No abstract available.
Digoxin* ; Reserpine* ; Tachycardia*

The purpose of this paper is to investigate the possible correlation between the choroidal blood flow and the amplitude of the b-wave in albino rabbits. The following vasoactive drugs were administered intravenously in order to change the blood flow, and the blood flow and the ERG were measured in the dark room after 30 minutes' dark adaptation. Epinephrine (0.5 mg/kg) produced slight reduction in the b-potential only when the blood flow decreased more than 10%. Pitressin (0.1 micro/kg) induced marked degree of blood flow reduction and this changes were always associated with parallel reduction in the b-potentiaI. Papaverine (2 mg/kg) also produced marked increase in blood flow and marked increase in the bpotential parallel to it. Hexamethonium bromide (1 mg/kg) produced parallel changes in the blood flow and the b-potential only when the blood flow decreased. Reserpine (0.2 mg/kg) induced moderate increase in the blood flow and this increase was associated with the increase in the b-potential. The possible applications of these results in the clinical practice were discussed.
Choroid* ; Dark Adaptation ; Epinephrine ; Hexamethonium ; Papaverine ; Rabbits* ; Reserpine ; Vasopressins

The effect of Pheniramine(Avil), a histaminergic-1 receptor blocking agent presently employed in treating various allergic diseases on pressor actions of norepinephring(NE) and tyramine (TR) was studied in the rabbit. Pheniramine, when given into a femoral vein with a dose(3mg/kg) enough to block H1-receptor, potentiated markedly the pressor responses of NE and TR. The pressor action of NE augmented by pheniramine was not affected by additional adminstration of debrisoquin (Drenergic neuron blocker) or phenelzine(monoamine oxidase inhibitor) or desipramine(U1-uptake blocker), or while potentiated by additional treatment with chlorisondamine(ganglionic blocker)or reserpine(catecholamine depleter). The hypertensive response of NE to phenelzine or desipramine was reinforced significantly by addition of pheniramine, but the response of NE in rabbits treated with reserpine or chlorisondamine or debrisoquin was not influenced by pheniramine-addition. Elevation of blood pressure to TR potentiated by pheniramine was attenuated significantly by reserpine treatment with chlorisondamine made the significant augmentation of pressor action to TR after pheniramine. Tyramine-induced response of blood pressure after pheniramine, but the response of blood pressure to TR caused by phenelzine or desipramine was enhanced markedly by pheniramine-treatment. From the above experimental results, it is thought that the pressor effect of NE and TR potentiated by pheniramine is similar to that of debrisoquin, i.e. the sensitization of effector cell, and that central action of pheniramine can not ruled out.
Blood Pressure ; Chlorisondamine ; Debrisoquin ; Desipramine ; Femoral Vein ; Neurons ; Norepinephrine* ; Oxidoreductases ; Phenelzine ; Pheniramine ; Rabbits ; Reserpine ; Tyramine*

Although the conclusion is controversial, there has long been an appealing notion that catecholamines may be involved in some way in the pathogenesis of primary hypertension and almost invariably most of hypotensive drugs involve at various sites of the neuron and produce their effect by depletion of norepinephrine in the sympathetic nerve ending. The authors undertook the comparative study on catecholamine depleting action of 3 most effective drugs available for the treatment of hypertension, reserpine, guanethidine and alpha-methyldopa, measuring the plasma catecholamine levels and urinary exceretion of caecholamine by the modified fluorometric method of Weil-Malherbe and Bone during the treatment of hypertension. The results are as follows: 1) Before the administration of hypotensive drugs, mean blood pressure was 180/110mmH, mean psalma epinephrine level was 0.36+/-0.23gamma%, mean plasma norepinephrine level was 0.48+/-0.35gamma%, 24 hours urinary excretion of epinephrine was 3.6+/-0.12gamma/day and 24 hours urinary excretion of norepinephrine was 68.9+/-0.34gamma/day. 2) In group 1 (reserpin administered group), the mean blood pressure was 190/110mmHg before the treatment and which was declined to 155/89mmHg on the last day of 4th week, in group 2 (guanethidine administered group), the mean blood pressure measured before the treatment was 185/110mmHg and which was declined to 150/85mmHg on the last day of 4th week, and in group 3 (alpha-methylodpa administered group), the mean blood measured pressure measured before the treatment was 182/110mmHg and which was declined to 153/88mmHg on the last day of 4th week. 3) After the treatment for 4 weeks with reserpin guanethidine and alpha-methyldopa, the mean plasma epinephrine levels were declined from 0.37+/-0.12gamma% to 0.11+/-0.08gamma% in group 1, from 0.38+/-0.16gamma% to 0.14+/-0.10gamma% in group 2 and from 0.33+/-0.23gamma% to 0.10+/-0.09gamma% in group 3. 4) The mean plasma norepinephrine levels were declined from 0.05+/-0.21gamma% to 0.22+/-0.12gamma% in group 1, from 0.51+/-0.25gamma% to 0.20+/-0.10gamma% in group 2 and from 0.51+/-0.21gamma% to 0.20+/-0.11gamma% in group 3 after the treatment of 4 weeks respectively. 5) Urinary exceretion of epinephine was declined from 32.3+/-0.16gamma/day to 10.4+/-0.10gamma/day in group 1, from 34.5+/-0.34gamma/day to 17.2+/-0.16gamma/day in group 2, and from 28.2+/-0.14gamma/day to 10.3+/-0.11gamma/day in group in group 3 after the treatment of 4weeks duration. 6) The mean value of 24 hours urinary excretion of norepinephrine was declined to from 72.2+/-0.35gamma/day to 28.5+/-0.14gamma/day in group1, from 69.2+/-0.34gamma/day to 22.6+/-0.21gamma/day in group 2 and from 68.6+/-0.34gamma/day to 18.2+/-0.10gamma/day in group 3 after the treatment of 4 weeks duration. 7) From the above result we can summarized as follows: Antihypertensive effect of each drugs was; guanethidine>alpha-methylodopa>reserpin in order but depressing action plasma norepinephrine levels was; alpha-methyldopa>guanethidine>reserpin and depressing effect of urinary norepinephrine excretion was; alpha-methyldopa>guanethidine>reserpin, in order.
Antihypertensive Agents* ; Blood Pressure ; Catecholamines ; Epinephrine ; Guanethidine ; Humans ; Hypertension ; Methyldopa ; Nerve Endings ; Neurons ; Norepinephrine ; Plasma* ; Reserpine

