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

Subtetanic contractions of the guinea-pig isolated soleus, a slow-contracting skeletal muscle, were evoked by transmural field-stimulation. Isoprenaline caused a dose-dependent depression of the contractions. This effect was inhibited by propranolol and H 35/25 (1-(p-tolyl-2-isopropylamino-1-propanol) but not by practolol. Similar results were obtained for terbutaline. Tazolol and H 80/62 (1-isopropylamino-3-(p-hydroxyphenoxy)-2-propanol (HCl), selective beta1-agonists, had no effect per se but inhibited the effect of terbutaline. Adrenaline, noradrenaline, and dopamine all caused a dose-dependent decrease in the force of the soleus contractions, their potencies being in that order. Tyramine did not appreciably affect the contractions nor did it inhibit the effect of terbutaline. Pretreatment with reserpine, if anything, increased the response to terbutaline. It is concluded, in conformity with previous in vivo studies, that the adrenergic receptor mediating the effect on the soleus muscle contractions is of the beta2-type. Indirect sympathomimetic effects do not contribute to the responses observed on the isolated soleus muscle.
 ...
PMID:Analysis of the beta-receptor mediated effect on slow-contracting skeletal muscle in vitro. 2 Dec 60

1 The effects of isoprenaline, propranolol and phentolamine, were studied on tritiated noradrenaline overflow elicited by postganglionic nerve stimulation in guinea-pig isolated atria. 2 Isoprenaline (1.2 times 10-minus 8M) increased while propranolol (1.0 times 10-minus 7M) reduced the overflow of tritiated noradrenaline evoked by nerve stimulation. These effects were less than those of phentolamine (3.1 times 10-minus 6M), which increased by approximately three-fold the overflow of [3H]-noradrenaline elicited by nerve stimulation. 3 Neuronal accumulation of tritiated noradrenaline in guinea-pig atria was not affected by isoprenaline, propranolol or phentolamine at the concentration employed in this study. 4 Isoprenaline (1.2 times 10-minus 8M) induced a positive chronotropic effect of about 80 percent of the maximum. On the other hand, propranolol produced a shift to the right in the frequency-response curve to nerve stimulation and in the concentration-response curve to exogenous noradrenaline in guinea-pig atria. 5 In the isolated nictitating membrane of the cat, the frequency-response curve to nerve stimulation was not modified by propranolol, while in the presence of 3.9 times 10-minus 6M of N,-2-(2,6-dimethylphenoxy)propyl-N,N,N-trimethylammonium (beta-methyl-TM 10) there was a shift to the right and a depression of slope. Neither propranolol nor beta-methyl-TM 10 affected responses to exogenous noradrenaline. 6. The effects of isoprenaline and of propranolol on transmitter release are compatible with the view that in addition to the presynaptic negative feed-back mechanism for noradrenaline release by nerve stimulation mediated via alpha-adrenoceptors a positive feed-back mechanism exists in adrenergic nerve endings which is triggered through the activation of presynaptic beta-adrenoceptors.
 ...
PMID:Possible role of a beta-adrenoceptor in the regulation of noradrenaline release by nerve stimulation through a positive feed-back mechanism. 16 67

The effects of verapamil on myocardial isometric force on contraction, cardiac adenosine 3,'5'-monophosphate (cyclic AMP) and heart phosphorylase alpha activity were studied in the isolated perfused rat heart. When hearts were perfused with verapamil (5.98 times 10- minus 8 M), force of contraction was reduced approximately 50% within 4 to 5 minutes; at this point, the concentration of cyclic AMP was significantly lower than control but phosphorylase alpha activity was unchanged. In hearts perfused continuously for 60 minutes with verapamil, force of contraction and cyclic AMP levels returned to normal within 20 minutes after administration of verapamil was begun. Isoproterenol (0.355 nmol/min) reversed the depressant effect of verapamil on cardiac contractility and restored heart cyclic AMP levels to normal. Methoxamine (35.5 nmol/min) given to verapamil-depressed hearts, caused contractile force to return to normal, but cardiac cyclic AMP levels remained low. Mephentermine (23.0 nmol/min) had no effect on cardiac contraction, cyclic AMP or phosphorylase alpha activity in hearts depressed by verapamil. It was concluded that with the concentration of verapamil used in these experiments, the drug caused a transient decrease in force of contraction and myocardial cyclic AMP. Both the depression in myocardial contractility and in cardiac cyclic AMP caused by verapamil were reversed promptly by isoproterenol, whereas methoxamine overcame acutely only the negative inotropic effect of verapamil. Mephentermine had no effect on hearts depressed by verapamil.
 ...
PMID:Effects of verapamil on myocardial contractility, cardiac adenosine 3,'5'-monophosphate and heart phosphorylase. 16 48

