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PubMed2007

Differential contribution of storage pools to the extracellular amount of accumbal dopamine in high and low responders to novelty: effects of reserpine.

The present study examined the effects of reserpine on the extracellular concentration of accumbal dopamine in high responders (HR) and low responders (LR) to novelty rats. Reserpine reduced the baseline concentration of extracellular accumbal dopamine more in HR than in LR, indicating that the dopamine release is more dependent on reserpine-sensitive storage vesicles in non-challenged HR than in non-challenged LR. In addition, reserpine reduced the novelty-induced increase of the extracellular concentration of accumbal dopamine in LR, but not in HR, indicating that the dopamine release in response to novelty depends on reserpine-sensitive storage vesicles only in LR, not in HR. Our data clearly demonstrate that HR and LR differ in the characteristics of those monoaminergic storage vesicles that mediate accumbal dopamine release.

Acidosis↗
PubMed1959

Some effects of reserpine and hydraliazine upon tissue respiration and the concentration of adenosine nucleotides in certain tissues.

The effects of reserpine and hydrallazine upon the oxygen uptake of preparations of rat brain, liver, and kidney and rabbit aorta have been investigated using the Warburg "Direct" method. In these tissues reserpine did not significantly stimulate respiration at any of the doses used. Concentrations of 10 or 50 mug./ml. had no significant effect upon respiration, but higher doses (330 mug./ml.) depressed it in all the tissues studied. This effect was also seen in rat brain at a reserpine concentration of 100 mug./ml. which had no significant effect in other tissues. Hydrallazine (50 or 100 mug./ml.) depressed respiration in all tissues studied. Stimulation at lower doses was not seen.After sublethal doses of reserpine, depletion of energy rich phosphate compounds occurred in brain and liver but not in skeletal muscle and heart. Hydrallazine also depleted brain of energy rich phosphate compounds, but did not affect liver, heart, or skeletal muscle. The bearing of these results on the mode of action of reserpine and hydrallazine is discussed.

Adenosine↗
PubMed1959

Mechanism of action of reserpine in producing gastric haemorrhage and erosion in the mouse.

Gastric haemorrhage was produced regularly in mice within 6 hours of the subcutaneous injection of a large dose (2 to 10 mg./kg.) of reserpine or of deserpidine. Rescinnamine, syrosingopine (SU-3118), and tetrabenazine (Ro 1-9569) were less active. Gastric haemorrhage was also produced within 6 hours when 5-hydroxytryptamine (10 mg./kg.) was injected every half-hour. Neither reserpine nor 5-hydroxytryptamine produced gastric haemorrhage in mice which had been vagotomized by tying the oesophagus at the cardio-oesophageal junction or which had been pre-treated with iproniazid. Amphetamine was less effective than iproniazid in preventing gastric haemorrhage after reserpine, and the following drugs were ineffective: cocaine, methyl phenidate (Ritalin), amarin, caffeine, nikethamide, lysergic acid diethylamide and its 2-bromo derivative (BOL148). Gastric haemorrhage was not observed in mice which had been given substantial doses of atropine or of hexamethonium before reserpine. The incidence of haemorrhage was substantially reduced by treatment with an antacid mixture. It is concluded that reserpine-like drugs cause gastric haemorrhage by a mechanism which has an important central component and which involves the liberation of 5-hydroxytryptamine.

Amphetamine↗
PubMed1962

Effect of reserpine pretreatment on the response of isolated papillary muscle to ephedrine.

Reserpine pretreatment of cats abolished the action of ephedrine to induce spontaneous beating in papillary muscles obtained from these animals. This spontaneous beating was viewed as resulting solely from catechol amine release. The positive inotropic action of ephedrine was diminished but not abolished by reserpine pretreatment. Reserpine reduced the heart rate in vivo, but it did not affect the peak contraction height or the rate of failure of the isolated papillary muscle. The contractile response to adrenaline (0.1 mug/ml.) was not affected by reserpine pretreatment. However, in this concentration adrenaline induced spontaneous beating only after reserpine.

