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Norman Dublin - One of the best experts on this subject based on the ideXlab platform.
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anticholinergic drugs versus other medications for overactive bladder syndrome in adults
Cochrane Database of Systematic Reviews, 2007Co-Authors: Campbell S D Roxburgh, Jonathan A Cook, Norman DublinAbstract:Background Overactive bladder syndrome is defined as "urgency with or without urge incontinence, usually with frequency and nocturia". It is a common condition with significant economic and quality of life implications. While the condition's pathophysiology remains to be fully elucidated, pharmacotherapy is the main treatment option. Despite uncertainty as to drug treatment of choice, anticholinergics are increasingly being used in primary and secondary care settings. This review compares anticholinergic drugs with other types or classes of drugs for treating overactive bladder syndromes. Objectives To compare anticholinergic drugs with other types or classes of drugs for treating overactive bladder symptoms. Search strategy We searched the Cochrane Incontinence Group Specialised Trials Register (searched 20 December 2006) and the reference lists of relevant articles. No language or other limits were imposed. Selection criteria All randomised and quasi-randomised controlled trials comparing anticholinergic drugs with other drugs for the treatment of overactive bladder symptoms. At least one arm of the study used an anticholinergic drug and at least one other arm used a non-anticholinergic drug. Data collection and analysis Two reviewers assessed the identified studies for eligibility and methodological quality and independently extracted data from the included studies. Data analysis was performed using RevMan software (version 4.2.8). Main results Twelve trials were included in the review. There were seven crossover trials and five parallel group studies. For the comparisons between anticholinergic drugs with tricyclic antidepressants, alpha adrenergic Agonists, afferent nerve inhibitors, and calcium channel blocker a single trial was identified for each. Nine trials compared flavoxate with anticholinergics. There was no evidence of a difference in cure rates between anticholinergics and flavoxate. Adverse effects were more frequent in anticholinergic groups versus flavoxate groups (RR 2.28 95% CI 1.45 to 3.56). There was no strong evidence to favour either anticholinergic drugs or the comparators. Authors' conclusions Many of the drugs considered in trials in this review are no longer used in clinical practice (and this includes the most commonly tested - flavoxate). There is inadequate evidence as to determine whether any of the available drugs are better or worse than anticholinergic medications. Larger randomised controlled trials in clinical settings are required to further establish the role of these medications in the management of overactive bladder syndrome.
R G Victor - One of the best experts on this subject based on the ideXlab platform.
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inhibition of alpha 2 adrenergic vasoconstriction during contraction of glycolytic not oxidative rat hindlimb muscle
American Journal of Physiology-heart and Circulatory Physiology, 1994Co-Authors: Gail D Thomas, J Hansen, R G VictorAbstract:Previous studies have produced conflicting evidence as to whether sympathetic vasoconstriction is impaired in active skeletal muscle. Because alpha 2-, not alpha 1-, adrenergic vasoconstriction is attenuated by mild acidosis, we hypothesized that alpha 2-mediated sympathetic vasoconstriction would be attenuated in contracting glycolytic muscle, which produces more acidosis than oxidative muscle. We compared effects of lumbar sympathetic nerve stimulation and Alpha-Adrenergic Agonists on arterial pressure, femoral blood flow, and force output during contractions of oxidative or glycolytic muscles in anesthetized rats. We found that 1) sympathetic vasoconstriction was preserved during contractions of oxidative soleus muscle and during low-intensity contractions of glycolytic gastrocnemiusplantaris muscles but was abolished during maximal contractions of these glycolytic muscles; 2) this sympatholytic effect was caused by impaired alpha 2-, not alpha 1-, vasoconstriction; and 3) the increased muscle blood flow resulting from a combination of impaired vasconstriction and increased arterial pressure was paralleled by increased force of gastrocnemius-plantaris muscle contraction. Thus contraction-induced impairment of alpha 2-vasoconstriction can augment muscle blood flow and muscle contraction, but the degree of impairment depends on fiber type and intensity of muscle contraction.
Campbell S D Roxburgh - One of the best experts on this subject based on the ideXlab platform.
