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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pesticide chlordimeform (CDM) depressed the electrically-induced twitch responses of the guinea pig longitudinal muscle ED50 = 3 X 10(-5)M). Naloxone reversed twitch depression induced by morphine but not by CDM. Phentolamine reversed twitch depression induced by either norepinephrine or clonidine, but not by CDM. PGE2 completely reversed twitch depression induced by either CDM or indomethacin, but only partially reversed twitch depression induced by lidocaine. The actions of CDM best resemble those of the nonsteroidal anti-inflammatory agents. The reversibility of the CDM depression by washing indicates that the guinea pig ileal preparation is a convenient screen for distinguishing reversible from irreversible inhibitors of prostaglandin biosynthesis.
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PMID:Reversible depression of electrically-induced contractions of guinea pig longitudinal muscle by a reversible inhibitor of prostaglandin synthetase. 12 9

Pressure increases elicited by contractions of the circular muscle of the isolated guinea-pig vas deferens in response to nerve stimulation were recorded. In contrast to longitudinal muscle which contracted in response to 1--50 pulses, circular muscle responded only to longer trains of pulses (10--500) at a frequency of 10 Hz. Atropine (1.4 muM) caused a slight depression of responses to 100 shocks. Phentolamine at a concentration of 2.6 muM failed to inhibit the response to stimulation, but a higher concentration (53 muM) caused a definite blockade. Guanethidine (25 muM) strongly reduced the responses. With a stimulus train of 100 pulses no inhibition by prostaglandin E1 (PGE1) (0.028 muM) could be demonstrated; however, at a lower number of shocks (20--50) a clearcut depression was observed. The lower the number of pulses the more marked was the depression. The observation that PGE1 failed to block the contractions evoked by noradrenaline (59 muM) suggests a presynaptic inhibitory action of the prostaglandin. It is suggested that noradrenaline is the transmitter in both muscle coats of the guinea-pig vas deferens and that the neuroeffector junctions are sensitive to the effect of PGE1.
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PMID:Inhibition of neuromuscular transmission by prostaglandin E1 in the circular muscle of the guinea-pig vas deferens. 18 81

The normal depression of plasma insulin concentration during exercise has been ascribed to adrenergic inhibition of insulin release and the role of humoral catecholamines in this hormonal adjustment has repeatedly been stressed. In the present study this contention has been investigated in 6 bilaterally adrenalectomized patients and in 6 sex- and age-matched controls who undertook exercise on an ergometer until they were exhausted. No differences were observed in any cardiovascular or metabolic adjustments between the two groups during strenous exercise. Mean plasma insulin concentration fell by about 50% in both groups. Phentolamine effectively abolished the fall in plasma insulin concentration during exercise in 2 adrenalectomized patients. The results suggest that the adrenergic nerves that supply the B-cells have a functional role in man during exercise.
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PMID:The role of the adrenergic innervation to the pancreatic islets in the control of insulin release during exercise in man. 23 Apr 55

The profile of spontaneous contractions as well as the influences of prostacyclin (PGI2) on the motility of human ovarian veins obtained during the estrogenic phase of the sex cycle were explored. The preparations exhibited a distinct phasic activity, which progressively decreased as isolation time progresses, dissapearing almost completely following more than two hours. PGI2 produced a biphasic influence on quiescent preparations. After the threshold is attained lower concentrations caused depression of tone whereas higher ones enhanced the basal tone and induced phasic contractile cycles. Phentolamine reduced markedly the stimulating influence of PGI2 but had no action on the inhibitory effects, whereas propranolol failed to alter either the excitatory of the depressive action. The results suggest a participation of alpha-adrenoceptive-mediated mechanisms in the stimulatory effect of PGI2. On the other hand, PGI2 may be of importance in the regulation of venous flow and the spontaneous or PGI2-induced contractions could play a role in the counter current mechanism between veins and arteries in the ovarian pedicle.
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PMID:Spontaneous contractile activity of isolated ovarian human vein. A dual influence of prostacyclin (PGI2). 39 50