Animals↗
PubMed1970

Restoration of tyramine responses by bretylium, BW392C60, bethanidine and monoamine oxidase inhibitors in reserpine-treated rats.

1. Bretylium, BW392C60, bethanidine, nialamide and pheniprazine, but not guanethidine or ouabain, were all capable of restoring the cardiovascular response to tyramine in reserpine pretreated rats anaesthetized with sodium pentobarbitone.2. In parallel with their recorded in vitro activity as monoamine oxidase inhibitors, BW392C60 was found to be more potent at restoring the response to tyramine than bretylium or bethanidine.3. The restored responses to tyramine were completely blocked by desmethyl-imipramine or by a combination of phentolamine and propranolol.4. The effect of bretylium on the tyramine response was not influenced by bilateral adrenal demedullation, urethane anaesthesia, the dose or duration of the reserpine pretreatment and was not dependent upon the frequency of the tyramine injections.5. Bretylium, BW392C60 or bethanidine did not alter the pressor response to intravenous noradrenaline.6. Nialamide-induced restorations of the responses to tyramine were not further enhanced by the administration of bretylium, BW392C60 or bethanidine.7. In pithed reserpine-treated rats the ability of bretylium and BW392C60 to restore the response to tyramine was reduced.8. It is concluded that all the drugs which reversed the reserpine-induced subsensitivity to tyramine were acting as monoamine oxidase inhibitors, thus allowing the intra-neuronal accumulation of endogenously formed catecholamines. The presence of nerve impulses in the adrenergic fibres of reserpinized rats appears to be an important factor in mediating this effect.

Adrenalectomy↗
PubMed1971

Effect of reserpine on the activity of adrenal enzymes involved in the synthesis of adrenaline.

1. After administration of reserpine to rats, the tyrosine hydroxylase (TH) and phenylethanolamine-N-methyl transferase (PNMT) activity in their adrenal glands was found to be increased under in vitro conditions.2. The increase in TH activity occurred at 12-18 h after reserpine whereas the PNMT activity increased at 30 hours. Unlike the TH, the increase in PNMT activity did not appear to be neuronally mediated since ganglion blockade by chlorisondamine failed to antagonize the reserpine-induced increase in PNMT activity. The increase in PNMT activity may be a response to increased utilization of catecholamines.3. Hypophysectomy resulted in a diminution of the activities of both enzymes; the activity of TH, but not of PNMT, could be partially restored by reserpine. ACTH restored the activities of both enzymes almost to normal.4. The differential effect of reserpine suggests that the activities of these two enzymes are controlled by different mechanisms.

Adrenal Glands↗
PubMed1975

An electrophysiological analysis of the effects of reserpine on adrenergic neuromuscular transmission.

1 An electrophysiological study has been made of the effects of depleting synaptic vesicles (i.e. small vesicles less than 60 nm diameter) of their transmitter with reserpine on the quantity of transmitter released by nerve impulses, using the amplitude of the synaptic potential as a measure of transmitter release. 2 Pretreatment of adrenergic nerve terminals with reserpine sufficient to deplete the terminals of 70% of their noradrenaline (NA) did not change the total number of synaptic vesicles in the terminals, but did reduce the number with a large granular core as well as the quantity of NA released by a single nerve impulse by 80%. 3 Pretreatment of adrenergic nerve terminals with reserpine and iproniazid, to decrease vesicular NA but enhance cytoplasmic NA, had the same effect on synaptic vesicles and on the NA released by a single nerve impulse as did reserpine alone. 4 During a short train of impulses at high frequencies in reserpine pretreated terminals, the quantity of NA released by successive impulses increased until a steady-state release was reached comparable to that in untreated preparations. This facilitated release could be quantitatively predicted in terms of the addition of the individual potentiations introduced by each impulse in the train. 5 These results are consistent with the idea that each quantum of transmitter is stored in a synaptic vesicle, and that these may be released by nerve impulses directly from the terminal by a process of exocytosis.

