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PubMedDate not supplied

[Prinzmetal's angina. Response to the treatment with reserpine. Review of its physiopathological mechanisms].

A case of Prinzmetal angina refractory to classic medical treatment, in which the angina attacks were suppressed with the administration qf reserpine is presented. The possible physiopathologic mecanisms of this entity are reviewed. The possibility of coronary spasm due to an alteration in the regulation of the coronary arterial tone from an autonomic.nervous system illness is established, an abnormal coronary vascular reactivity is also reviewed. It is emphasized that the Prinzmetal angina is an original entity, idfferent from the coronary arteriosclerotic heart disease, which may coexist with it but which cannot be treated in the same way, because its physiopathologic mecanisms are different.

Angina Pectoris↗
PubMed1977

[Changes in the bioelectrical activity of pacemaker cells of the desympathized and reserpinized frog heart under conditions of parasympathetic rhythm acceleration].

A study was made of the mechanism of parasympathetic acceleration on Rana temporaria hearts with the preliminarily exhausted catecholamine stores due to desympathization and reserpinization of the animals. Bioelectrical activity of the cells of the isolated pace-maker was recorded. Parasympathetic acceleration was accompanied by an increase in the rate of accretion of slow diastolic depolarization (this indicating an active mechanism of this acceleration), and also a slight hyperpolarization and a decrease of the action potential duration. The acceleration effect and the changes of the form of the action potential were absent after atropine treatment of the preparation, this confirming the cholinergic nature of the parasympathetic acceleration. It is supposed that the parasympathetic system mediator acetylcholine--could decrease potassium or increase sodium permeability of the Pacemaker cell membrane, this leading to increase of the slow diastolic depolarization rate and to discharge acceleration.

Action Potentials↗
PubMedDate not supplied

[The effect of lithium chloride on the desynchronization of "reserpine-induced depression"].

Lithium chloride (5 mg/kg i.m. for 10 days in the morning but not in the evening) prevented effectively desynchronization of "reserpine depression" in mice and rats: the spectra and structure of the rhythms of behavioral parameters (open field), body temperature, content of serotonin and its metabolites in the brain and that of glucocorticoids in blood plasma were almost the same as those in intact animals; the circadian harmony of all parameters were correlated in the best manner and their mean circadian values were restored.

Adrenergic Uptake Inhibitors↗
PubMed1977

The effects of reserpine on myocardial lesions in dogs subjected to hemorrhagic shock.

Anesthetized dogs were subjected to severe hemorrhagic hypotension, with blood pressure maintained at 35 mm Hg for 30 or 90 minutes. In these dogs myocardial zonal lesions were present and subendocardial hemorrhage and necrosis resulted. In two other groups of dogs, similarly subjected to hemorrhage but previously depleted of catecholamines by a 3-day regime of reserpine treatment, there was a markedly lower or no incidence of myocardia lesions.

Animals↗
PubMed1982

Psychiatric side effects of antihypertensive drugs other than reserpine.

The psychiatric side effects of the major antihypertensive drugs other than reserpine are reviewed, including centrally acting drugs such as methyldopa and clonidine, peripheral adrenergic drugs such as guanethidine, beta-adrenoceptor blockers such as propranolol, and diuretics. Problems with differential diagnosis and with the interpretation of case reports make assessment of psychiatric side effects difficult. Sedation and sleep disturbances are the most common side effects, occurring with methyldopa, clonidine, and propranolol. Only methyldopa is clearly associated with depression. Other reported effects are toxic confusional states and psychotic reactions. These are rare, however, and no clear patterns of development have been recognized.

Adrenergic beta-Antagonists↗
PubMed1976

[Effects of lithium chloride administered in combination with methamphetamine or a reserpine- like drug on brain norepinephrine and dopamine metabolism in rats].

Lithium chloride (LiCl) was injected acutely (2.4 mEq/kg, i.p.) or subacutely (2.5 mEq/kg X 2/day for 4.5 days, i.p.) in rats treated concurrently with methamphetamine (MAPT) or a reserpine-like drug (Ro4-1284), and effects of LiCl on behavior as well as metabolism of brain norepinephrine (NE) and dopamine (DA) were investigated. Acute administration of LiCl suppressed the MAPT-induced hyper-locomotor activity but did not affect the Ro4-1284-induced behavioral depression. LiCl administered subacutely increased the MAPT-induced stereotyped behavior, and it reduced the Ro4-1284-induced initial transient excitation in spontaneous locomotor activity and tended to facilitate the recovery from behavioral depression. As for NE and DA metabolism, LiCl administered subacutely inhibited the MAPT-induced decrease of the deaminated NE metabolites and Ro4-1284-induced decrease of DA metabolism and the Ro4-1284-induced alterations in NE metabolism. From these results, it is likely that the inhibitory effect of LiCl on the MAPT and Ro-1284-induced changes in NE and DA metabolism may to some extent be involved in the therapeutic effects on manic-depressive illness.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed1980

The effect of pargyline pretreatment on the enhancement of the exocytotic release of norepinephrine during nerve stimulation which is induced by a benzoquinolizine compound with reserpine-like properties.

Pretreatment of guinea pigs with paragyline (100 mg/kg i.p., 18 hr before sacrifice) resulted in a significant depression in the overflow of endogenous norepinephrine (NE), total 3H, [3H]NE and dopamine beta-hydroxylase associated with stimulation of the sympathetic nerves to the isolated heart. The depression was pronounced at 5 Hz. At 10 Hz, pargyline pretreatment was without effect. The effect on dopamine beta-hydroxylase output was not as great as that on total 3H, [3H]NE or endogenous NE release, suggesting the possibility that more than one mechanism is responsible for the depressant effect of monoamine oxidase (MAO) inhibition on sympathetic neurotransmission. A benzoquinolizine compound with reserpine-like properties, 2-hydroxy-2-ethyl-3-isobutyl-9, 10-dimethoxy,1,2,3,4,6,7-hexahydro-11b-H-benzo[alpha]quinolizine (RO 4-1284), increased the nerve stimulation-mediated overflow of all the measured indices of neurotransmitter release, in addition to producing a significant increase in the spontaneous overflow of 3H from hearts of untreated guinea pigs. The augmentation of nerve-stimulated NE release by RO 4-1284 was even greater in hearts from pargyline pretreated guinea pigs. These results would tend to eliminate a causal role for a deaminated metabolite of NE in the augmenting effect on release seen with RO 4-1284. Conversely, the inhibition of neurotransmitter release associated with MAO inhibition is not mediated by the blockade in the formation of deaminated catecholamine metabolites. Enhancement in the negative feedback mechanism on release and the accumulation of false transmitter probably account for the local effects of MAO inhibitors on neurally mediated norepinephrine release.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