Evaluation of several antihypertensive regimens involving reserpine, hydrochlorothiazide (Esidrex(R)) and clonidine (Catapres(R)) was conducted on 230 subjects with mild to severe hypertension. Chlordiaxepoxide (Librium(R)) which is a sedative was also administered to observe the effect in patients with mild labile hypertension. The results obtained were as follows; 1. All five regimens of chlordiazepoxide, reserpine, hydrochlorothiazide, hydrochlorothiazide plus reserpine and hydrochlorothiazide plus clonidine produced a significant decrease in average mean arterial pressure (systolic+diastolicc pressure/2) compared to control values (p<0.01). 2. Hydrochlorothiazide plus clonidine was the most effective pressure lowering regimen, resulting in an average fall of 39.3 mmHg in average mean arterial pressure and obtaining excellent result in 28.6% of the cases. 3. The order in the pressure lowering effect was hydrochlorothiazide plus clonidine, hydrochlorothiazide plus reserpine, hydrochlorothiazide, reserpine, and chlordiazide 4. There was no significant difference between hydrochlorothiazide plus clonidine and hydrochlorothiazide plus reserpine (p>0.1). 5. More reduction in diastolic pressure than systolic was observed with hydrochlorothiazide plus clonidine. 6. The results of hydrochlorothiazide alone, hydrochlorothiazide-reserpine and hydrochlorothaizide-clonidine were better than those of chlordiazepoxide and reserpine alone in patients with fundoscopic findings of Keith-Wagener Grade II. 7. There was difference in pressure lowering effect with hydrochlorothiazide plus clonidine between the group with and without albuminuria. 8. Hydrochlorothiazide plus clonidine were extremely effective in patients with severe hypertension, hydrochlorothiazide plus reserpine in patients with moderately severe hypertension, and reserpine and hydrochlorothiazide alone in patients with mild hypertension.
Albuminuria ; Antihypertensive Agents* ; Arterial Pressure ; Blood Pressure ; Chlordiazepoxide ; Clonidine ; Humans ; Hydrochlorothiazide ; Hypertension ; Reserpine

Parenteral reserpine was given intramuscularly to 32 hospitalized hypertensive patients: 10 hypertensive patients without renal insufficiency, 3 hypertensive patients with heart failure, 10 hypertensive patients of malignant phase or with uremia, and 9 hypertensive patients with cerebrovascular accident. Follwoings were the result. 1. In the majority of patients, the effective dose of reserpine was 2 to 3 mg. 2. Reserpine given intramuscularly lowered blood pressure in 2 to 4 hours, had its maximum effect in 3 to 6 hours and had a duration of 3 to more than 24 hours (average 9 hours). 3. When effective dose of reserpine was given, blood pressure was lowered significantly (more than 30mmHg in mean blood pressure) in 18 patients (81.7%) of 22 hypertensive patients without renal insufficiency, and in 4 patients (40%) of 10 hypertensive patients with renal insufficiency. 4. Major side effect was drowsiness which was more evident in the patients with renal insufficiency. 5. Reserpine administered parenterally is an effective and safe agent for the treatment of hypertensive emergencies on a short term basis especially in the patient without renal insufficiency.
Blood Pressure ; Emergencies ; Heart Failure ; Humans ; Renal Insufficiency ; Reserpine* ; Sleep Stages ; Stroke ; Uremia

