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 effects of somatostatin on lateral hypothalamic self-stimulation were investigated in rats pretreated with haloperidol, bicuculline, phenoxybenzamine or propranolol. Somatostatin decreased the rate of self-stimulation. Halperidol, bicuculline and phenoxybenzamine potentiated the somatostatin-induced depression of self-stimulation behaviour. Propranolol had no effect. It is suggested that dopaminergic, GABAergic and noradrenergic systems are involved in the somatostatin-induced depression of self-stimulation.
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PMID:Effects of somatostatin on self-stimulation behaviour in rats pretreated with a receptor blocker. 289 12

The present study was performed in order to evaluate whether norepinephrine (NE) can modulate the synthesis and release of 1 and 2 series of prostaglandins (PGs) by the isthmic region of preovulatory sow oviducts and also to clarify whether the action of the neurotransmitter is mediated through alpha, through beta or through both types of tissue adrenoreceptors. NE, at a concentration of 1 microgram/ml, depressed significantly (P less than 0.05) the basal output of PGE1 and enhanced (P less than 0.01) the release of PGE2 but, did not modify, the output of "PGF2 alpha-like material". Propranolol (10(-7)M) failed to alter the basal output of "PGE1, PGE2 or PGF2 alpha-like material". In the presence of this beta-adrenoreceptor blocker, the depression induced by NE on PGE1 output, was abolished; its stimulatory influence on the release of PGE2, was eliminated and no effect was detected regarding PGF2 alpha. On the other hand, phentolamine (10(-6)M) did not alter the basal output of "PGE1, PGE2 or PGF2 alpha-like material" and also failed to modify the depression induced by NE on PGE1 release. However, this alpha adrenoceptor blocker completely inhibited the stimulatory action of NE on the output of PGE2 into the incubating medium. The foregoing results document opposite actions of NE on PGE1 and PGE2 outputs from the isthmic region of proestrous sow oviducts and suggest the involvement of beta-adrenoreceptors in both disparate influences. The activation of alpha adrenoreceptors also appears associated with the enhancing effect of the agonist on the release of PGE2. The possible physiological significance of these findings is discussed in terms of the function of the isthmic region as an "adrenergic sphincter" able to influence ovum transport around the moment of ovulation.
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PMID:On the synthesis of prostaglandins E1, E2 and E2 alpha by sow oviducts. Differential modulation of 1 and 2 series of prostaglandins by norepinephrine. 298 54

Because both long-term adrenoceptor agonist administration and antidepressant treatment in animals down-regulate CNS beta-adrenoceptors and attenuate brain adenylate cyclase activity, beta-adrenoceptor agonists may also possess antidepressant properties. We compared the effects of the centrally acting beta-adrenoceptor agonist clenbuterol (5, 10 and 35 mg/kg per day), and the combination of propranolol (5 mg/kg per day) and clenbuterol (10 mg/kg per day), with desipramine (15 mg/kg per day) on forced swim test performance and on cortical beta-adrenoceptors in rats following 7 days of drug administration. Desipramine (15 mg/kg per day), and clenbuterol (10 and 35 mg/kg per day, but not 5 mg/kg per day) both significantly reduced immobility in the forced swim test. Frontal cortex beta-adrenoceptors were significantly down-regulated after desipramine and all 3 doses of clenbuterol. The co-administration of propranolol (5 mg/kg per day) blocked both the reduction in immobility and down-regulation of cortical beta-receptors induced by clenbuterol (10 mg/kg per day). Propranolol (5 mg/kg per day) alone up-regulated frontal cortex beta-adrenoceptors, but had no significant effect on swimming performance. These data suggest that the physiological consequences of beta-adrenoceptor down-regulation are important in the mechanism of action of antidepressants. The results also suggest that clenbuterol may be useful in the treatment of depression.
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PMID:A comparison of the neurochemical and behavioral effects of clenbuterol and desipramine. 303 50

