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PubMed1994

Effect of reserpine pretreatment on avian erythrocyte carbonic anhydrase activation by isoproterenol.

We studied the action of beta-adrenergic agonists on Japanese quail erythrocyte carbonic anhydrase (CA) in vitro. Earlier we had reported that epinephrine increased CA activity by 14%; the present study focused on an attempt to increase the size of this response. Washed erythrocytes from reserpine-treated (1 mg/kg daily i.m. for 3 days) and control birds were incubated for 40 min in the presence of isoproterenol 10(-6) mol/l. The activity of CA expressed as Wilbur-Anderson units/mg hemoglobin was increased by as much as 42% in reserpine-treated birds over the control depending on the conditions. Addition of 10(-5) mol/l of the beta-adrenergic antagonist propranolol inhibited the isoproterenol-induced effect in nonreserpinized birds. We conclude that pretreatment with reserpine, which was accompanied by a fall in plasma catecholamine levels, particularly epinephrine levels, enhanced the activation of CA by isoproterenol.

Animals↗
PubMed1975

Volumetric and histochemical studies of the adrenal medulla of mouse after reserpine administration.

The effect of single and consecutive doses of reserpine on the morphology and cellular and nuclear sizes of adrenaline and noradrenaline cells in the adrenals of mice were compared with the normal controls receiving saline injections as a placebo. Adopting micrometric measurements for apparent cellular and nuclear diameters, the pooled mean volumes of adrenaline- and noradrenaline-secreting cells and nuclei were calculated. Normal controls, subjected to consecutive daily saline injections for a period of 2 weeks, presented an increase in the intensity of the chromaffin reaction and higher values of cellular and nuclear sized of both cell types than those receiving single saline injection. These findings are believed to be a result of increased cell activity due to the stress of repeated, regular daily handling and injections. The increased measurements of cellular and nuclear sized of both types of adrenomedullary cells are believed to be due to hypermetabolic activity of the cells, thus exceeding action of reserpine shown by the decreased intensity of chromaffin reaction. Mice receiving daily consecutive reserpine injections showed a decrease in the intensity of chromaffin reaction as well as cellular and nuclear sizes compared with their controls. This is attributed to a decrease in the catecholamine content of the adrenal medulla.

Adrenal Medulla↗
PubMed1978

[Effect of reserpine on the formation of 9,10-dimethyl-1,2-benzanthracene induced tumors in pinealectomized and thymectomized rats].

After reserpine treatment the incidence of dimethylbenzanthracene-induced tumors was found to be significantly higher in pinealectomized rats than in intact or thymectomized ones. A very high rate of DMBA-leukemia was observed in immune-deficient pinealectomized rats after reserpine administration. It is therefore suggested that the neuroendocrine disturbances due to removal of the pineal gland in the newborn animals, are latent and become evident after reserpine administration as reflected in an increased tumor incidence.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1978

Effects of reserpine on the incidence of 9,10-dimethyl-1,2-benzanthracene-induced tumors in pinealectomised and thymectomised rats.

After reserpine treatment the incidence of dimethyl-benzathrance-induced tumors was found to be significantly higher in pinealectomised rats than in intact or thymectomised ones. A very high rate of DMBA-leukemia was observed in immune deficient pinealectomised rats after reserpine administration. It is therefore suggested that the neuro-endocrine disturbances, due to removal of the pineal gland in the new-born animals, are latent and become evident after reserpine administration, as reflected in an increased tumor incidence.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1976

Patient acceptance of guanethidine as therapy for mild to moderate hypertension. A comparison with reserpine.

The relative benefits and risks of reserpine and guanethidine were compared in patients with thiazide-treated mild to moderate hypertension (diastolic pressure 95-115 mm Hg). Forty-nine ambulant patients )30 men, 19 women) were treated throughout the study with hydrochlorothiazide, 50 mg/day. In this double blind crossover study each drug was added in graded increments until a predetermined therapeutic response was obtained, blood pressure measurements and side effect scores were evaluated biweekly. Major conclusions of the study were: 1) guanethidine, as well as reserpine, will reduce mild to moderate blood pressures to normal; 2) in most cases, side effects which did occur while taking guanethidine or reserpine were well tolerated and neither drug was clearly superior. Side effects associated with larger doses of guanethidine employed in severe hypertension were absent or only slightly bothersome. Thus, guanethidine apppears to have a good benefit-to-risk ratio in the therapy of mild to moderate hypertension and offers a number of advantages over drugs commonly used in this syndrome. This study refutes the common belief that guanethidine must be reserved only for the treatment of more severe degrees of hypertension.

