Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 10 patients with stress stenocardia pharmacodynamics of Isoptin was studied with the aid of identical physical loads on the treadmill repeated with an hour's interval for 5-6 hours. A clearcut antianginal effect was recorded which consisted in the reduction of ST segment depression and of the pain syndrome for 5 hours after administration of 3 tablets over 5 hours and for 6 hrs 20 min after administration of 5 tablets of both drugs. The degree of effect increased considerably after the dose of isoptin was enhanced and was not changed after the dose of corinfar was enhanced. Difference in the haemodynamic effect of the drugs was found in their effect on the cardiac rate. Corinfar increased the cardiac rate, isoptin decreased it.
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PMID:[Calcium antagonists in stress angina pectoris (pharmacodynamic study)]. 715 4

The effects of phentolamine on rabbit basilar artery were studied and compared with those on other smooth muscles. The drug showed a dose-dependent depressing effect on high-potassium-induced contracture of rabbit basilar artery. The depressing effect was stronger on tonic than on phasic contraction. When phentolamine was applied during high-potassium-induced tonic contraction, dose-dependent relaxation was observed. The degree of phentolamine-induced-relaxation of high-potassium-induced tonic contraction was not affected by surgical denervation of the basilar artery, although catecholamine content was almost completely lost, as indicated by chemical and histochemical experiments. The relaxed tension caused by phentolamine was reversed by addition of Ca in a dose-dependent manner. Verapamil also showed a dose-dependent relaxing effect on high-potassium-induced contracture, with this relaxed tension being reversed by the addition of Ca in a dose-dependent manner. The relaxing effect of phentolamine on rabbit basilar artery was stronger than on rabbit aorta or guinea-pig taenia coli. Phentolamine depressed serotonin- or histamine-induced contraction at a concentration more than 10 times higher than the concentration for depression of noradrenaline-induced contraction. The depression of high-potassium-induced contracture and reversal by additional Ca, especially in denervated preparations, indicates that phentolamine acts directly on smooth muscle in a similar manner to that of Ca antagonists.
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PMID:The direct inhibitory action of phentolamine on the contraction of rabbit basilar artery. 718 56

We evaluated efficacy and mechanisms of the antiarrhythmic action of verapamil in 20 patients with sustained supraventricular tachycardia. Two patients had sinus nodal re-entrant tachycardia, nine atrioventricular (AV) nodal re-entrant tachycardia, and nine AV reciprocating tachycardia associated with the Wolff-Parkinson-White syndrome. The study design comprised a double-blind, randomized, cross-over phase using a 0.075 mg/kg dose of verapamil versus placebo and an open-label phase using a 0.15 mg/kg dose of verapamil. The overall results of both phases showed that 15 of 19 patients converted to sinus rhythm with verapamil while only one of 16 converted to sinus rhythm with placebo. The effective plasma verapamil concentration measured 123 +/- 40 ng/mL (mean +/- SD). Verapamil suppressed sinus nodal and AV nodal re-entry but exerted no selective depression between fast and slow AV nodal pathways. It had no significant effect on accessory AV bypass tract but was effective in terminating AV reciprocating tachycardia by its depressive action on the AV node.
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PMID:Intravenous verapamil for termination of re-entrant supraventricular tachycardias: intracardiac studies correlated with plasma verapamil concentrations. 721 75

Atrioventricular (AV) conduction was studied in isolated, perfused rabbit hearts. Total AV interval was subdivided into the intraatrial, intranodal and His-Purkinje conduction times. Concentrations of Ca, K and Na in the control perfusate were 2.4, 4.5 and 144.8 mM, respectively. Generalized ischemia or hypoxia almost selectively depressed intranodal conduction, engendering a second degree block. Low Ca (0.8 mM) slightly prolonged the intranodal conduction time, whereas high Ca (4.8-7.2 mM) caused a greater prolongation of this interval, often causing intranodal block. High Ca-induced depression of intranodal conduction was antagonized by high K (7.5 mM). Verapamil (0.5-1.0 mg/L) produced a second degree intranodal block. Subsequent elevation of Na concentration to 172 mM (but not high Ca) restored a 1:1 conduction. Tetrodotoxin (2-10 mg/L) did not affect, whereas low Na (108.6 mM) severely depressed intranodal conduction. These results suggest that (1) AV nodal conduction is most vulnerable to reduced oxygen supply, (2) an optimal Ca concentration for AV nodal conduction exists, (3) high K counteracts high Ca-induced depression of AV nodal conduction, and (4) slow Na current may play a major role in generating AV nodal action potentials. Voltage clamp experiments on the AV node substantiated some of these observations.
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PMID:Peculiarities of AV nodal conduction and the role of slow Na current. 721 99

