Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The electrophysiologic properties of bepridil, a calcium channel blocker with additional effects on fast response tissues, were investigated in 10 patients with atrioventricular accessory pathways. Seven patients had Wolff-Parkinson-White syndrome, and three had concealed atrioventricular pre-excitation. A dose of 4 mg/kg was administered intravenously over five minutes. Bepridil increased the AH interval and the functional refractory period of the atrioventricular node. The effective refractory periods of the right atrium and right ventricle were also increased. Bepridil prolonged refractoriness in the accessory pathway both in the anterograde and retrograde direction. After bepridil administration it was impossible to induce reciprocating tachycardia electrically in two patients because of conduction block in the normal pathway. On the other hand, the zone of tachycardia was often increased after bepridil. Nevertheless, the heart rate during tachycardia was slowed by depression of conduction in both the normal and accessory pathways. The findings of this study provide a basis for the antiarrhythmic action of bepridil in patients with atrioventricular accessory pathways.
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PMID:Electrophysiological action of bepridil on atrioventricular accessory pathways. 349 24

The short- and long-term effects of two calcium channel blocking drugs, verapamil and nifedipine, on blood pressure, heart rate, plasma catecholamines, plasma renin activity, plasma volume and cardiac performance (echocardiography) were studied in essential hypertensive patients and in normal subjects. Verapamil, 160 mg orally, reduced blood pressure within 60 minutes in 22 hypertensive patients, but not in 12 normotensive subjects. Nifedipine, 10 mg sublingually, reduced blood pressure within 15 minutes in 19 hypertensive patients, but not in 7 normotensive subjects. Plasma noradrenaline was significantly increased both in normal subjects and in hypertensive patients only after nifedipine was administered. Verapamil (80 mg three times a day) first, and nifedipine (10 mg three times a day) thereafter, or vice versa, were given to 12 hospitalized hypertensive patients on a fixed sodium and potassium intake; the drugs produced similar blood pressure reductions, but heart rate and plasma catecholamines were increased only after nifedipine (p less than 0.05). Neither drug affected plasma volume, aldosterone or plasma renin activity. Long-term ambulatory treatment with verapamil (80 or 160 mg three times a day for 2 to 4 months) or nifedipine (10 mg three times a day for 2 months) produced changes in all variables that were similar to those observed in the hospital (controlled) study. Shortening fraction was significantly increased after nifedipine (p less than 0.05) but no change was observed after verapamil. In conclusion, blood pressure is effectively reduced by both verapamil and nifedipine; an appreciable adrenergic stimulation may be caused by nifedipine, but usually not by verapamil, and fluid retention, renin release or myocardial depression is not observed during verapamil or nifedipine treatment.
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PMID:Similarities and differences in the antihypertensive effect of two calcium antagonist drugs, verapamil and nifedipine. 351 29

Calcium channel blockers seem to be particularly suitable for elderly hypertensive patients since these agents do not cause salt and fluid retention, postural hypotension, sedation, depression, or biochemical abnormalities. Moreover, their use is compatible with several common diseases of old age, such as diabetes, obstructive lung disease, and peripheral vascular disease. We recently conducted a study in 21 patients (average age, 79 +/- 2 years) who completed an eight-week trial with 20-mg nifedipine tablets taken twice daily. Mean blood pressure decreased from 191 +/- 2/96 +/- 2 mm Hg to 151 +/- 4/80 +/- 3 mm Hg. In 15 patients (71 percent), blood pressure decreased to less than or equal to 160/90 mm Hg; in four additional patients (19 percent), diastolic blood pressure decreased by 15 to 25 percent. Thus, there was a sustained lowering of blood pressure in 90 percent of the participants receiving nifedipine monotherapy. A review of recent studies in elderly hypertensive patients revealed similarly favorable results with calcium channel blockers given alone or in combination with other agents. The accumulating data suggest that these compounds may offer a useful new approach to the treatment of hypertension in old age. However, in these studies, the number of patients and the duration of follow-up need to be extended to confirm the favorable impression obtained thus far.
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PMID:Calcium channel blockers in the management of hypertension in the elderly. 354 97