The bradycardiac and presor to intravenous and intraventricular methoxamine were examined in urethane-anesthetized rabbits 1) Intravenous methoxamine produced bradycardiac pressor responses. Atropine (2 mg/kg, i,v.) weakened but not abloished the bradycardiac effect. 2) The bradycardiac effect elicited by intravenous methoxamine was not affected by int-ravenous prazosin, rehimbiine, guanethidine and propranolol, butt was attenuated by intra venous chlorisondamine reserpine. 3) The pressor effect elioited by intravenous methoxamine was weakened by prazosin, but was scarcely affected, rather potentiated, by intraTenous yohimblne, guanethidine, chlorisondamine, propranolol and resperpine. 4) Intraventricular methoxamine produced pressor and bradycardiac responses. 5) The bradycardiac effect elicited by intraventricular methoxamine was net affected by intravenous atropine, prasosin and yohimbine. This was attenuated by intravenous guane- thidine, chlorisondamine, propranolol and reserpine, and by intraventricular atropine prazosin and propranolol, respectively. 6) The pressor effect elicited by intraventricular methoxamine was attenuated by intra- ventricular and intravenous prazosin. This was not affected by intravenous atropine, gua-nethidine, chlorisondamine, propranolol, reserpine and yohimbine, and by intraventricular atropine, prasosin and Propranolol, respectivelr. 7) From these results it was inferred that bradycardiac effect elicited by methoxamine was not an action through the mediation of aleph 1-adrenoceptors but was a result from non-specific actions on some brain receptors.
Atropine ; Brain ; Chlorisondamine ; Guanethidine ; Methoxamine* ; Negotiating ; Prazosin ; Propranolol ; Rabbits* ; Reserpine ; Yohimbine

Reserpine is a well-known medicine for the treatment of hypertension, however the role of reserpine in cell signaling is not fully understood. Here, we report that reserpine treatment induces the phosphorylation of AMP activated protein kinase (AMPK) at threonine 172 (T172) in PC12 cells. Phosphorylation of AMPK T172 is regulated by upstream signaling molecules, and the increase of phospho-T172 indicates that AMPK is activated. When we examined the FOXO3a dependent transcription by using the FHRE-Luc reporter assay, reserpine treatment repressed the FHRE-Luc reporter activity in a dose dependent manner. Finally, we showed that reserpine treatment induced the phosphorylation of AMPK as well as cell death in MCF-7 cells. These results suggest that AMPK is a potential cellular target of reserpine.
AMP-Activated Protein Kinases* ; Animals ; Cell Death ; Hypertension ; MCF-7 Cells ; PC12 Cells ; Phosphorylation ; Reserpine* ; Threonine

Preliminary in vitro experiments were performed to define the contraction effects of the serotonin and prostaglandin F2 alpha in cat's internal carotid artery. Subsquently 12 cats were used to study changes in contractility resulting from pretreatment with reserpine. The arteries, which were exposed to serotonin and prostaglandin F2 alpha contracted significantly just after exposure time. And by addition of higher concentrated serotonin and prostaglandin F2 alpha more contractions were noted. Arteries isolated from reserpine-pretreated cats responded to the serotonin and prostaglandin F2 alpha with similar pattern to those seen in control groups, but the contractility showed some what more decreased slope compared to those with high concentration of serotonin only. These results suggested that reserpine might have yet unknown effects which were different from known mechnism of serotonin to cerebral arteries.
Animals ; Arteries ; Carotid Artery, Internal ; Cats ; Cerebral Arteries ; Dinoprost ; Reserpine* ; Serotonin

Reflex sympathetic dystrophy is a common posttraumatic pain syndrome for which no relia- bly effective method of therapy has been found. Oral therapy has been attempted with steroid, tricyclic antidepressant, beta-blocker, and antiseizure medications, none of which are predictably helpful. Multiple invasive treatment, including sympathetic blockade and intravenous regional local anesthetic, reserpine, or guanethidine blocks, have been employed, but again with inconsistent success. Transcutaneous nerve stimulation is effective in some patients but aggravates symptoms in others. Following a report of the use of subarachnoid block in the treatment of reflex sympathetic dystrophy, a symptom that is characterized by vasospasm and cold intolerance, we experienced the ability of subarachnoid block to relieve the symptoms of reflex sympthetic dystrophy.
Guanethidine ; Humans ; Reflex Sympathetic Dystrophy* ; Reflex* ; Reserpine ; Transcutaneous Electric Nerve Stimulation