Body Weight↗
PubMed1977

Influence of prostaglandin E2, indomethacin, and reserpine on renal vascular responses to nerve stimulation, pressor and depressor hormones.

The effects of prostaglandin E2 (PGE2) indomethacin, and reserpine were evaluated in the rabbit renal vascular bed in situ under conditions of controlled blood flow. Intrarenal infusion of PGE2, 0.03 and 0.3 microgram/min, decreased responses to renal nerve stimulation, intra-arterial norepinephrine, and angiotensin. Responses to nerve stimulation were decreased to a greater extent than responses to norepinephrine. At lower concentrations the effects of PGE2 on pressor responses and on vascular resistance could be separated. Reserpine decreased the histochemical evidence of adrenergic innervation and reduced the response to renal nerve stimulation, enhanced the response to norepinephrine, and was without effect on the response to angiotensin. Indomethacin decreased depressor responses to arachidonic acid, produced a small increase in renal vascular resistance but did not enhance renal pressor responses. The increase in renal vascular resistance after indomethacin was not modified by reserpine pretreatment. Indomethacin enhanced the renal response to bradykinin. These data show that PGE2 possesses the ability to modulate pressor responses in the kidney. However, experiments with indomethacin suggest that endogenous prostaglandins neither modulate pressor responses nor mediate the response of the renal vascular bed to bradykinin. In addition, these data suggest that the increase in renal resistance after indomethacin is not dependent on the adrenergic nervous system.

Adrenergic Fibers↗
PubMed1983

Case report of adverse effect of reserpine on tardive dyskinesia.

The authors used reserpine to treat a case of tardive dyskinesia. Like neuroleptics, reserpine improved the symptoms of tardive dyskinesia during administration but appeared to aggravate the underlying illness, as evidenced by increased symptoms after reserpine discontinuation.

Adult↗
PubMed1979

Effect of chronic reserpine administration on K+ and amylase release from the rat parotid gland.

After chronic administration of reserpine, slices of the rat parotid gland incubated in vitro were found to release significantly more K+ and significantly less amylase than similar slices from untreated control animals. The extent of K+ release in the gland slices of the drug-treated animals shows no dependency on external Na+ or Ca++ and is probably enhanced because of a decreased activation of K+ uptake by the Na+-K+ pump. This effect may also involve a defective generation of cyclic GMP, which was found to enhance K+ uptake and, thus, to inhibit K+ release in control slices. The inhibition of amylase release observed after treatment with reserpine most likely results from a deficient level or utilization of the energy or nucleotide sources required for enzyme secretion, because a similar inhibition was observed in control slices after incubation in the absence of the purines inosine and adenine. These results indicate that chronic reserpine administration impairs the stimulus-secretion coupling mechanism in the rat parotid gland and results in abnormal responses from both alpha and beta adrenergic receptors.

Adrenergic beta-Agonists↗
PubMed1980

Exocrine pancreatic secretion in rats treated with reserpine after stimulation with pilocarpine, dopamine, and caerulein.

Pancreatic juice was collected in vivo from control and reserpine-treated rats after stimulation with pilocarpine (0.2 mg/100 g body weight), dopamine (6--7 mg/100 g body weight), caerulein (90--100 pmole total dose) or with a combination of caerulein and secretin (6 u/100 g body weight) and the volume, amylase, bicarbonate and chloride outputs were compared. The results indicate that the secretory response to the three secretagogues was significantly reduced in the drug treated animals. Thus, the volumes of pancreatic juice were 57.0, 60.5, and 15.7% of those obtained in control rats after stimulation with, respectively, pilocarpine, dopamine, and caerulein. Amylase output was 63.8, 67.1, and 21.0% and bicarbonate output was 29.9, 46.8, and 6.2% of those observed in untreated rats after the same stimulants. Fluid secretion increased in the treated animals to 71.3% of that of controls when both caerulein and secretin were administered together and amylase output became greater than in control rats (151%). However, bicarbonate output was still 55.2% of that of controls with this combined stimulation. It is concluded that chronic reserpine administration impairs exocrine pancreatic secretion and that this effect involves both the acinar and ductal portions of the gland. This impairment involves the physiologic responses of these two segments of the glandular epithelium to both neural and hormonal stimulants. These findings suggest that the exocrine pancreatic disturbance in reserpine-treated rats may be similar to that observed in cystic fibrosis (CF), and because the treated rat has been proposed as a model for the human disease, they suggest the use of this model as a test system for the study of the pancreatic secretory abnormality in CF.