The effect of verapamil on myocardial contractility, heart adenosine 3', 5'-monophosphate (cyclic AMP) and cardiac phosphorylase a activity was studied in isolated perfused rat hearts. In a concentration of 0.025 mug/ml, verapamil decreased force of contraction 50% and caused a significant fall in heart cyclic AMP within 4 to 5 min after perfusion with the drug was begun. When perfusion of the heart with medium containing verapamil was continued for 60 min, contractile force gradually returned to control. at the end of 60 min of perfusion with verapamil, the myocardial concentration of cyclic AMP was not different from that measured in hearts perfused with contro medium for a similar time period. Isoproterenol, given at the point of maximal contractile depression induced by verapamil, restored normal force of contraction and raised cardiac cyclic AMP to the same level as that observed when the catecholamine was given to untreated hearts; When methoxamine was administered to hearts depressed by verapamil, contractility returned to normal, but cyclic AMP content remained below control values.
 ...
PMID:Metabolic and inotropic effects of verapamil in perfused rat heart. 17 69

The beta-adrenergic receptors were studied in vitro in lymphocytes obtained from patients with major affective disorders and controls. Specific L-[3H]-dihydroalprenolol binding was decreased in both depressed and manic patients compared to controls and euthymic patients. Isoproterenol-stimulated, but not prostaglandin El-stimulated, cyclic adenosine-3',5'-monophosphate production was decreased in manic and depressed patients. These results suggest decreased lymphocyte beta-receptor functioning in depression and mania. This decrease may be an index of changes in brain beta-receptors in mania and depression, or may simply reflect homeostatic regulation of peripheral beta-receptors in response to stress-induced increases in circulating catecholamines.
 ...
PMID:Changes in lymphocyte beta-adrenergic receptors in depression and mania. 23 57

Isoproterenol infusions depress pentagastrin (PG)-stimulated secretion of acid and pepsin from both gastric fistulae and denervated (Heidenhain) pouches in conscious dogs. It was not found to do so if methacholine replaced gastrin. Propranolol reversed the isoproterenol depression of PG stimulation but had no effect on isoproterenol plus methacholine except on the fistula where both acid and pepsin were depressed. It is felt that PG and methacholine act by differing mechanisms both on chief and parietal cells.
 ...
PMID:Adrenergic activity and gastric secretion. 77 88

Quantitation of peripheral vascular versus direct cardiac effects of isoproterenol (0.002 mg/kg) was attempted in a new pharmacologic animal model, the unanesthetized calf, before and after replacement of its natural heart with a pneumatically driven artificial heart (AH). Isoproterenol significantly increased (rho less then 0.01) cardiac output and pulmonary shunt and decreased aortic blood pressure before and after AH replacment. Elevation of cardiac output and pulmonary shunt was greater (rho less than 0.05) and depression of aortic pressure less (rho less than 0.05) before AH replacement than after. Isoproterenol did not change pulmonary artery (PA) or right atrial (RA) blood pressures before AH implantation but did reduce (rho less than 0.05) PA diastolic and mean pressures and increase mean RA pressures after. Systemic vascular resistance was significantly (rho less than 0.01) reduced by isoproterenol before and after AH implantation. Heart rate, 02 uptake, respiratory rate, tidal volume, and minute volume were all markedly increased before AH implantation but unchanged after. These findings demonstrate that approximately half the increase in output and pulmonary shunt and all changes in 02 uptake and respiratory dynamics after administration of isoproterenol are related to cardiac effects of the drug. Our data also suggest that the unanesthetized bovine before and after AH replacement is a unique model for study of the differential pharmacology of drugs with respiratory, cardiac, and peripheral vascular effects.
 ...
PMID:Cardiovascular and respiratory effects of isoproterenol before and after artificial heart implantation. 94 61

