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Adrenergic modulation of IKH was studied in isolated canine atrial cardiomyocytes with whole-cell patch-clamping, and action-potential consequences were assessed in multicellular preparations with fine-tipped microelectrodes. Isoproterenol increased IKH in a concentration-dependent manner (maximum 103+/-22% increase), an effect mimicked by forskolin and 8-bromo-cyclic AMP. Isoproterenol effects were prevented by propranolol and the selective beta1-adrenoceptor blocker CGP-20712A, but not the beta2-blocker ICI-118551. Isoproterenol enhancement was prevented by pipette-administered protein kinase A (PKA) inhibitor peptide or by superfusion of H89 (PKA blocker). Phenylephrine decreased IKH in a reversible, concentration-dependent way. This effect was blocked by the alpha-antagonist prazosin and the selective alpha1A-blocker niguldipine, but not the alpha1B-blocker chloroethylclonidine or the alpha1D inhibitor BMY-7378. Phenylephrine effects were prevented by the phospholipase C (PLC) inhibitor U73122 and the protein kinase C (PKC) inhibitor bisindolylmaleimide. The PKC-activating phorbol ester PDD (but not its inactive analogue alpha-PDD) mimicked phenylephrine effects. Action potential recordings in the presence and absence of the selective IKH blocker tertiapin indicated a functional role of alpha- and beta-adrenergic actions on IKH. Adrenergic regulation of cholinergic agonist-induced K+ current paralleled that of IKH.
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BFOS and morphine showed marked analgesic activities (p<0.001); the pretreatment of animals with naloxone, metergoline and l-arginine significantly (p<0.05 and p<0.001) reduced the analgesic activity of BFOS; however, pretreatment with prazosin, yohimbine, propranolol and glinbenclamide showed no effect on its analgesic activity.
In the present study we investigated the characteristics of medullary raphe serotonergic neurons. Specifically, we sought to examine further the similarities between medullospinal 5-HT neurons and the more extensively studied neurons of the dorsal raphe. Intravenous administration of 5-methoxy-dimethyltryptamine (5-MeODMT) produced a dose-related inhibition of the firing of midline medullary 5-HT neurons. Microiontophoretically applied 5-MeODMT also inhibited medullary 5-HT neurons. The inhibitory potency of 5-MeODMT was nearly identical to that observed for dorsal raphe 5-HT neurons. Microiontophoretic or intravenous administration of the 5-HT2 receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) did not alter the firing rate of medullary 5-HT neurons. Intravenous administration of the alpha 1-receptor antagonist prazosin resulted in an inhibition of the medullary 5-HT neuronal firing. The discharge of medullary 5-HT neurons increased during iontophoresis of norepinephrine. These data are discussed in relation to the identification and characterization of medullary 5-HT neurons. In addition, the data suggest that the firing rate of medullary 5-HT neurons is regulated in part by a tonic excitatory noradrenergic input.
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S-doxazosin decreases the carotid blood pressure and left ventricular pressure of the heart less than R-doxazosin and rac-doxazosin, but its effect on the vesical micturition pressure is similar to R-doxazosin and rac-doxazosin, indicating that S-doxazosin has chiral selectivity between cardiovascular system and urinary system in anesthetized rats.
The purpose of this study was to investigate the relationship between norepinephrine-induced contraction and hydrolysis of phosphatidylinositols in rat aorta. Norepinephrine-induced contraction was associated with increased accumulation of the hydrolytic products of the phosphatidylinositols, inositol monophosphate and phosphatidic acid. Norepinephrine also induced significant decreases in phosphatidylinositol phosphate and phosphatidylinositol bisphosphate. The alpha-1 adrenoceptor antagonist, prazosin, exposure to the Ca++ channel modulator, nifedipine, and removal of extracellular Ca++ inhibited the accumulation of inositol monophosphate and contraction due to norepinephrine. These results suggest that the contraction induced by norepinephrine may be mediated by processes associated with hydrolysis of phosphatidylinositols. The hydrolysis may occur through Ca++-dependent activation of phospholipase C by alpha-1 adrenoceptor agonists.
