical value of reserpine or related drugs in the treatment of these disorders.

Animals↗
PubMed1993

Vacuous jaw movements in rats induced by acute reserpine administration: interactions with different doses of apomorphine.

Two experiments were conducted to study the vacuous jaw movements induced in rats by acute administration of the monoamine-depleting agent reserpine. In the first experiment, different doses of reserpine (1.25, 2.5, and 5.0 mg/kg) were assessed for their ability to induce vacuous jaw movements. Acute administration of reserpine induced a dose-related increase in vacuous jaw movements, with the two highest doses being significantly different from the vehicle control. In the second experiment, interactions between 5.0 mg/kg reserpine and the dopamine agonist apomorphine were investigated. Coadministration of reserpine with the lowest dose of apomorphine (0.1 mg/kg) significantly increased vacuous jaw movements relative to reserpine alone. The two higher doses of apomorphine (0.5 and 1.0 mg/kg) significantly decreased vacuous jaw movements in reserpine-treated rats. These results demonstrate that vacuous jaw movements are induced by acute reserpine treatment in a dose-related manner. In addition, the interactions with apomorphine suggest that vacuous jaw movements are stimulated by decreases in dopamine release produced by low doses of apomorphine that are thought to have mainly presynaptic actions, but that these movements are decreased by higher doses of apomorphine that are known to act postsynaptically.

Animals↗
PubMed1996

Vacuous jaw movements induced by acute reserpine and low-dose apomorphine: possible model of parkinsonian tremor.

Coadministration of the monoamine-depleting agent reserpine with a low dose of apomorphine has been shown to result in high levels of vacuous jaw movements in rats. Two experiments were conducted to study the pharmacologic and motoric characteristics of the vacuous jaw movements induced by 5.0 mg/kg reserpine plus 0.1 mg/kg apomorphine. The first experiment was undertaken to determine whether the vacuous jaw movements induced by reserpine plus apomorphine could be reduced by coadministration of the muscarinic antagonist scopolamine. Injections of scopolamine produced a dose-related decrease in vacuous jaw movements induced by reserpine plus apomorphine, with the two highest doses (0.5 and 1.0 mg/kg scopolamine) producing significant differences relative to the control group that received reserpine plus apomorphine. In the second experiment, a slow-motion videotape system was used to study the temporal characteristics of the vacuous jaw movements induced by reserpine and apomorphine, and to study the effects of 1.0 mg/kg scopolamine on these movements. Most of the vacuous jaw movements shown by rats treated with reserpine and apomorphine occurred in rapid bursts of jaw movement. Analysis of the interresponse times (i.e., time between each jaw movement) showed that most of the jaw movements had a local frequency in the range of 2.86-6.67 Hz. Cotreatment with scopolamine significantly affected several measures of jaw movements. Thus, the vacuous jaw movements induced by reserpine plus apomorphine can be reversed by anticholinergic treatment, and these movements tend to occur as periodic oscillations of the lower jaw with a frequency of 3-7 Hz. Vacuous jaw movements in rats share some characteristics with parkinsonian symptoms and may represent an animal model of parkinsonian tremor.

Animals↗
PubMed1990

Neuronal and adrenal enkephalins and catecholamines in response to acute CNS ischemia and reserpine in pig.

Co-storage of enkephalins and catecholamines in coronary artery, mesenteric artery and vein, middle cerebral artery, vas deferens and adrenal medulla was studied in domestic pig (Sus scrofa). Responses to acute CNS ischemia were correlated with time to peak plasma levels of central venous and adrenal vein outflow samples in controls, during reserpine treatment and after drug withdrawal. Endogenous enkephalins are co-stored in chromaffin granules of adrenal epinephrine-type cells and large dense cored vesicles of noradrenergic terminals. After a lag period, reserpine at near 'therapeutic' doses caused an apparent induction of opioid peptide precursor synthesis accompanied by processing to enkephalins in adrenal medulla up to 8-fold by 30 days and in mesenteric vein up to 4.5-fold by 14 days. Upon 14 days recovery from reserpine, elevated adrenal enkephalins were maintained and depleted catecholamines were largely replenished. Acute CNS ischemia produced rises in MAP (approx. 80 mmHg), marked net depletions of noradrenergic enkephalin stores, and net increases in adrenal vein outflow and central venous levels of enkephalins and catecholamines. Noradrenergic terminals contributed significantly to circulating enkephalins as well as norepinephrine. Reserpine for 7 days nearly abolished all tested responses to acute CNS ischemia, but immediate net 200-400% elevations of endogenous enkephalin stores occurred in coronary artery and mesenteric artery and vein (apparent processing of reserpine-induced neuronal precursor stores). Thus, induction of new synthesis of precursor opioid peptides by reserpine, with or without parallel processing to enkephalins, occurs in noradrenergic terminals in many tissues. All effects of reserpine on endogenous enkephalins implicate a central mechanism to inhibit sympathoadrenal outflow to the periphery. At 14 days recovery from reserpine, when near normal cardiovascular responses to acute CNS ischemia were regained, there was increased net release of the elevated adrenal enkephalins, exaggerated peak plasma enkephalin concentrations, but only minimal depletions of enkephalins from noradrenergic terminals.