The effects of nifedipine (60 to 90 mg/day) and propranolol (240 mg/day) on symptoms, angina threshold and cardiac function were compared in a placebo-controlled, double-blind, crossover study. Five-week treatment periods with nifedipine and propranolol were compared with 2 weeks of placebo treatment in 21 men with chronic stable angina pectoris, 13 of whom had symptoms both at rest and on exertion. Compared with placebo, New York Heart Association functional class improved in patients equally with nifedipine (p = 0.001) and propranolol (p = 0.006). Frequency of chest pain decreased with nifedipine (p = 0.001) and propranolol (p = 0.01), and nitroglycerin consumption similarly decreased with both treatments. Nifedipine significantly delayed the onset of chest pain (p = 0.01) and 1 mm of ST-segment depression (p = 0.002) during bicycle exercise; smaller increases with propranolol were not statistically significant. A preferential clinical response to nifedipine (9 patients) or propranolol (6 patients) was unrelated to the presence or absence of pain at rest or to any baseline hemodynamic finding. Nifedipine and propranolol were equally effective in relieving exertional ischemia as shown by improvements in ejection fraction at identical workloads, from 0.48 +/- 0.11 to 0.58 +/- 0.12 (p less than 0.001) and 0.56 +/- 0.14 (p less than 0.001), respectively. Exercise wall motion, assessed by a semiquantitative wall motion score, also improved with both drugs. Propranolol treatment decreased exercise cardiac output by 14% (p = 0.01) through its effect on heart rate. In contrast, nifedipine treatment had no effect on cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of nifedipine alone with propranolol alone for stable angina pectoris including hemodynamics at rest and during exercise. 308 64

Propranolol hydrochloride is a beta-adrenergic blocking drug used in a variety of clinical conditions. Overdoses can result in severe hypotensive states usually associated with bradycardia or asystole or with profound myocardial depression. We report on an 18-year-old man who ingested a massive dose of propranolol HCl in a suicide attempt. The patient was brought to the hospital in an unresponsive state within 30 minutes of ingestion. He was initially stabilized but subsequently died nine hours after the drug was ingested. Invasive monitoring during this period revealed the shock to be secondary to marked depression of his systemic vascular resistance. Cardiac rhythm and left ventricular output were maintained throughout the attempted resuscitation. This hemodynamic picture suggests that decreased systemic vascular resistance may be another mechanism of shock in significant propranolol HCl overdoses.
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PMID:A fatal case of propranolol poisoning. 322 44

The effects of a novel piperazine derivative (INO 2628) on sinus node pacemaker activity and atrial contractile force were investigated in isolated, blood-perfused dog atrium. Injections of INO 2628 (0.03-100 mumol) into the sinus node artery of the isolated atrium induced a dose-dependent decrease in sinus rate and an increase in contractile force. The positive inotropic effects at more than 10 mumol were accompanied by a transient negative inotropism. Propranolol did not affect the positive inotropic response to INO 2628, but it significantly suppressed positive chronotropic and inotropic responses to norepinephrine. Atropine at a dose which completely blocked negative chronotropic and inotropic responses to carbachol, produced a slight but significant depression of INO 2628-induced negative chronotropic responses; inotropic responses were unaffected. These results suggest that INO 2628 induces noncholinergic negative chronotropic and nonadrenergic positive inotropic responses in isolated dog atria.
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PMID:Negative chronotropic and positive inotropic effects of a unique cardioactive agent, N,N'-dicyclopropyl methyl piperazine (bis) hydrochloride (INO 2628), in isolated, blood-perfused dog atria. 324 39

1. Ambulatory electrocardiography was used to compare the effects of propranolol and pindolol on symptoms, heart rate, arrhythmias and ST segments. Seventeen males (mean age 54 years) with a diagnosis of chronic stable angina pectoris (New York Heart Association Class II-III) were studied. Patients were treated on a double-blind cross-over basis with propranolol 80 mg three times daily or pindolol 5 mg three times daily for 14 days each. During the last 48 h of each treatment period ambulatory electrocardiography was performed. 2. Propranolol resulted in a significantly lower mean hourly, mean 24 h and minimum heart rate. Likewise propranolol caused a lower mean daytime and nocturnal heart rate. There was no significant difference in the frequency of angina between the treatments. The number of episodes of ST segment depression was not significantly different between the two drugs, although there was a trend in favour of propranolol. 3. Both the mean 24 h ST level and the maximum ST segment depression were lower during treatment with pindolol. Propranolol was associated with a total of 117 nocturnal pauses or episodes of asystole ranging in length from 1.5 to 2.8 s. During treatment with pindolol only one such period occurred. The number of premature ventricular contractions occurring during treatment with pindolol (1316 beats) was less than on propranolol (2010) and the mean hourly frequency of premature ventricular contractions was significantly lower during pindolol administration. 4. Pindolol is not significantly different from propranolol in the control of symptomatic and asymptomatic myocardial ischaemia and is associated with fewer premature ventricular contractions. However, there is no advantage in using pindolol in chronic stable angina.
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PMID:The influence of beta-adrenoceptor blockers with and without intrinsic sympathomimetic activity on heart rate, arrhythmias and ST-T segments, using ambulatory electrocardiography. 335 81