The cardiovascular effects of the administration of nifedipine and nifedipine combined with propranolol were examined in 15 monkeys during 0.75 and 1.25 MAC of anesthesia with isoflurane, enflurane, or halothane. Hemodynamic variables measured included heart rate (HR), mean arterial pressure (MAP), left ventricular end-diastolic pressure (LVEDP), maximum rate of increase of the Left ventricular pressure (max LV dP/dt), and thermodilution cardiac output (CO). The infusion of nifedipine at a rate adequate to produce therapeutic blood levels during 0.75 MAC with each anesthetic decreased MAP and SVR, but had no effect on cardiac index (CI), max LV dP/dt, or HR. Increasing the anesthetic concentration from 0.75 to 1.25 MAC during nifedipine administration decreased HR and MAP in all groups and decreased CI with halothane and enflurane, but not with isoflurane. Addition of propranolol by infusion in amounts adequate to produce 75% beta-adrenergic blockade caused a further depression of CI, max LV dP/dt, HR, and MAP. However, the hemodynamic depression was significantly greater with halothane and enflurane than with isoflurane. Intravenous administration of calcium chloride (10 mg/kg) after calcium channel and beta-adrenergic blockade only partially reversed the hemodynamic depression that occurred with all three anesthetics. It was concluded that acute loading with nifedipine with and without propranolol exerts a greater cardiovascular depressant effect during enflurane or halothane anesthesia than during isoflurane anesthesia. The myocardial depressant effects of nifedipine and propranolol myocardial depressant effects of nifedipine and propranolol may be synergistic with the depressant effects of potent inhalation anesthetics.
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PMID:Cardiovascular responses to acute loading with nifedipine alone and nifedipine plus propranolol during inhalation anesthesia in monkeys. 366 54

The effect of inorganic lead in vitro in several aspects of [3H]dopamine release from superfused rat striatal synaptosomes was examined. Under conditions of spontaneous release, lead (1-30 microM) induced dopamine release in a concentration-dependent manner. The onset of the lead-induced release was delayed by approximately 15-30 sec. The magnitude of dopamine release induced by lead was increased when calcium was removed from the superfusing buffer. Lead-induced release was unaffected in the presence of putative calcium, sodium, and/or potassium channel blockers (nickel, tetrodotoxin, tetraethylammonium, respectively). Depolarization-evoked dopamine release, produced by a 1-sec exposure to 61 mM potassium, was diminished at calcium concentrations below 0.254 mM. The onset of depolarization-evoked release was essentially immediate following exposure of the synaptosomes to high potassium. The combination of lead (3 or 10 microM) with high potassium reduced the magnitude of depolarization-evoked dopamine release. This depression of depolarization-evoked release by lead was greater in the presence of 0.25 mM than 2.54 mM calcium in the superfusing buffer. These findings demonstrate multiple actions of lead on synaptosomal dopamine release. Lead can induce dopamine release by yet unidentified neuronal mechanisms independent of external calcium. Lead can also reduce depolarization-evoked dopamine release by apparent competition with calcium influx at the neuronal membrane calcium channel.
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PMID:Effect of in vitro inorganic lead on dopamine release from superfused rat striatal synaptosomes. 371 85

Effects of s.c. doses of morphine and verapamil, alone and in combination, on arterial blood gases and pH, mean blood pressure and heart rate were assessed in partially restrained, awake Fischer-344 rats. As expected, morphine (4-16 mg/kg) produced a dose-dependent respiratory depression, as indicated by hypoxia, hypercapnia and acidosis. Verapamil, a calcium channel antagonist, alone (10 mg/kg) did not affect these parameters; however, it significantly attenuated and delayed the aforementioned effects of morphine. Morphine caused a slight increase in mean blood pressure, which was not dose dependent, whereas verapamil reduced blood pressure dramatically even in the presence of morphine. All groups showed some tachycardia, but rats treated with morphine alone showed the most pronounced increase in heart rate, which was antagonized by verapamil. The authors conclude that the interaction of verapamil with morphine's respiratory depressant effects differs from the previously reported potentiation of morphine's antinociceptive and hypothermic actions.
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PMID:Interactions between verapamil and morphine on physiological parameters in rats. 372 97

The authors report two cases of Bipolar Affective Disorder which were responsive to Lithium therapy in the past, but could no longer be treated with Lithium due to hyperparathyroidism in the first case and noncompliance in the second. In both cases, successful control of hypomania was achieved with Verapamil, but treatment of depression required the addition of Trazodone. The rationale for employing a calcium channel blocking agent, such as Verapamil, in bipolar illness is reviewed.
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PMID:Verapamil in bipolar illness. 373 Oct 14

