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These results suggest that olanzapine might be efficacious for essential tremor. Further clinical trials are indicated to establish the efficacy of olanzapine in patients with ET.
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According to this systematic literature review, postmenopausal vasomotor treatments that have been shown to be safe and effective in short-term use include black cohosh, exercise, gabapentin, medroxyprogesterone acetate, SSRIs (ie, paroxetine hydrochloride), and soy protein. Initial, small reports are suggestive for efficacy in menopausal vasomotor symptoms with megestrol acetate and venlafaxine.
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We have evaluated the effect of the vanilloid receptor agonists resiniferatoxin (RTX), capsaicin and piperine and of the vanilloid receptor antagonist capsazepine on the resting tone in the isolated rat ileum. Capsazepine (10(-8)-3 x 10(-5) M) produced a concentration-related relaxation (8 +/-3%-49 +/-3%) of the rat ileum. By contrast RTX (up to 10(-8) M), capsaicin (up to 10(-6) M) and piperine (up to 10(-5) M) were without effect. Pre-treatment with capsaicin [either in vivo (50 mg/kg s.c.) or in vitro (10(-6) M)] did not modify the inhibitory effect of capsazepine. The L-type Ca2+ channel antagonist nifedipine (10(-6) M), but not the N-type Ca2+ channel antagonist omega-conotoxin GVIA (3 x 10(-8) M) nor the Na+ channel blocker tetrodotoxin (3 x 10(-7) M), counteracted the inhibitory effect of capsazepine. The NK1 receptor antagonist SR 140333 (10(-7) M), the NK2 receptor antagonist SR 48968 (10(-6) M), the NK3 receptor antagonist SR 142801 (10(-7) M), atropine (10(-6) M), hexamethonium (10(-4) M), phentolamine (10(-6) M) plus propranolol (10(-6) M), N(G)-nitro- L-arginine methyl ester ( L-NAME 3 x 10(-4) M), apamin (10(-7) M), methysergide (10(-6) M), the calcitonin gene-related peptide (CGRP) antagonist hCGRP 8-37 (1.5 x 10(-6) M), the VIP antagonist hGRF 1-29 (10(-5) M) did not modify the inhibitory effect of capsazepine. Capsazepine (2.5-40 mg/kg) also decreased upper gastrointestinal transit in vivo. It is concluded that the vanilloid antagonist capsazepine has a direct relaxing effect on rat intestinal smooth muscle which could involve L-type calcium channels. We found no evidence to suggest that capsazepine is antagonizing an endogenous vanilloid.
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The aim of the present study was to investigate the in vitro effects of the short-acting beta2-adrenoceptor agonist salbutamol and the long-acting beta2-adrenoceptor agonist salmeterol on hypoxia-induced rat diaphragm force reduction. In vitro diaphragm twitch force (Pt) and maximal tetanic force (Po) of isolated diaphragm muscle strips were measured for 90 min during hyperoxia (tissue bath PO2 83.8 +/- 0.9 kPa and PCO2 3.9 +/- 0.1 kPa) or severe hypoxia (PO2 7.1 +/- 0.3 kPa and PCO2 3.9 +/- 0.1 kPa) in the presence and absence of 1 microM salbutamol or 1 microM salmeterol. During hyperoxia, salbutamol and salmeterol did not significantly alter the time-related decreases in Pt and Po (to approximately 50% of initial values). Salbutamol had no effects on Po or the Pt-to-Po ratio. Salmeterol treatment significantly reduced Po and increased the Pt-to-Po ratio during hyperoxia (P < 0.05 compared with control value). Hypoxia resulted in a severe decrease in Pt (to approximately 30% of initial value) and Po after 90 min. Both salbutamol and salmeterol significantly reduced the decline in Pt during hypoxia (P < 0.05). The reduction in Po was not prevented. Salbutamol increased Pt rapidly but transiently. Salmeterol had a delayed onset of effect and a longer duration of action. Addition of 1 microM propranolol (a nonselective beta-adrenoceptor antagonist) did not alter Pt, Po, or the Pt-to-Po ratio during hypoxia but completely blocked the inotropic effects of salbutamol and salmeterol, indicating that these effects are dependent on beta2-adrenoceptor agonist-related processes.