Intravenous infusion of 10 to 30 gamma/min. of Isuprel for 3 to 7 minutes is accurate in diagnosing coronary disease in at least 80% of cases in our series of 100 patients with segmental coronary artery stenoses of 50% or more, demonstrated by coronary angiography. By comparing these 100 patients with a control group of 30 healthy subjects we can state that the late "ST" segment changes (persisting or appearing 3 minutes after stopping the infusion) are typical of coronary insufficiency. In patients without previous infarction, coronary insufficiency is expressed by a horizontal "ST" depression of 1 mm or more. In patients with previous infarction we observed either an "ST" depression or an "ST" elevation. The "ST" elevation, never observed in the control group, seems to have a different significance depending on whether or not a previous myocardial infarction has occurred. If there was no previous necrosis, severe coronary artery disease seems to be suggested and is a bad prognostic sign. This is not so if the patient has previously presented a myocardial infarction.
 ...
PMID:[The isoproterenol test in the electrocardiographic diagnosis of coronary insufficiency. Experience in 100 cases of ischemic cardiopathy]. 120 42

Significant depression of mucociliary function occurs during general anesthesia. One possible mechanism to account for this effect is a change in ion and water transport across airway epithelium. To determine if anesthetics alter epithelial cell function, we used electrophysiologic techniques to measure the effects of halothane on ion transport of in vitro canine tracheal epithelial. Epithelial tissues were mounted in an Ussing chamber and the short-circuit current (Isc) (a measure of active ion transport) and transepithelial resistance were determined in the absence and presence of halothane. Halothane induced a rapid and reversible decrease in Isc that was dose-dependent. Four percent halothane reversibly decreased Isc from 90 +/- 11 to 39 +/- 6 microA/cm2 (n = 12; P = 0.001) and increased transepithelial resistance. Isoproterenol is a well-known activator of chloride secretion that acts via beta-adrenergic receptors and cyclic adenosine monophosphate (cAMP). Pretreatment with isoproterenol or dibutyryl cAMP (a cell permeable analogue of cAMP) increased the percent inhibition of Isc by 4% halothane. These effects are consistent with preferential inhibition of chloride secretion by halothane but rule out a primary action of halothane on the beta-adrenergic system. In the presence of indomethacin, which eliminates the contribution of chloride secretion to Isc, 4% halothane induced a much smaller but still significant inhibition. This suggests that sodium absorption is also affected. We conclude that halothane significantly decreases ion and water transport in canine epithelia and that impaired fluid secretion may contribute to decreased mucous clearance in the perioperative period.
 ...
PMID:Halothane inhibition of ion transport of the tracheal epithelium. A possible mechanism for anesthetic-induced impairment of mucociliary clearance. 131 9

Earlier experiments performed in this laboratory have demonstrated that naloxone infusion (1 mg/kg/min i.v.) into conscious rats results in a bradycardia that has a peripheral component, is dependent on a certain level of sympathetic activity and is sensitive to alpha adrenoceptor blockade (5 mg/kg of phentolamine i.v.). The main objective of this investigation was to examine the underlying mechanism(s) responsible for the peripherally mediated naloxone-induced bradycardia, and to test the hypothesis that naloxone interacts with peripheral inhibitory alpha adrenoceptors associated with depression of peripheral sympathetic activity. Naloxone infusion (1 mg/kg/min i.v.) in pithed rats, in the absence of sympathetic nerve activation, resulted in a bradycardia that could not be blocked by 1 mg/kg (i.v.) of atropine, 5 mg/kg (i.v.) of phentolamine, 0.1 mg/kg (i.v.) of prazosin or 0.5 mg/kg (i.v.) of rauwolscine. Isoproterenol or norepinephrine-induced tachycardia was not blocked by naloxone infusion, suggesting that naloxone does not antagonize the postjunctional activation of cardiac adrenoceptors to cause bradycardia. In the presence of sympathetic nerve activity, naloxone depresses neurogenic tachycardia. This effect was blocked completely by 5 mg/kg (i.v.) of phentolamine or 0.5 mg/kg (i.v.) of rauwolscine, but not 0.1 mg/kg (i.v.) of prazosin or 1 mg/kg (i.v.) of atropine. The results of this investigation suggest that the naloxone-induced bradycardia in pithed rats is mediated postjunctionally and prejunctionally, and that this prejunctional effect is dependent on sympathetic nerve activity and inhibitory alpha-2 adrenoceptors. Furthermore, these results confirm results obtained from conscious rats in an earlier investigation.
 ...
PMID:Naloxone-induced bradycardia in pithed rats: evidence for an interaction with the peripheral sympathetic nervous system and alpha-2 adrenoceptors. 133 70


1 2 3 4 5 6 7 8 9 Next >>