Amylases↗
PubMed1981

The chronically reserpinized rat as a model for cystic fibrosis: alterations in pancreatic enzyme secretion and storage.

Alterations in the pancreatic secretion of fluid and of enzymes in response to either pilocarpine (15 mg/kg) or an octapeptide of cholecystokinin (0.1 microgram/kg) have been found in rats that received daily injections of reserpine (0.5 mg/kg) for 7 days. During a 3-hr secretory period, significant reductions in the volume of pancreatic juice and in the total output of protein, amylase, and trypsin were observed in these animals. In the first hour of the secretory response, however, protease output was increased in the treated animals, particularly that of chymotrypsin, which was also increased in the longer secretory period following pilocarpine, but not cholecystokinin, stimulation. Zymogen granules isolated from the pancreas of the treated rats by differential centrifugation in a 0.3 M sucrose buffer had increased specific activities of the proteases when compared to those of untreated controls. Ultrastructurally, zymogen granules isolated from the pancreas of the treated rats showed changes in density, with bizonal and trizonal configurations being frequently observed, and had less distinct limiting membranes. In some, the membrane appeared broken at intervals, and there was granular material, presumably derived from the granule contents, lining the surface of the granule. It is concluded that pretreatment with reserpine inhibits fluid secretion and alters enzyme secretion in the rat exocrine pancreas. The latter effect is related to a nonparallel storage of amylase and proteases in the secretory granules induced by the drug treatment, probably through an action on protein synthesis or intracellular transport. An accumulation of proteases may lead to activation of these enzymes and to granule lysis. Inasmuch as the reserpine-treated rat has been proposed as an experimental model for cystic fibrosis, these findings are relevant in terms of possibly pathogenetic mechanisms in this disease.

Amylases↗
PubMed1982

Pancreatic function in the reserpinized rabbit--a model for cystic fibrosis. I. Effect of secretin.

Pancreatic juice was collected from rabbits treated with reserpine and from untreated controls. The volume of pancreatic juice secreted, flow rate and the bicarbonate output were all significantly reduced in the treated animals during both spontaneous flow and during secretin-stimulated flow. On the other hand, the total protein concentration, the amylase activity and the calcium concentration of the pancreatic juice were all significantly elevated in the treated animals. The elevation in the total protein concentration appeared to be due to both increased amounts of protein and decreased amounts of water. Of particular interest was that secretin stimulation caused the same % increase in the flow rate and output of pancreatic juice in both control and reserpine treated rabbits. The method by which fluid is secreted by the treated animal, therefore, appeared to be depressed at all times and under all conditions. Decreased volumes of pancreatic juice, a decreased bicarbonate output and increased concentrations of protein and calcium are found in this model and are consistent with clinical findings present in the pancreatic secretions obtained from individuals with cystic fibrosis. Therefore, the similarities between secretions of the reserpine treated rabbit and those observed in the cystic fibrosis patient support its use as an experimental model for investigating the abnormal pancreatic secretions in this disease.

Amylases↗
PubMed1988

The reserpine-treated rat as an experimental animal model for cystic fibrosis: abnormal Cl transport in pancreatic acinar cells.