Animals↗
PubMed1979

Reversal of DOPA-induced arousal in reserpine-treated rabbits and mice by histidine.

1 The behavioural effects induced by histidine were studied in two species. In rabbits, sedation was assessed by the presence of blepharospasm, loss of righting reflex, and loss of response to painful stimuli. In mice, sedation and arousal were assessed by changes in the locomotor activity, exploratory activity, and minimal electroshock seizure threshold.2 The administration of histidine to normal rabbits or mice, in doses of 800 mg/kg and 1000 mg/kg respectively, had no apparent effect on behaviour. Moreover, it did not affect the behavioural excitation induced by L-DOPA (100 mg/kg i.v. in rabbits and 750 mg/kg i.p. in mice) in these animals.3 The administration of histidine with or after L-DOPA in reserpine-treated rabbits (2.5 mg/kg i.v.) or mice (5 mg/kg, i.p.) produced sedation. This sedative effect was dose-dependent.4 The sedative effects induced by histidine after DOPA-induced arousal in reserpine-treated rabbits and mice were prevented by prior injection of the histamine H(1)-receptor blockers, chlorpheniramine (2.5 mg/kg) or diphenhydramine (5 mg/kg).5 Imipramine (7 to 10 mg/kg, i.v.)-induced arousal in reserpine-treated rabbits was also reversed by histidine infusion.6 The infusion of 5-hydroxytryptophan (100 mg/kg, i.v.) with L-DOPA, or of arginine (450 mg/kg, i.v.) with or after L-DOPA, or of histamine (100 mug/kg), i.v.) after L-DOPA, did not affect the DOPA-induced arousal in reserpine-treated rabbits.7 These findings indicate that histamine, formed centrally from exogenous histidine, and released in increased amounts at the synapses in reserpine-treated animals, possesses a central sedative effect. This effect may be sufficient to antagonize the behavioural excitation induced by high levels of catecholamines in the brain of these animals when aroused by L-DOPA administration.8 It is concluded that in addition to the other monoamines, histamine may also be implicated in the regulation of brain excitability.

Animals↗
PubMed1987

The effect of reserpine on sympathetic, purinergic neurotransmission in the isolated mesenteric artery of the dog: a pharmacological study.

Electrical transmural stimulation evoked a transient contraction in the isolated mesenteric artery of the dog. This contraction was abolished by guanethidine or tetrodotoxin and was partially inhibited by prazosin. Noradrenaline was competitively antagonized by prazosin. Similarly, in the reserpine-treated artery, electrical transmural stimulation produced a transient contraction which was abolished by guanethidine or tetrodotoxin. However, prazosin failed to inhibit this contraction. The contraction to noradrenaline was not significantly different from the response it produced in control vessels. Tyramine (10(-5) M), which acts on sympathetic nerves to release noradrenaline, evoked a tonic contraction in the untreated artery. This contraction was abolished or markedly attenuated by prazosin or guanethidine. The response was not observed in the reserpine-treated artery, indicating that reserpine had depleted the nerves of noradrenaline. In the control vessel alpha,beta-methylene-ATP produced a transient contraction which was followed by a complete relaxation to the basal level. This contractile response was not significantly different in the presence of guanethidine or prazosin or in the reserpine-treated artery. After desensitization of the vessel to alpha,beta-methylene ATP (5 X 10(-6) M) the prazosin-resistant contractions induced by electrical transmural stimulation were abolished both in reserpine-treated and untreated arteries. Also the contractile responses to ATP and alpha-beta-methylene-ATP were abolished but the responses to tyramine (control vessels), noradrenaline and KCl were not affected. 8-Phenyltheophylline (10(-5) M) showed no inhibitory effect on the contractile responses to electrical transmural stimulation, tyramine, ATP or alpha,beta-methylene-ATP. 7. Neuropeptide Y, peptide YY, vasoactive intestinal polypeptide, bombesin and substance P (10-7 and 10-6 M for each peptide) caused no contractile response in the dog mesenteric artery. 8. These experiments provide further evidence that the sympathetic contraction of the isolated mesenteric artery of the dog induced by electrical transmural stimulation consists ofan adrenergic and a purinergic component and that the latter component is mediated through postsynaptic P2- purinoceptors.