Acute Disease↗
PubMed1989

Effect of reserpine on N-methylthiobenzamide-induced pulmonary edema: role of lung norepinephrine and hypothermia.

N-Methylthiobenzamide (NMTB) is a pneumotoxin which causes pulmonary edema and hydrothorax in rodents. Reserpine has been shown to attenuate the pneumotoxicity induced by NMTB. Some of that evidence suggests that the protection afforded by reserpine occurs independently of its capacity to reduce peripheral 5-hydroxytryptamine (5-HT). We therefore investigated 2 other pharmacologic properties of reserpine, namely: (1) its capacity to reduce lung norepinephrine (NE); and (2) its capacity to induce hypothermia, in order to more fully understand its mechanism of protection. Pretreatment of mice or rats with 6-hydroxydopamine at a dose which reduced lung NE by approximately 80% did not affect the pneumotoxic response to NMTB. Thus a decrease in lung NE probably does not account for reserpine's protective effect. An investigation of reserpine's effects on core temperature revealed that mice dosed with a combination of reserpine + NMTB presented with core temperatures lower than mice treated with either compound alone. Mice placed in a cold environment (2 degrees C) and dosed with NMTB presented with hypothermia and an attenuated toxic response to NMTB. Thus a reserpine-induced hypothermia could be allowing for a reduction of NMTB metabolism and consequent diminution of toxicity. These observations suggest that reserpine's capacity to protect animals against NMTB-induced pulmonary edema may in part be due to its capacity to induce hypothermia.

Amides↗
PubMed1992

Chronic reserpine administration selectively up-regulates beta 1- and alpha 1b-adrenergic receptors in rat brain: an autoradiographic study.

Rats were treated for 15 days with reserpine or vehicle. One day after the last treatment, animals were killed and frozen brain sections were prepared for in vitro autoradiography. Binding to beta-adrenergic receptors was measured with [125I]iodocyanopindolol, and binding selective for beta 1 and beta 2 subtypes was assessed by including non-radioactive drugs that selectively mask beta receptor subtypes. Total alpha 1-adrenergic receptor binding was measured with [3H]prazosin, while alpha 1a binding was measured with [3H]WB4101 (in the presence of unlabeled serotonin). Quantitative densitometric analysis revealed that chronic reserpine treatment caused an increase in beta binding throughout the brain, including the cortex, thalamus, amygdala, hippocampus, caudate-putamen and hypothalamus. This effect of reserpine was entirely confined to the beta 1 subtype in all regions examined. [3H]Prazosin binding (alpha 1a plus alpha 1b) was also increased after chronic reserpine in several regions of the cortex and thalamus, as well as the ventral hippocampus and caudal amygdala. No effect of chronic reserpine was seen on [3H]WB4101 binding, indicating that the effect of reserpine on alpha 1 receptors is limited to the alpha 1b subtype. The increase in alpha 1b binding after reserpine administration in rats was generally smaller and less widespread than that seen with beta 1 binding. Thus the effect of reserpine upon noradrenergic neurotransmission demonstrates a high degree of receptor specificity and regional selectivity.

Animals↗
PubMedDate not supplied

Calcium inhibits catecholamine depletion by reserpine from carotid body glomus cells.

Histofluorescent and quantitative microfluorimetric studies have been performed on glomus cells of the rat carotid body, which fluoresce intently after treatment by paraformaldehyde vapor. Reserpine causes a reduction in intensity of fluorescence of about 90%. Subcutaneous injections of calcium chloride (100-300 mg/kg) were given before reserpine. Calcium prevents the depletion of catecholamies from the glomus cells by reserpine. This effect is dose related in that the depletion of catecholamines by heavy reserpine doses (15 mg/kg) cannot be overcome by calcium, medium doses (5 mg/kg) can be overcome but variably, and light doses (1 mg/kg) are always overcome substantially and can result in virtually complete inhibition of the depletion by reserpine. If calcium might counteract the effects of reserpine by occupying attachment sites of the vesicular membrane, thereby preventing reserpine from reaching its site of action, resulting in the usual uptake of catecholamines by the vesicles and suppression of the depleting action of reserpine.

Animals↗