Pancreatic acini of control and reserpine-treated rats were incubated with the isotopic tracer 36Cl to compare Cl accumulation in the absence and presence of secretagogues and transport inhibitors. Two phases of Cl accumulation were ascertained in resting control cells: an initial rate (0-5 min) and a steady state level (10-30 min) of accumulation. Both phases were enhanced by acetylcholine (1 microM) and caerulein (10 nM), but not by 10 nM vasointestinal peptide or 10 microM forskolin. Exposure to 1 mM DIDS (4,4'-diisothiocyano-2,2'-stilbene disulfonic acid) inhibited both phases of Cl accumulation, whereas exposure to 1 mM amiloride had a delayed effect on the initial rate and reduced the steady state phase in both resting (unstimulated) or acetylcholine-stimulated cells. Furosemide (1 mM) had no effect on Cl accumulation when added to the cells just before tracer, but reduced it when added 10 min before. Neither the initial phase nor the steady state level of Cl accumulation were enhanced by acetylcholine in acini of reserpine-treated rats and the effect of DIDS on the initial phase was smaller than in control cells. Continued exposure to this inhibitor resulted, furthermore, in a significantly larger steady state Cl content. The inhibitory effects of amiloride and of a 10-min preincubation with furosemide were similar to those observed in control cells. These results suggest that Cl accumulates in rat pancreatic acini by way of DIDS-sensitive mechanisms that are activated by Ca2+-mediated, but not by cAMP-mediated, secretagogues. These mechanisms are altered in acini of reserpine-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1983

Effects of cyproheptadine, reserpine, and synthetic corticotropin-releasing factor on pituitary glands from patients with Cushing's disease.

Direct effects of cyproheptadine, reserpine, synthetic ovine corticotropin-releasing factor (CRF), dexamethasone, and lysine-8-vasopressin (LVP) on the secretion of immunoreactive ACTH and beta-endorphin from the adenoma and the nonadenomatous tissue of patients with Cushing's disease were examined using a superfusion system. Cyproheptadine and reserpine (10(-9)-10(-7) M of each) suppressed immunoreactive ACTH and beta-endorphin secretion from both tissues. CRF (10(10)-10(7) M) stimulated the secretion of both peptides from the nonadenomatous tissue, but only a high dose of CRF could stimulate the secretion of these peptides from some adenomas. Such CRF-induced secretion was partially suppressed by dexamethasone. LVP (10(-9)-10(-7) M) stimulated peptide secretion from both types of tissue. These results suggest direct inhibitory effects of cyproheptadine and reserpine on the secretion of these peptides from the pituitary of patients with Cushing's disease, a different stimulatory mechanism of LVP from that of CRF in these tissues, and low sensitivity of the adenoma to CRF.

Adenoma↗
PubMed2000

N-Methyl-D-aspartate receptor antagonists enhance the head-twitch response, a 5-hydroxytryptamine2 receptor-mediated behaviour, in reserpine-treated mice.

In this study, N-methyl-D-aspartate (NMDA)-receptor antagonists enhanced the head-twitch response induced by 5-hydroxytryptamine (5-HT) in reserpine-treated mice. To minimize the risk of any indirect involvement of NMDA-receptor antagonists (D(-)-2-amino-5-phosphonopentanoic acid (AP-5), D(-)-3-(2-carboxypiperazine-4-yl)-propyl-1-phosphonic acid (CPP), (+)-5-methyl-10,11-dihydroxy-5H-dibenzo-[a,d]-cyclohepten-5,10-imi ne (MK-801), ketamine, dextrorphan and dextromethorphan) with 5-HT neurones, vesicle stores of monoamines, especially 5-HT, were depleted with reserpine. In addition, the enhancement of 5-HT-induced head-twitch response was inhibited by apomorphine and NMDA as well as ritanserin in reserpine-treated mice. These results support our previous conclusion that NMDA receptors play important roles in the glutamatergic modulation of 5-HTergic function at the postsynaptic 5-HT2 receptors in mice.

Adrenergic Uptake Inhibitors↗
PubMed1996

Effect of cabergoline, a long-acting dopamine D2 agonist, on reserpine-treated rodents.