Adenosine Diphosphate↗
PubMed1987

Effects of reserpine and 6-hydroxydopamine on the adrenergic and purinergic components of sympathetic nerve responses of the rabbit saphenous artery.

1 The effects of reserpine and of 6-hydroxydopamine on the contractions of the rabbit isolated saphenous artery produced by stimulation of the sympathetic nerves were studied. 2 In vessels exposed to reserpine, substantial contractions to nerve stimulation were recorded despite a 95.7% reduction in the noradrenaline content of the tissue. These responses of the vessel were not significantly affected by the alpha 1-antagonist, prazosin, whereas after desensitization of the P2-purinoceptor with alpha, beta-methylene ATP, no response to nerve stimulation remained. 3 In vessels exposed to 6-hydroxydopamine, no nerve-mediated responses were observed. 4 Noradrenaline-containing nerves were observed by fluorescence histochemistry in control tissues, but were not observed in tissues treated with reserpine or 6-hydroxydopamine. 5 The potencies of ATP and histamine were not significantly affected by reserpine or 6-hydroxydopamine treatment. However, there was a slight supersensitivity to noradrenaline in reserpine-treated and 6-hydroxydopamine-treated vessels compared with that of control vessels. Prazosin was selective for alpha-adrenoceptors, while alpha, beta-methylene ATP was selective for P2-purinoceptors. 6 These results substantiate the finding that ATP and noradrenaline are sympathetic cotransmitters in the rabbit isolated saphenous artery, and demonstrate that ATP can act as a transmitter independently of noradrenaline in this vessel.

Adenosine Triphosphate↗
PubMed1989

The enhanced responsiveness of hypophyseal DA receptors in female rats induced by repeated reserpine treatment is not due to decreased oestrogen secretion.

In a previous study we have demonstrated that repeated reserpine treatment markedly enhances the intrinsic activity of the partial dopamine (DA) agonist (-)-3-PPP (preclamol) on pituitary DA receptors in female rats. This effect was attributed to the DA-depleting action of reserpine. However, since reserpine may also decrease oestrogen secretion, and since this hormone is known to affect dopaminergic transmission, experiments with ovariectomized, oestrogen-replaced female rats were undertaken. Ovariectomized rats were administered a depot preparation of oestradiol valerate in a dose that, according to literature data, yields physiological or slightly supraphysiological plasma concentrations of oestrogen. In spite of this treatment, repeated reserpine administration was found to substantially increase the intrinsic activity of (-)-3-PPP, as well as that of the partial DA agonist TDHL (terguride), on female pituitary DA receptors. It was concluded that repeated reserpine treatment increases pituitary DA receptor responsiveness in female rats by depleting DA, rather than by decreasing oestrogen secretion.

Animals↗
PubMed1988

Sympathetic vascular control of the pig nasal mucosa (2): Reserpine-resistant, non-adrenergic nervous responses in relation to neuropeptide Y and ATP.