Verapamil (0.15 mg/kg) intravenously, was administered to 19 patients with recurrent supraventricular tachycardia (SVT) undergoing electrophysiological evaluation. Twelve patients had overt Wolff-Parkinson-White (WPW) syndrome and seven patients had concealed accessory pathways conducting in the retrograde direction only. Verapamil had a significant effect in delaying conduction and prolonging refractoriness in the atrioventricular (AV) node, but no significant actions on any of the other cardiac tissues that formed the tachycardia circuit in these patients. In particular, it had no significant effects on anterograde or retrograde bypass conduction or refractoriness. Sustained SVT was initiated in 15 patients, and was terminated within 60 to 105 seconds of a 30-second injection of verapamil in 13 patients. Cycle length alternation during SVT was seen in six patients prior to reversion, and spontaneous ventricular complexes (VPCs) were observed following verapamil administration in five patients. Two patients with apparently normal sinus node function showed prolongation of their sinus node recovery times immediately following reversion of SVT by verapamil. Echo zones were assessed before and after verapamil, and sustained or self-terminating SVT could still be induced after the drug in 13 of the 15 patients who had sustained SVT beforehand. It was concluded that intravenous verapamil was effective in terminating sustained SVT in the majority of patients with overt or concealed WPW and that, despite a potential for sinus node depression and the initiation of VPCs, it had no clinically significant side effects. The ability to reinitiate SVT following its administration suggests the need for immediate follow-up with maintenance drug therapy.
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PMID:Effects of verapamil on supraventricular tachycardia in patients with overt and concealed Wolff-Parkinson-White syndrome. 722 99

1 The effects of Ca2+ -antagonists on the relationships between alternate changes in the ST-T complex in the epicardial electrogram, ST-T alternans, and associated excitation-conduction abnormalities during coronary occlusion were examined in anaesthetized dogs. 2 Epicardial unipolar electrograms, bipolar electrograms (BPEG) and monophasic action potentials (MAP) were recorded with unipolar, composite and suction electrodes, respectively. 3 ST-T alternans was associated with serious conduction delay. During the period of ST-T alternans, the amplitude of MAP changed alternately and the negative deflection of the ST-T complex was associated with a larger MAP. A depression of the TQ level and decrease in the resting potential of MAP were marked. 4 Verapamil (0.2 mg/kg) and diltiazem (0.5 mg/kg) inhibited ST-T alternans, conduction abnormalities, TQ depression and changes in MAP. However, after these drugs, the TQ depression and the decrease in the resting potential were evident after a longer period of occlusion at a time when ST-T alternans, conduction abnormalities and alternate changes in MAP were still inhibited. Dipyridamole (0.5 mg/kg) had no effect on either ST-T alternans or the conduction abnormalities. 5 Verapamil and diltiazem inhibited ST-T alternans and the associated excitation and conduction abnormalities. The effects of these two drugs cannot be explained on the basis of attenuation of the decrease in the resting potential.
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PMID:Effects of calcium antagonists on the alternation of the ST-T complex and associated conduction abnormalities during coronary occlusion in dogs. 731 86

Changes in the exercise ECG caused by five different drugs are presented. Analysis of these changes indicate that these are related to the hemodynamic effects of the drugs, rather than to reduction of myocardial ischemia. Calcium antagonists (Verapamil) as well as drugs which reduce heart rate (Alinidine, Propranolol) do not change the relation between ST depression and heart rate in a given patient. Drugs which lower ventricular volume (Molsidomine, Nitroglycerine) reduce the amount of ST depression at the same heart rate during exercise.
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PMID:The effects of drugs on the exercise electrocardiogram. 731 92

The role of L-type Ca2+ channels on the kappa opioid-induced depression of spinal afferent transmission was assessed in spinalized rats, through recording of the C-fiber-evoked spinal flexor reflex. Six successive i.t. doses of the K agonist U-50,488H produced a dose-dependent decrease of the C-reflex duration (ID50: 25.7 nmol), the log dose-response relationship being shifted to left by pretreatment with 5 mg/kg i.v. of the calcium channel blocker verapamil, or to right by pretreatment with .25 mg/kg i.v. of the calcium channel agonist Bay K8644. Verapamil and Bay K8644, administered i.v. after U-50,488H i.t., respectively potentiated or antagonized the depressor effect of the K ligand on the reflex. The results point to a role for Ca2+ availability as a factor involved in depression of afferent nociceptive transmission by K opioids at the spinal cord.
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PMID:Calcium channel modulators modify K opioid-induced inhibition of C-fiber-evoked spinal reflexes in rat. 751 Nov 32