We studied the characterization of cabergoline, a new ergot alkaloid derivative and a selective dopamine D2 receptor agonist, in comparison to bromocriptine and pergolide in reserpine-treated rodents. Cabergoline (0.25-1.0 mg/kg, s.c.) improved dose-dependently the reserpine-induced akinesia that was assessed on the locomotor activity, and the efficacy lasted longer than those of bromocriptine (1.25-5.0 mg/kg, s.c.) or pergolide (0.0625-0.5 mg/kg s.c.). Cabergoline (ED50 = 1.10 mg/kg, at 4 h after the administration of drugs) also reversed catalepsy, the failure to correct an externally imposed posture, and its efficacy was stronger and longer than bromocriptine (ED50 = 4.65 mg/kg, at 4 h). Further, reserpine-induced rigidity was improved equally by cabergoline (0.125-1.0 mg/kg, i.v) and bromocriptine (1.0 mg/kg, i.v.). When cabergoline was administered together with 3(3,4-dihydroxyphenyl)-L-alanine (L-DOPA), the effects were additive. Our results indicate that the long-lasting effects of cabergoline could be beneficial for treating Parkinson's disease.

Animals↗
PubMed1979

Response of urinary noradrenaline excretion to reserpine administration in normal and hypertensive subjects.

Reserpine was administered in purpose to determine the "Noradrenaline store" in sympathetic nerve endings. The marked increase of urinary noradrenaline excretion was observed by reserpine 0.4 mg/day administration. Total amount of noradrenaline in urine for first three days of 0.4 mg/day of reserpine administration was considered as a good indicators of "Noradrenaline store". There was no difference of "Noradrenaline store" between normal and hypertensive subjects. The increase % of urinary noradrenaline was higher in labile hypertension than in established hypertension as well as in normal subjects. Though the relationship between "Noradrenaline store" or the increase % of noradrenaline and sympathetic nerve activity was not clear, it is suspected that the releasable noradrenaline in sympathetic nerve granule was higher in labile hypertension than in established hypertension or normal subjects.

Adult↗
PubMed1975

Modifications of responses to adrenergic drugs in arterial strip by treatment in vivo with ephedrine and reserpine.

The aim of the present experiment was to investigate effects of ephedrine and reserpine, administered in vivo, on responses of dog isolated arterial strips to adrenergic drugs, and to study a possible mechanism involved in the reversal of blood pressure responses to dopamine. Dose-dependent contractile responses to adrenaline (A), dopamine (DA) and ephedrine (ED) were depressed in the femoral strips isolated from the ED-treated dogs as compared with those isolated from the untreated dogs. Those to noradrenaline (NA) were potentiated in low concentration and in hibited in high concentration, though those to tyramine (TY) were not altered. Relaxing and contractile responses to isoprenaline (IP) were inhibited. DA did not induce a relaxing effect but a contractile one even in the strips brought to a state of moderate tone with ED or phelypressin. In the strips isolated from the reserpine-treated dogs, contractile responses were to some extent potentiated by NA, A and DA, and significantly by ED, while those to TY were inhibited. Relaxing responses to IP were reduced and contractile responses potentiated. In the strips extirpated from the reserpine and ED-treated dogs, contractile responses to NA and A were potentiated in low concentration and tended to be potentiated in high concentration whereas those to DA and ED were not affected. Dose-dependent relaxing effects of DA in the dog renal and mesenteric strips contracted previously by KCl after phenoxybenzamine were attenuated by treatment with ephedrine in vivo. The results suggested that the dopamine reversal in the blood pressure may be mainly due to actions other than its peripheral effect on the blood vessels.

Animals↗
PubMed1985

Effect of nicotine, alcohol and caffeine pretreatment on the gastric mucosal damage induced by aspirin, phenylbutazone and reserpine in rats.

The effects of nicotine (2.5 mg/100 ml), alcohol (25% v/v) and caffeine (30 mg/100 ml base) and their combination (nicotine, 2.5 mg/100 ml; alcohol, 25% v/v; and caffeine, 30 mg/100 ml base) fed in drinking water ad libitum for 21 days were studied on the gastric mucosal damage induced by aspirin, phenylbutazone and reserpine in rats. When given alone, none of them produced any visibly discernible gastric lesions. Their concurrent administration, however, produced some injury to the gastric mucosa which was far less severe than the lesions induced by any of the ulcerogenic drugs used in this study. Pretreatment with nicotine, alcohol and caffeine and their combination resulted in a significant augmentation of gastric lesions produced by aspirin, phenylbutazone and reserpine. These results establish an association between nicotine, alcohol and caffeine in the pathogenesis of gastric ulcers and also implicate them as modifying factors in the genesis of gastric lesions induced by aspirin, phenylbutazone and reserpine.

Animals↗