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Participating centres entered data on all of their patients who had completed treatment with oral propranolol for IHs, using an online data capture tool.
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Adrenergic control of cardiovascular function is a common component of regulation in embryonic birds studied to date. Our goal was to investigate adrenergic and cholinergic cardiovascular regulation in two goose species, the Canada goose (Branta canadensis) and the related domestic goose (Anser anser domesticus) to determine if these species possess similar regulation during embryonic development. We determined mean arterial pressure (Pm) and heart rate (fH) responses to serial blockade of cholinergic, β-adrenergic and α-adrenergic receptors in B. canadensis and A. domesticus at 70 and 90% of total incubation (28days). Both species possessed cholinergic and β-adrenergic tone on fH at 70% of incubation that increased in intensity with development. In addition, a constant α-adrenergic tone on Pm was present in both species. Our findings indicate that these geese species possess both cholinergic and adrenergic cardiovascular regulation providing information needed for speculation regarding the commonalities in the ontogeny of these cardiovascular regulatory elements in birds.
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A literature search of Ovid, Embase, the Cochrane database, Google™ Scholar, and Medline using PubMed as the search engine was performed to identify studies that analysed the effect of propranolol treatment in children with airway haemangiomas. Random-effect meta-analytical techniques were conducted for the outcome measures.
In young children with unintentional, single drug exposure to the most popular antihypertensive medication (i.e., metoprolol, bisoprolol, ramipril, enalapril, lisinopril, captopril, candesartan, valsartan, amlodipine, and verapamil), only mild symptoms occurred, and hospital evaluation is not a must. However, children with recent exposure to clonidine or moxonidine should be evaluated at a hospital due to an increased likelihood of poisonings of at least moderate severity.
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Tongue tremor is commonly associated with essential tremor, but rarely presents as an initial finding. Essential tremor is the most common movement disorder and is characterised by 4-12 Hz postural and kinetic tremor, but there is no universally accepted diagnostic criterion. It commonly affects the arms, and to a lesser extent, other regions of the body, and signs and symptoms tend to worsen during emotional or physiological stress. We describe a rare isolated presentation of tongue tremor as a part of essential tremor, its management, and the diagnostic dilemma. To our knowledge isolated tongue tremor as a presentation of essential tremor has not previously been described in maxillofacial publications.
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Recent controversial publications, citing studies purporting to show that P-gp mediates the transport of propranolol, proposed that passive biological membrane transport is negligible. Based on the BDDCS, the extensively metabolized-highly permeable-highly soluble BDDCS class 1 drug, propranolol, shows a high passive permeability at concentrations unrestricted by solubility that can overwhelm any potential transporter effects. Here we reinvestigate the effects of passive diffusion and carrier-mediated transport on S-propranolol.
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Changes in maternal catecholamines that accompany the onset of labor analgesia include a decrease in epinephrine (EPI) but no change in norepinephrine (NE). Because EPI exerts predominantly beta-adrenergic, and NE predominantly alpha-adrenergic effects in circulating concentrations, we hypothesized that these changes could lead to uterine arteriole vasoconstriction.
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Basic autonomic nervous function was evaluated in patients with neurocardiogenic syncope (NCS). Atropine, isoproterenol, propranolol, phenylephrine, and phentolamine were administered successively, and parasympathetic nerve activity and beta- (and alpha-) activity, sensitivity, and secretion of the sympathetic nerve were determined in patients with NCS and control subjects. In patients with NCS, beta- and alpha- sensitivity were higher and beta-activity and beta- and alpha-secretion lower than in control subjects. In patients with NCS, the increased basic beta-sensitivity may contribute to induce strong cardiac contractions and augment ventricular mechanoreceptor response, and a compensatory state against diminished neuronal sympathetic activity is suggested by the increased alpha-sensitivity.