1. NiCl2 (cumulative concentrations of 0.56-1.91 mmol 1(-1)) produced concentration-dependent depression of tension developed (Td) and the maximum rate of rise of tension (dT/dt max) of isometric contraction of the isolated rat hemidiaphragm, during direct subtetanic (DST) electrical stimulation, only. EC50 values for NiCl2-induced depression of Td and Dt/dt max were 0.88 +/- 0.06 and 0.83 +/- 0.13 mmol 1(-1), respectively. NiCl2 did not significantly change either parameter of the isometric contraction during direct single-pulse (DSP) electrical stimulation. 2. Maximal depression of Td and dT/dt max, produced by a single concentration of NiCl2 (1 mmol 1(-1)) during DST electrical stimulation was obtained 20 min after addition of the drug in the bathing medium. 3. In the normal Tyrode solution, addition of CaCl2 (final concentration of 5.86 mmol 1(-1)) almost completely antagonized the depressant effect of NiCl2 (1 mmol 1(-1)) on Td and dT/dt max during DST electrical stimulation. In the calcium-free solution, the depression both of Td and dT/dt max produced by NiCl2 (1 mmol 1(-1)) was significantly more pronounced in comparison with the effect of NiCl2 in the normal Tyrode solution. 4. L-calcium channel activator, Bay K 8644 (25 mumol 1(-1)), significantly potentiated both Td and dT/dt max during DST electrical stimulation, but NiCl2 (1 mmol 1(-1)) decreased both parameters of the isometric contraction even in the presence of this concentration of Bay K 8644. On the other hand Bay K 8644 (25 mumol 1(-1)) did not antagonize NiCl2-induced depression of Td and dT/dt max. 5. Verapamil (2.5 mumol 1(-1); 45 min of incubation) and lidocaine (0.10 mmol 1(-1); 30 min of incubation) significantly potentiated the depression of Td and dT/dt max, produced by NiCl2 (1 mmol 1(-1), during DST electrical stimulation. The addition of CaCl2 (final concentration of 7.20 mmol 1(-1)) in the bathing medium only partially antagonized the depressant synergistic action of both verapamil or lidocaine and NiCl2 on Td and dT/dt max. 6. Forskolin (cumulative concentrations of 2.60-44.20 mumol 1(-1)) fully antagonized NiCl2-induced depression of both Td and dT/dt max; propranolol (1 mumol 1(-1)) did not abolish this antagonizing action of forskolin. Also, NiCl2 (cumulative concentrations of 0.56 -1.54 mmol 1(-1)) did not change potentiating effect of forskolin (23.4 mumol 1(-1)).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effect of nickel chloride on the isolated hemidiaphragm of the rat. 755 56

Epileptic activity induced by the GABAA receptor antagonist bicuculline is known to be blocked by organic calcium antagonists. To further analyse the mechanism underlying convulsant activity induced by substances reducing GABA-mediated synaptic transmission, the effect of organic calcium channel blockers on epileptic activity induced by the GABAA channel blocker picrotoxin in hippocampal and neocortical slices of guinea pigs were investigated. Verapamil and flunarizine suppressed paroxysmal depolarization shifts (PDS) of single neurons and accompanying epileptic field potentials (EFP). As a measure of drug action the repetition rate of epileptic events were used. The depression down to 10% the initial value (90% depression) is indicated. In the hippocampus verapamil suppressed PDS/EFP within 70 +/- 16 min (40 mumol/l) and within 39 +/- 5 min (60 mumol/l). This suppression was reversible with washout of verapamil. Flunarizine irreversibly blocked EFP/PDS within 108 +/- 14 min (18 mumol/l). In the neocortex verapamil reversibly suppressed EFP within 146 +/- 6 min (40 mumol/l) and 127 +/- 26 min (60 mumol/l). Flunarizine irreversibly blocked EFP within 181 +/- 30 min (3 mumol/l) and 109 +/- 13 min (18 mumol/l). The results suggest that voltage dependent calcium channels are essentially involved in picrotoxin-induced epileptic activity.
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PMID:Picrotoxin-induced epileptic activity in hippocampal and neocortical slices (guinea pig): suppression by organic calcium channel blockers. 783 32


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