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

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

BACKGROUND: Ischemic preconditioning reduces the infarct size and the severity of arrhythmia in a post-ischemic reperfused heart although the detailed mechanism is unknown. In the ischemic heart, a large amount of catecholamine is released from the adrenergic nerve terminal and this aggravates cell destruction and arrhythmia. In this study, the possibility for ischemic preconditioning to inhibit the release of endogenous catecholamine from the ischemic heart was tested to investigate the probable cardioprotective mechanism of ischemic preconditioning. METHODS: In the isolated, Langendorff perfused rat hearts, we observed the protective effect of ischemic preconditioning against post-ischemic reperfusion injury, and measured the amount of catecholamine released into coronary effuent. In addition, we observed the effect of catecholamine depletion on reperfusion injury in non-preconditioned and preconditioned hearts. RESULTS: During the reperfusion(20min) after ischemia(30min), the cardiac function was markedly depressed with the development of severe contracture. In the heart preconditioned by three sequential episodes of 5min ischemia and 5min reperfusion, the reperfusion contracture decreased significantly and the cardiac function was almost recovered to normal after 20min reperfusion. The release of lactate dehydrogenase was also decreased in the preconditioned heart. The release of endogenous catecholamine was abruptly increased immediately after the reperfusion and the release was exponentially decreased throughout the reperfusion period. THe pattern of catecholamine release was much different from that of lactate dehydrogenase release. In the preconditioned heart, the release was significantly decreased to about half of that in non-preconditioned t\heart. Endogenous catecholamine depletion by reserpine treatment did not affect the post-ischemic functional recovery in both non-preconditioned and preconditioned hearts. CONCLUSION: It is suggested from these results that ischemic preconditioning inhibis the release of endogenous catecholamine during ischemic period, which may be partly related to cardioporotective effect of preconditioning in ischemic and reperfused heart.
Animals ; Arrhythmias, Cardiac ; Contracture ; Heart* ; Ischemia ; Ischemic Preconditioning* ; L-Lactate Dehydrogenase ; Rats* ; Reperfusion ; Reperfusion Injury ; Reserpine

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

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

The mechanism of the positive inotropic responses to quaternary ammonium compounds (tetraethylam-monium, tetra-n-propylammouium, trimethylethylamm-onium trimethyl-n-butylammonium, trimethyl-n-penty-lammonium, trimethyl-n-hexylammonium, trimethyI-phenylammonium, trimethylbenzylammonium, triethyl-phenylammonium and m-hydroxyphenyltrimethylam-monium) was examined on the atropinized papillarymuscle of cats. After pretreatment with dichloro-isoproterenol, all the quaternary ammonium compounds failed to produce their usual positive inotropic activities. Bretylium or TM-10, which specifically interferes with the release and/or synthesis of adrenergic mediators, rendered papillary muscle unresponsive to quaternary ammonium compounds but responsive to norepinephrine. Quaternary ammonium compounds also failed to produce their positive inotropic activity on papillary muscle whose catecholamines were a1most completely dep1eted by treatment with reserpine. Surgical removal of the sympathetic innervation to the heart resulted in a marked reduction of myocardial catecholamines. The positive inotropic responses to quaternary ammonium compounds were markedly suppressed in papillary muscle obtained from bilaterally-sympathectomized cats with degenerated postganglionic sympathetic nerve fibers to the heart. From the above results, it appears that quaternary ammonium compounds act at a common site to effect positive inotropic activities which are mediated via a catecholamine-release mechanism.
Animals ; Catecholamines ; Cats ; Heart ; Nerve Fibers ; Norepinephrine ; Papillary Muscles ; Quaternary Ammonium Compounds* ; Reserpine

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

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