The possible occurrence of non-adrenergic mechanisms in the sympathetic vascular control of the nasal mucosa was studied in vivo using reserpine-treated pigs (1 mg kg-1, i.v., 24 h earlier) in combination with pharmacological blockade of alpha-adrenoceptors by local phenoxybenzamine (1 mg kg-1, i.a.) infusion. The nasal mucosal depletion (99%) of the content of noradrenaline (NA) in reserpinized animals was not influenced by preganglionic denervation while the depletion (44%) of neuropeptide Y (NPY) was prevented. Upon stimulation with single shocks, 25% of the arterial blood flow reduction and 47% of the nasal mucosal volume reduction (reflecting contraction of venous sinusoids) were still present after reserpine as compared with controls. In reserpinized animals, the vascular responses were slow developing and long-lasting, and about 60% remained at 0.59 Hz and more than 80% at 6.9 Hz. The vascular effects after reserpine were, however, subjected to fatigue, which may explain why phenoxybenzamine treatment still reduced the functional effects in the absence of NA. Local intra-arterial injections of NA, NPY and the metabolically stable adenosine-5'-triphosphate analogue alpha, beta-methylene ATP (mATP) caused reduction in both arterial blood flow and nasal mucosal volume. The C-terminal fragment of NPY (NPY 13-36) also induced nasal vasoconstriction although with a fivefold lower potency than NPY 1-36. Adenosine-5'-triphosphate caused a biphasic vascular effect with vasodilatatory actions at low doses and a short-lasting vasoconstriction followed by vasodilatation at very high doses (100-fold higher than the threshold response to mATP). In contrast to the response to NA, the long-lasting vascular effects of NPY and mATP were resistant to phenoxybenzamine treatment. In conclusion, although NA is likely to mediate most of the sympathetic vascular responses to low-frequency stimulation in the pig nasal mucosa, a large resistance and capacitance vessel component upon high-frequency stimulation seems to be non-adrenergic and mimicked by NPY rather than ATP.

Adenosine Triphosphate↗
PubMed1991

Detection of reserpine in horses by high-performance liquid chromatography.

A high-performance liquid chromatography (HPLC) assay was developed for the detection of reserpine. The assay was used to monitor the plasma concentrations of the drug given intramuscularly on one or two occasions to five horses. The blood concentrations of reserpine varied quite considerably between horses given the same dose of the drug. However, on average, reserpine could be detected consistently, and quantified, for 48 h after a single dose of 2.5 mg, and for a similar period after the second of two 2.5 mg doses given 13 d apart. Because of the apparently large variability in the pharmacokinetics of reserpine in horses, exact times cannot be given beyond which the drug will no longer be detectable in the plasma. However, following two doses of 2.5 mg reserpine given 13 d apart, at least 7 d must elapse after the second dose before there is no drug detectable in the plasma of most horses.

Animals↗
PubMed1985

A study on the aetiology of reserpine ulceration and the antiulcer action of solcoseryl in rat stomach.

The aetiology of reserpine-induced gastric ulcer formation and the antiulcer effects of solcoseryl were studied in rats. Intraperitoneal injection of reserpine produced severe ulceration, as well as mast cell and histamine depletion, in the gastric glandular mucosa. Mepyramine and cimetidine markedly antagonized the gastric lesions, but did not influence the reduced mast cell count; atropine pretreatment significantly inhibited both parameters. Intramuscular injection of solcoseryl lessened ulcer severity and prevented the decreased mast cell counts and histamine levels in reserpine-treated rats. However, the same dose of solcoseryl injected intraperitoneally was ineffective. Solcoseryl, irrespective of the route of administration, did not influence the gastric secretory activities of reserpine. It is concluded that reserpine ulceration is both cholinergic- and histamine-mediated, and that the antiulcer effects of solcoseryl appear to be due to prevention of histamine depletion in the gastric mucosa.

Actihaemyl↗
PubMed1987

The effects of acute reserpine administration on the sensitivity of the isolated pacemaker from rat heart to isoprenaline and noradrenaline.

The effects of reserpine on the sensitivity of the isolated pacemaker from rat heart to the chronotropic effect of isoprenaline and noradrenaline were studied. A single large dose of reserpine (2.5 mg kg-1) administered to rats 24 h before killing induces supersensitivity of the isolated pacemaker to isoprenaline, leaving unaltered the responsiveness of the pacemaker to noradrenaline. Reserpine at the dose of 1.0 mg kg-1 did not alter the sensitivity of the pacemaker to the catecholamines. Only the larger dose of reserpine raised the corticosterone plasma level. It is possible that a corticosterone-mediated inhibition of the extraneuronal uptake process is responsible for the supersensitivity to isoprenaline. Large doses of reserpine should not be used in experiments aimed to study cardiac sensitivity to isoprenaline or extraneuronal uptake and metabolism of the catecholamine.