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Pulpal vessels are innervated with sympathetic adrenergic vasoconstrictor fibers. Electrical stimulation of the cervical sympathetic nerve causes pulpal arteriolar constriction and a reduction of arteriolar and venular flow rate (in mm3/s) in rat incisor pulps and a decrease in pulpal blood flow (in ml/min/100 g) in canine pulps of cats and dogs. The alpha-antagonist phenoxybenzamine and the alpha-1 antagonist prazosin attenuated the decrease in pulpal blood flow (PBF) caused by sympathetic stimulation. Reflex excitation of the sympathetic nerve system by hemorrhage caused pulpal vasoconstriction and a reduction of PBF. Induction of hemorrhagic hypotension in dogs subjected to cervical sympathectomy and adrenalectomy caused less pronounced pulpal vasoconstriction and flow reduction than in normal dogs. Pulpal vessels are also equipped with alpha-1, alpha-2 and beta-adrenergic receptors. Activation of alpha-1 and alpha-2 receptors by intraarterial injection of phenylephrine and clonidine caused a reduction in PBF in dogs and decreases in arteriolar and venular diameters and volumetric flow in rats. These responses were blocked by the alpha-1 and alpha-2 antagonists. Activation of beta-2 receptors by i.a. injection of isoproterenol caused a paradoxical reduction of PBF in dogs. In rats isoproterenol caused a transient increase in the flow rate followed by a reduction, and arteriolar dilation was accompanied by venular constriction. These flow responses to isoproterenol were blocked by the beta-2 antagonist propranolol. Results of microcirculatory studies in dogs and rats indicate that pulpal hemodynamics are regulated significantly by the sympathetic adrenergic system.
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The treatment for 7 days with 4 mg of sustained release doxazosin shows greater success when removing the catheter after suffering AUR due to BPH. With this treatment, 60% of the patients could spontaneously urinate again. By increasing the dose to 8 mg, the catheter can be removed in half the patients that did not initially respond. Before removing the catheter it is not possible to predict which patients would be able to spontaneously urinate.
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The responses of the dilator layer of the rat iris to sympathetic nerve stimulation were examined using intracellular recording techniques. Three different cell types were detected. In two of these, which were assumed to reflect recordings from myoepithelial cells, sympathetic nerve stimulation initiated excitatory junction potentials. These started after a delay of several hundred milliseconds and lasted for several seconds. The excitatory junction potentials were abolished by low concentrations of prazosin and were relatively insensitive to yohimbine, indicating that neurally released noradrenaline activated an alpha 1-adrenoceptor. The adrenoceptor was further characterised as being of the alpha 1b subtype using chlorethylclonidine. The time course of excitatory junction potentials was slowed when the preparation was cooled, suggesting that a second messenger pathway was being activated. The contractions triggered by sympathetic nerve stimulation persisted after excitatory junction potentials had been abolished by reducing the external concentration of chloride ions and after adding the organic calcium antagonist, nifedipine. Thus it seems likely that contractions of the dilator are triggered by the release of calcium ions from internal stores. These observations are discussed in relation to the idea that alpha 1b-adrenoceptors are coupled to a messenger pathway which involves inositol triphosphate and the pulsatile release of calcium ions from internal stores. The second section of the paper deals with the structure of neuro-myoepithelial contacts in the dilator layer. The majority of sympathetic varicosities formed organized neuroeffector junctions with either myoepithelial cells or melanophores. At the junctions the effector cell membrane and varicosity membrane were separated by less than 80 nm, with synaptic vesicles concentrated towards the neuroeffector junction. The synaptic vesicles in varicosities that failed to form junctions did not aggregate towards their regions of exposed membrane. These observations are discussed in relation to the idea that transmission at autonomic varicosities occurs at organised neuroeffector junctions.