Propranolol (100mug) ivc together with phentolamine (60 mug) decreased spontaneous locomotor activity and weakened post-nialamide locomotor activity in rat. When applied separately in the above doses, neither of the two compounds had this action. Depression of amphetamine-induced locomotor activity was observed after propranolol (250 mug) together with phetolamine (60 mug). Phentolamine alone, had hypothermic action but when applied together with propranolol, it increased after 4 hrs body temperature. The tested compounds prolonged hexobarbital-induced sleeping time but did not affect noradrenaline or dopamine levels in rat's brain.
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PMID:The central action of intraventricularly (ivc) administered propranolol and phentolamine in rat. 116 21

In experiments with rabbits, glucagon prolonged the half-period of absorption of sodium iodide 125J in the left ventricular myocardium. Regitine prevented acceleration of the heart rate and impairment of capillary flow after glucagon. In healthy rabbits hippurate 125J clearance was unaffected by glucagon. After injury of the heart muscle by injection of silver nitrate solution into the left ventricular wall and depression of blood pressure, glucagon partly normalized renal clearance of hippurate 125J.
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PMID:The influence of glucagon on the blood supply of the heart and kidneys in rabbits. 121 13

On the endothelium-intact rat aorta some studies have shown prazosin to cause nonparallel rightward shifts of alpha 1-adrenoceptor agonist response curves. The aim of the present study was to analyze the inhibitory effect of prazosin on the phenylephrine responses of the endothelium-intact and endothelium-denuded rat aorta. Firstly I used phenoxybenzamine treatment to characterize the phenylephrine responses. The KA values for phenylephrine were 0.13-0.18 microM and 0.07-0.16 microM in the endothelium-intact and endothelium-denuded rat aorta, respectively. In order to produce maximal responses of the endothelium-intact or--denuded preparation, phenylephrine had to occupy 95-99% of the alpha 1-adrenoceptors. Secondly I compared the inhibitory effects of phentolamine and prazosin on the endothelium-intact rat aorta. Phentolamine at 0.1 and 1 microM caused parallel rightward shifts of phenylephrine response curves with no effect on phenylephrine maximal responses (phentolamine pA2 = 7.9). The inhibitory effects of phentolamine were readily reversible. Prazosin at 0.1-10 nM caused nonparallel rightward shifts of the phenylephrine response curves with a depression of the maximal response. These inhibitory effects of prazosin were either irreversible or only very slowly reversible in drug-free solution and slowly reversible in the presence of phentolamine. Ninety min was required for the inhibitory effect of prazosin to reach equilibrium whereas phentolamine was at equilibrium after 45 min. Finally I have characterized the inhibitory actions of prazosin on the endothelium-denuded rat aorta. Prazosin caused parallel rightward shifts of phenylephrine response curves with no effect on phenylephrine maximal responses. The inhibitory effects of prazosin were at equilibrium after 45 min and were readily reversible.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An analysis of the inhibitory effects of prazosin on the phenylephrine response curves of the rat aorta. 140 16

The mode of interaction of some alpha-adrenoceptor ligands with the 5-HT2-receptor system was investigated in the calf coronary artery. Isometric contractions caused by 5-hydroxytryptamine (5-HT) were studied on strips without endothelium. Phentolamine antagonized competitively (pKB = 7.4) the effects of 5-HT. Phentolamine also prevented the methysergide-induced depression of contractions elicited by 5-HT. The alpha 1-selective ligand 127I-HEAT depressed the responses to 5-HT. Both phentolamine and ketanserin prevented the depressant effects of I-HEAT on 5-HT-induced contractions. These and previous experiments are consistent with the existence of the 5-HT2 receptor in two interconvertible states R in equilibrium with R'. Interconversions between the high affinity state R and low affinity state R' (for 5-HT) appear to be modulated by an allosteric site A. The present and previous data suggest four possible modes of interaction of alpha-adrenoceptor ligands with the 5-HT2-receptor system: (a) ligands that compete with 5-HT for the 5-HT2 receptor in the R state (examples are nonselective phentolamine, alpha 1-selective ketanserin and corynanthine, and alpha 2-selective yohimbine and rauwolscine); (b) ligands such as I-HEAT that through binding to A depress the response to 5-HT by favouring the R' state; (c) ligands, such as ketanserin and phentolamine, that through binding to A favour the R state; and (d) ligands, such as phenoxybenzamine, that cause a covalent modification of the R state but not of the R' state. Qualitative and quantitative considerations suggest that in the calf coronary artery the described features are unrelated to alpha 1- and alpha 2-adrenoceptors.
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PMID:A two-state model for the 5-HT2 receptor: effects of alpha-adrenoceptor ligands. 245 22