Animals↗
PubMed1988

The role of adrenoceptors in the mechanism of reserpine-induced stimulation of gastric acid secretion in the rat.

The role of alpha- and beta-adrenoceptors in the mechanism of reserpine-induced stimulation of gastric acid secretion in the rat has been examined. After 6 h reserpine (0.1 mg kg-1 i.p.) significantly stimulated acid secretion relative to control values (176 +/- 4 vs 60 +/- 3 mumol, mean +/- s.e.m., n = 10, P less than 0.001). Neither coeliac ganglionectomy nor propranolol (5-15 mg kg-1) influenced this action. Vagotomy prevented acid stimulation by reserpine and was associated with H+ output similar to that of vagotomy controls (13 +/- 1 vs 14 +/- 1 mumol, mean +/- s.e.m., n = 10). Dose-dependent inhibition of the reserpine-induced acid secretion was produced by phenoxybenzamine or phentolamine; an inhibition similar to that achieved by vagotomy was noted with the 15 mg kg-1 dose (13 +/- 1 and 15 +/- 1 mumol, respectively, vs 176 +/- 4 mumol, mean +/- s.e.m., n = 10, P less than 0.001). The similarity in action between vagotomy and large doses of phenoxybenzamine or phentolamine suggests that, in the rat, vagal alpha-adrenoceptor stimulation is directly involved in the mechanism of reserpine-induced stimulation of gastric acid secretion.

Animals↗
PubMed1994

Increased potency of carbachol in isolated rat left atria after chronic reserpine pretreatment.

Chronic reserpine pretreatment has been shown to produce postjunctional beta-adrenergic supersensitivity in cardiac tissue. The present investigation was undertaken to determine whether chronic reserpine administration also alters the heart's sensitivity to muscarinic cholinoceptor agonists. The direct and indirect (antiadrenergic) negative inotropic effects of muscarinic agonists were examined in isolated rat left atria at various times after initiation of reserpine pretreatment (1.0 mg.kg-1 x day-1 for 7 days). Supersensitivity to the positive inotropic effects of isoproterenol was demonstrated at 1, 2, and 3 wk after initiation of treatment. Concentration-response curves were then obtained for the muscarinic agonist carbachol and the adenosine A1 receptor agonist (-)-N6-(2-phenylisopropyl)-adenosine (PIA) in reducing the inotropic response to isoproterenol (3.16 microM). The potency of carbachol was increased by approximately 2.0-fold at 1, 2, and 3 wk. Also, sensitivity to the direct negative inotropic effects of carbachol was increased 1.7-fold at 1 wk but not at 2 and 3 wk. At 1 wk, reserpine pretreatment did not alter either the direct or the indirect negative inotropic effects of PIA. These results show that postjunctional beta-adrenergic supersensitivity produced by chronic reserpine pretreatment is accompanied by a reciprocal increase in sensitivity of isolated rat left atria to the negative inotropic effects of muscarinic agonists.

Analysis of Variance↗
PubMed1976

Chronic treatment with reserpine and adrenocortical activation.

Daily i.p. injection of reserpine for 9 days strongly depletes hypothalamic norephinephrine (NE); after an initial activation, adrenocortical function returns to control values by the 5th day. Tyrosine hydroxylase (TH) activity in the brain stem of reserpine-treated rats exhibits a progressive increase. Alpha-methyl-para-tyrosine (chi-MpT) in rats chronically pretreated with reserpine provokes adrenocortical activation and a further decrease of hypothalamic NE. Exogenous ACTH in the same animals revealed an unimpaired adrenocortical reactivity after prolonged treatment with reserpine. These results seem to suggest that the disappearance of adrenocortical activation following long-term treatment with reserpine is due to the stimulated formation of a small functional pool of NE available for the tonic inhibition of CRF-ACTH secretion.

Adrenal Cortex↗