The novel competitive N-methyl-D-aspartate (NMDA) receptor antagonist DL-(E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid (CGP 37849) was found to produce a phencyclidine (PCP)-like behavioral syndrome (ataxia, locomotion, stereotypies) in amygdala-kindled rats, whereas the amphetamine-like behavioral alterations of the syndrome (locomotion, stereotypies) were only infrequently seen in nonkindled rats. In dose-response experiments in kindled and nonkindled rats, behavioral effects were scored using a ranked intensity scale, and the behaviors and behavioural scores determined after CGP 37849 were compared with those determined after i.p. administration of the noncompetitive NMDA receptor antagonist dizocilpine maleate (MK-801). In kindled rats, 20 mg/kg of CGP 37849 produced about the same scores for hyperlocomotion and head weaving as 0.1 mg/kg of MK-801. Kindled rats exhibited higher behavioral scores than nonkindled rats, especially in the case of CGP 37849. The behavioral effects produced by CGP 37849 in kindled rats were almost indistinguishable from the PCP-like behavioral effects induced by MK-801, indicating that CGP 37849 indeed produces a PCP-like pattern of behavior in kindled rats. Hyperlocomotion and head weaving induced by CGP 37849 in kindled rats could be attenuated or totally prevented by pretreatment with ipsapirone, a partial agonist/antagonist at postsynaptic 5-hydroxytryptamine (5-HT) receptors of the 5-HT1A subtype. Furthermore, these behavioural effects were attenuated or blocked by the dopamine antagonist haloperidol and the alpha-1 adrenoceptor antagonist, prazosin. The data demonstrate that kindling induces a hypersensitivity to PCP-like behavioral effects of competitive and noncompetitive NMDA receptor antagonists, which could relate to the recent finding of increased function of NMDA receptors following kindling.(ABSTRACT TRUNCATED AT 250 WORDS)
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The effects of prazosin, an alpha1/alpha2-adrenergic receptor antagonist, on the production of interleukin (IL)-1beta and IL-10 induced by LPS was studied in mice selected for their paw preference.
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The meta-analysis did not provide details of the data abstraction process. Urinary symptom score was measured using two different tools: the Boyarsky Symptom Index (BSI) and American Urology Association Symptom Index (AUA-SI). The BSI was used in seven studies and AUA-SI in two studies. The authors calculated a common symptom score, based on the common items from both questionnaires, that had all but one item used in the AUA-SI. Questions from AUA-SI are scored on a 0 to 5 scale and those on BSI on a 0 to 3 scale. To adjust for this difference, the authors performed a nonlinear rescaling of the AUA-SI to adjust for these scoring differences.
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(1) In the non-medication period, all the patients with PHEO were characterized by a steep elevation of the arterial pressure and a variability of the high blood pressure events more remarkably than the patients with EHT. The changes in arterial pressure in the patients with PHEO were accompanied by headaches, feelings of fear, trembling, sweating and palpitation. (2) At the medication period, prazosin sufficiently suppressed the sudden elevation of blood pressure. However, the paroxysmal elevation of blood pressure after voiding was not prevented in 2 of 3 patients with ectopic PHEO in the urinary bladder. Urinary and plasma catecholamine (CA) were normal in 2 of our 3 cases. Voiding elevated plasma CA which provided better diagnostic determinant in patients with this bladder tumor as well as the CDPR. (3) The CDPR provided good operative removal results through the 24-hour monitoring, and the recovery was uneventful.
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Prepulse inhibition (PPI) of the acoustic startle response is an operational measure of sensorimotor gating that can be assessed in both humans and animals. The noradrenergic system appears to play a role in PPI as the alpha1 agonist cirazoline disrupts PPI and the alpha1 antagonist prazosin blocks the disruptions in PPI produced by phencyclidine.
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Urinary retention is the most common complication after anorectal surgery, with rates as high as 52 percent reported. With the trend toward early discharge, avoidance of this complication is particularly important. Perioperative fluid restriction and the use of short-acting anesthetics have been shown to be effective in decreasing postoperative urinary retention rates but are not applicable in all cases. Reflex sympathetic stimulation, possibly as a result of perianal pain, may lead to increased muscular tone of the internal sphincter at the bladder neck. This theory had led to the effective use of alpha-adrenergic blockade in the treatment of established cases of urinary retention after anorectal surgery, herniorrhaphy, and major pelvic surgery. However, the prophylactic role of alpha blockade after anorectal surgery has not been studied. In a double-blind, prospective, randomized study, 51 patients were treated with either prazosin and alpha-adrenergic blocker or placebo prior to and immediately after elective anorectal surgery. Urinary retention rates were similar in the two groups. At this time, prophylactic alpha-adrenergic blockade is not recommended for the prevention of urinary retention after anorectal surgery.