β-Adrenergic signaling could contribute to initiation and progression of breast cancer. This research investigated some potential mechanisms of propranolol in amelioration of progression and survival in breast cancer.
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beta-adrenoceptor-mediated relaxation was investigated in ring preparations of rat isolated thoracic aorta. Rings were pre-constricted with a sub-maximal concentration of noradrenaline (1 microM) and relaxant responses to cumulative concentrations of beta-adrenoceptor agonists obtained. The concentration-response curve (CRC) to isoprenaline was shifted to the right by propranolol (0.3 microM) with a steepening of the slope. Estimation of the magnitude of the shift from EC(50) values gave a pA(2) of 7.6. Selective beta(1)- and beta(2)-adrenoceptor antagonists, CGP 20712A (0.1 microM) and ICI 118551 (0.1 microM), respectively, produced 4 and 14 fold shifts of the isoprenaline CRC. Atypical beta-adrenoceptor agonists also produced concentration-dependent relaxation of aortic rings. The order of potency of the beta-adrenoceptor agonists was (-log EC(50)): isoprenaline (6. 25)>cyanopindolol (5.59)>isoprenaline+propranolol (5.11)>CGP 12177A (4.40)>ZD 2079 (4.24)>ZM 215001 (4.07)>BRL 37344 (3.89). Relaxation to CGP 12177A and ZM 215001 was unaffected by propranolol (0.3 microM). SR 59230A (=1 microM) and cyanopindolol (1 microM), beta(3)-adrenoceptor antagonists, had no effect on the isoprenaline (in the presence of propranolol) or CGP 12177A CRCs. Bupranolol and CGP 20712A, at microM concentrations (beta(4)-adrenceptor antagonists), inhibited responses to isoprenaline (in the presence of propranolol) and CGP 12177A. In conclusion, atypical beta-adrenoceptors co-exist with beta(1)- and beta(2)-adrenoceptors in rat aorta. Although non-conventional partial agonists and selective beta(3)-adrenoceptor agonist cause relaxation, the vascular atypical beta-adrenoceptor does not appear to correspond to the beta(3)-adrenoceptor. There are, however, similarities with the putative beta(4)-adrenoceptor.
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The neurotransmitter dopamine (DA) at a 10 microM concentration elicited a stimulation of intracellular cyclic AMP (cAMP) accumulation in cultured astrocytes derived from embryonic rat striatum. This accumulation was partially blocked by the beta-adrenergic receptors antagonist propranolol, mimicked by the D(1) agonist SKF 38393 and by the mixed D(1)/D(2) agonist apomorphine. A regional heterogeneity in the magnitude of dopamine-induced cAMP accumulation was observed in cultured astrocytes obtained from different brain areas. The maximum effect was observed in striatal astrocytes, a lower effect in cortical astrocytes, and no increase was detected in cerebellar astrocytes. Reverse transcription-polymerase chain reaction (RT-PCR) coupled to Southern blot hybridization demonstrated that striatal astrocytes express only D(1) receptor mRNA and Western blot analysis confirmed the expression of the D(1) receptor protein in striatal astrocytes. In contrast to what found in neurons, the D(1)-dependent cAMP formation in striatal astrocytes is partially reduced by pertussis toxin (PTX) treatment. The stimulation of D(1) receptors or the activation of adenylyl cyclase by forskolin led to an increase of cytosolic and nuclear protein kinase A (PKA) catalytic activity. The presence of dopamine D(1) receptors in cultured striatal astrocytes suggests a role of dopamine in the regulation of cellular processes in striatal astrocytes.
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We searched for compounds that are pharmacologically active on ureteral motility for treating ureteral colic to ease retrograde access into the ureter and improve the clearance of stones or stone particles from the ureter. The effects of the alpha1-adrenergic receptor agonist phenylephrine, the nonselective beta and beta2-adrenergic receptor agonists isoproterenol and fenoterol, and the phosphodiesterase inhibitors papaverine (nonspecific) and rolipram (type IV) on the frequency and amplitude of ureteral contractions when administered intravenously or topically were investigated in pigs.