Propranolol HCl (7.5 mg X kg-1), timolol maleate (7.0 mg X kg-1), and sotalol HCl (10 mg X kg-1) were administered intracerebroventricularly (icv) to spontaneously breathing (SB) rats. The respiratory rate declined until the rats all died from respiratory arrest. Artificial ventilation resulted in survival of the rats for a 3-hr observation period. Intravenous (iv) administration of the same doses of the three beta blockers to SB rats did not result in either respiratory depression or death. Except for a decrease in heart rate (HR) the hemodynamic and respiratory parameters remained almost constant during the 3-hr observation period after iv administration to SB rats. After icv administration to SB as well as to ventilated rats no significant differences could be observed in the initial decrease in HR in comparison with iv administration. In SB rats at the end of the experiments a further decrease in HR was observed which might be ascribed to hypoxia since it did not occur in ventilated rats. After icv administration of each drug to the ventilated rats, mean arterial blood pressure showed a significantly greater decrease at the end of the 3-hr observation period than after iv administration. Plasma concentrations of the three drugs were determined just before death after icv administration in SB rats. In the other two groups they were measured at mean survival time and at the end of the experimental period. The plasma concentrations showed that the route of administration rather than the concentration of the beta blocker in plasma determines the occurrence of respiratory arrest. It was concluded that an overdose of propranolol, timolol, or sotalol can cause a centrally mediated respiratory arrest. Furthermore, a central mechanism appears to be implicated in the decrease in blood pressure.
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PMID:Central origin of respiratory arrest in beta-blocker intoxication in rats. 360 68

The effects of nine calcium ion antagonists on exercise tolerance, heart rate and ST-segment changes were compared with those of propranolol in two hundred and eighty patients with established chronic stable angina pectoris. These patients participated in clinical trials for anti-anginal efficacy against placebo, using identical methods and similar protocols, but the comparison reported here was retrospective. The trials were all fixed dose, and the dose was determined by previous upward titration to arrive at an average maximal tolerance level. All the drugs except prenylamine increased the exercise tolerance significantly when compared with placebo. Maximal ST-segment depression on exercise was reduced during treatment with propranolol while treatment with the calcium ion antagonists had no significant effect. The time to the development of 1 mm ST-segment depression was prolonged by all the drugs. Nifedipine, PY-108-068 and nicardipine increased the resting heart rate whereas verapamil, diltiazem, gallopamil, KB-944, prenylamine and tiapamil produced a slight reduction. Propranolol produced a highly significant reduction in the resting and maximal heart rates and the rate-pressure product, whereas gallopamil increased the rate-pressure product by +8% and prenylamine reduced it by -10%. At the doses used, diltiazem, gallopamil and verapamil produced a greater increase in exercise tolerance than did propranolol, while the other drugs were inferior. None of the calcium ion antagonists matched the increase in the time taken to develop 1 mm ST-segment depression with propranolol, although the results with verapamil and gallopamil were close. The calcium ion antagonists are effective antianginal agents which produce their effects by mechanisms which are very different to the beta-adrenoreceptor blocking agents.
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PMID:A comparison of nine calcium ion antagonists and propranolol: exercise tolerance, heart rate and ST-segment changes in patients with chronic stable angina pectoris. 365 22

In 14 patients with obstructive hypertrophic cardiomyopathy and angiographically normal coronary arteries, 8 with angina (group B) and 6 without (group A), the effects of intravenous isoproterenol, 2 to 4 micrograms/min, followed by intravenous propranolol, 0.2 mg/kg, were studied. An intraventricular systolic gradient less than 50 mm Hg, high-quality echocardiograms and cineangiograms and high-fidelity pressure tracings were selection criteria. Hemodynamic and metabolic variables were assessed during basal conditions, after 5 minutes of isoproterenol infusion or at angina and ST-segment depression, and 5 and 10 minutes after intravenous propranolol infusion. Isoproterenol increased the intraventricular systolic gradient more significantly in group B than in group A (102.4 +/- 8.3 vs 52.2 +/- 8.2, p less than 0.0001). Group B also had higher left ventricular end-diastolic pressure (32.5 +/- 3.9 vs 20.2 +/- 5.7), lower mean arterial pressure (69.7 +/- 3.5 vs 84.7 +/- 4.8) and a smaller increase in coronary sinus flow (176.1 +/- 9.2 vs 261.5 +/- 33.9, all p less than 0.0001), concomitant with lactate release and ST-segment depression. Propranolol promptly reversed hemodynamic and metabolic changes caused by isoproterenol, except for a further coronary sinus flow increase (from 176.1 +/- 9.2 to 219 +/- 14.2 ml/min, p less than 0.001), and heart rate decrease below basal values (57.8 +/- 7.5 vs 79.9 +/- 9.8 beats/min, p less than 0.001) in group B.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of isoproterenol-induced angina pectoris in patients with obstructive hypertrophic cardiomyopathy and normal coronary arteries. 366 32


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