1. Tested against the spontaneous tone of guinea-pig isolated trachealis, cromakalim (0.1-100 microM), isoprenaline (1 nM-1 microM) and theophylline (1 microM-1 mM) each produced concentration-dependent relaxation. 2. Glibenclamide (0.1-10 microM) did not itself alter the spontaneous tone of the trachea nor did it modify the relaxant actions of isoprenaline or theophylline. In contrast, glibenclamide (0.1 and 1 microM) caused a concentration-dependent rightward shift of the log concentration-effect curve of cromakalim. Glibenclamide (10 microM) reduced the slope of the log concentration-effect curve of cromakalim and moved the foot of the curve back towards the control position. 3. Phentolamine (1, 10 and 100 microm) did not itself alter the spontaneous tone of the trachea nor did it modify the relaxant actions of isoprenaline or theophylline. In contrast phentolamine caused concentration-dependent depression of the log concentration-effect curve of cromakalim. 4. Neither prazosin (1 microM) nor yohimbine (10 microM) modified the spontaneous tone of the trachea. Prazosin and yohimbine each failed to antagonise the effects of cromakalim, isoprenaline and theophylline. 5. Intracellular electrophysiological recording showed that glibenclamide (1 microM) and phentolamine (100 microM) caused minor change in the resting membrane potential of trachealis cells. Slow wave activity was slightly depressed by these agents. In contrast tetraethylammonium (TEA; 8 mM) caused marked depolarisation, and promoted the conversion of slow waves into regenerative action potentials. These electrical changes were accompanied by tonic tension development. 6. Phentolamine (100 microM) and glibenclamide (1 microM) reduced and reversed both the relaxation and the hyperpolarisation induced by cromakalim (10 microM). 7. It is concluded that glibenclamide and phentolamine each provide selective antagonism of the relaxant action of cromakalim in guinea-pig trachealis. These agents also inhibit the plasmalemmal hyperpolarisation induced by cromakalim. The effect of phentolamine is unrelated to the blockade of alpha 1- or alpha 2-adrenoceptors. If either glibenclamide or phentolamine act to block the K+ channels opened by cromakalim, then such channels are not identical to those which endow the trachealis plasmalemma with its powerful rectifying behaviour.
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PMID:Cromakalim-induced relaxation of guinea-pig isolated trachealis: antagonism by glibenclamide and by phentolamine. 251 95

Norepinephrine (NE) has been shown to have a biphasic effect on evoked potentials in the CA1 region of the hippocampus of the rat in vitro, with a beta receptor mediating an increase and an alpha receptor eliciting a decrease in the amplitude of the population spike. The purpose of this study was to use selective alpha-adrenergic agonists and antagonists to determine the subtype of receptor mediating the depressant response of NE. The present investigations demonstrated that the selective alpha 1 agonist, phenylephrine (2-50 microM) elicited a dose-dependent depression of the amplitude of the population spike. Clonidine, a relatively selective alpha 2-agonist, also depressed the amplitude of the population spike, but only at concentrations (10 microM) that were inconsistent with a selective action upon alpha 2-receptors. Another alpha 2-agonist, alpha-methylnorepinephrine (100-400 nM) did not depress the amplitude of the population spike. The depressant effect of NE was antagonized by the nonselective alpha antagonist, phentolamine (0.5-50 microM) and the alpha 1-selective antagonist, prazosin (1 microM), but not by the alpha 2-selective antagonist, idazoxan (1-10 microM). Phentolamine and prazosin antagonized the response to phenylephrine but not to clonidine. The depressant effect of NE was not antagonized by the antagonist of serotonin and dopamine, spiperone (100 nM); conversely, the effect of 8-hydroxy-2-(di-n-propylamine) tetralin (50 microM), a 5-HT1A receptor-selective agonist, which also depresses the amplitude of the population spike, was not antagonized by phentolamine (5 microM).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Noradrenergic depression of synaptic responses in hippocampus of rat: evidence for mediation by alpha 1-receptors. 284 79


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