The anti-anginal efficacy of tiapamil, a new calcium channel blocking agent was studied in 24 patients with established effort induced chronic stable angina pectoris. The patients were allocated randomly in a double-blind fashion to tiapamil 300 mg thrice daily or placebo for 2 weeks and thereafter all the patients received tiapamil 300 mg thrice daily in a single-blind fashion for a further 2 weeks. All patients performed symptom limited multistage graded exercise testing with computer-assisted analysis of the electrocardiogram before entering the study and at the end of the double-blind and single-blind phases. The mean exercise time to develop angina during the control test in the group which received placebo during the double-blind phase was 7.1 min; this increased to 8.5 min after 2 weeks of placebo and 9.7 min after 2 weeks of subsequent tiapamil therapy. Similarly in the group which received tiapamil during the double-blind phase the mean exercise time on control test was 6.4 min, increasing to 9.7 min and 9.7 min after 2 and 4 weeks of tiapamil therapy respectively. There were no statistical significant differences between the changes from control, seen with tiapamil and placebo during the double-blind phase. However, the changes observed between control and active therapy in the tiapamil group did reach statistical significance (p = 0.003). Similarly, 1 mm ST-segment depression time was prolonged by tiapamil therapy. The heart rate at rest and maximal exercise remained unaltered with tiapamil therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tiapamil, a new calcium channel blocking agent for the treatment of effort induced chronic stable angina pectoris. 374 14

The clinical and hemodynamic effects of propranolol, propranolol-verapamil (P-V), propranolol-nifedipine (P-N) and propranolol-diltiazem (P-D) were studied in 19 patients with chronic exertional angina pectoris. A placebo-controlled, double-blind, randomized, crossover study design was used in which patients took each treatment for a 4-week period. The 3 combinations equally reduced the incidence of angina attacks and decreased ST-segment depression. Left ventricular hypokinesia during exercise was lessened and end-systolic volume during exercise decreased with all combinations. Because of a corresponding reduction of normokinetic segmental function, global ejection fraction during exercise remained unchanged. Heart size increased (p less than 0.05) and the PR interval lengthened (p less than 0.001) with P-V and P-D compared to P-N. The largest number of adverse clinical reactions occurred with P-V, whereas the fewest occurred with P-D. Almost all patients preferred combined therapy over propranolol and many favored 1 combination over the others. In summary, when therapy with combined beta- and calcium channel-blocking drugs is planned, P-D should be considered the combination of first choice because of its low incidence of adverse clinical effects. In the presence of possible or definite abnormalities of atrioventricular nodal conduction or decreased left ventricular function, P-N should be considered. Although P-V is associated with frequent adverse reactions, a trial may be warranted if the other combinations are unsuccessful.
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PMID:Clinical and hemodynamic evaluation of propranolol in combination with verapamil, nifedipine and diltiazem in exertional angina pectoris: a placebo-controlled, double-blind, randomized, crossover study. 388 39

Concurrent therapy with the calcium channel blocker, verapamil, and the beta-blocking group of compounds is usually felt to be clinically contraindicated due to the former's potent dromotropic and negative inotropic actions. The basis of this assumption was examined in a rest and exercise hemodynamic study of the effects of verapamil and the cardioselective beta-blocking drug, metoprolol, in 22 patients with stable angina pectoris and angiographically confirmed coronary artery disease. In a randomized study, 11 patients were assessed following intravenous verapamil (16 mg) alone, 11 following intravenous metoprolol (10 mg) alone, and all 22 were assessed on combination therapy. The plasma levels achieved at the time of each hemodynamic assessment were in the therapeutic range. At rest, verapamil alone significantly lowered systemic arterial pressure and vascular resistance; metoprolol alone lowered heart rate and increased systemic vascular resistance without change in systemic arterial pressure. Combination therapy reduced systemic arterial pressure and heart rate without change in cardiac output and systemic vascular resistance. During upright bicycle exercise, the changes were directionally similar. Depression of cardiac function (i.e., reduced cardiac output at increased pulmonary artery occluded pressure) occurred following metoprolol but not following verapamil; the addition of verapamil did not accentuate the depression of function induced by metoprolol. These results suggested that in patients with stable coronary artery disease, without manifest conduction system abnormality, the cardiac depressant actions of verapamil were countered by its vasodilator properties.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects on left ventricular performance of verapamil and metoprolol singly and together in exercise-induced angina pectoris. 389 May 5


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