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anticholinergic drugs versus other medications for overactive bladder syndrome in adults
Cochrane Database of Systematic Reviews, 2007Co-Authors: Campbell S D Roxburgh, Jonathan A Cook, Norman DublinAbstract:Background Overactive bladder syndrome is defined as "urgency with or without urge incontinence, usually with frequency and nocturia". It is a common condition with significant economic and quality of life implications. While the condition's pathophysiology remains to be fully elucidated, pharmacotherapy is the main treatment option. Despite uncertainty as to drug treatment of choice, anticholinergics are increasingly being used in primary and secondary care settings. This review compares anticholinergic drugs with other types or classes of drugs for treating overactive bladder syndromes. Objectives To compare anticholinergic drugs with other types or classes of drugs for treating overactive bladder symptoms. Search strategy We searched the Cochrane Incontinence Group Specialised Trials Register (searched 20 December 2006) and the reference lists of relevant articles. No language or other limits were imposed. Selection criteria All randomised and quasi-randomised controlled trials comparing anticholinergic drugs with other drugs for the treatment of overactive bladder symptoms. At least one arm of the study used an anticholinergic drug and at least one other arm used a non-anticholinergic drug. Data collection and analysis Two reviewers assessed the identified studies for eligibility and methodological quality and independently extracted data from the included studies. Data analysis was performed using RevMan software (version 4.2.8). Main results Twelve trials were included in the review. There were seven crossover trials and five parallel group studies. For the comparisons between anticholinergic drugs with tricyclic antidepressants, alpha adrenergic Agonists, afferent nerve inhibitors, and calcium channel blocker a single trial was identified for each. Nine trials compared flavoxate with anticholinergics. There was no evidence of a difference in cure rates between anticholinergics and flavoxate. Adverse effects were more frequent in anticholinergic groups versus flavoxate groups (RR 2.28 95% CI 1.45 to 3.56). There was no strong evidence to favour either anticholinergic drugs or the comparators. Authors' conclusions Many of the drugs considered in trials in this review are no longer used in clinical practice (and this includes the most commonly tested - flavoxate). There is inadequate evidence as to determine whether any of the available drugs are better or worse than anticholinergic medications. Larger randomised controlled trials in clinical settings are required to further establish the role of these medications in the management of overactive bladder syndrome.
Jose Antunesrodrigues - One of the best experts on this subject based on the ideXlab platform.
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alpha adrenergic Agonists inhibit the dipsogenic effect of angiotensin ii by their stimulation of atrial natriuretic peptide release
Brain Research, 2001Co-Authors: Rosemary Bastos, A L Favaretto, Jolanta Gutkowska, Samuel M Mccann, Jose AntunesrodriguesAbstract:Angiotensin II (ANG-II) and atrial natriuretic peptide (ANP) have opposing actions on water and salt intake and excretion. Within the brain ANP inhibits drinking induced by ANG-II and blocks dehydration-induced drinking known to be caused by release of ANG-II. Alpha-Adrenergic Agonists are known to release ANP and antagonize ANG II-induced drinking. We examined the hypothesis that α Agonists block ANG-II-induced drinking by stimulating the release of ANP from ANP-secreting neurons (ANPergic neurons) within the brain that inhibit the effector neurons stimulated by ANG-II to induce drinking. Injection of ANG-II (12.5 ng) into the anteroventral region of the third ventricle (AV3V) at the effective dose to increase water intake increased plasma ANP concentrations (P<0.01) within 5 min. As described before, previous injection of phenylephrine (an α1-adrenergic agonist) or clonidine (an α2-adrenergic agonist) into the AV3V region significantly reduced ANG-II-induced water intake. Their injection also induced a significant increase in plasma ANP concentration and in ANP content in the olfactory bulb (OB), AV3V, medial basal hypothalamus (MBH) and median eminence (ME). These results suggest that the inhibitory effect of both α-adrenergic Agonists on ANG-II-induced water intake can be explained, at least in part, by the increase in ANP content and presumed release from these neural structures. The increased release of ANP from the axons of neurons terminating on the effector neurons of the drinking response by stimulation of ANP receptors would inhibit the stimulatory response evoked by the action of ANG-II on its receptors on these same effector neurons.
Edit Tothmolnar - One of the best experts on this subject based on the ideXlab platform.
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alpha adrenergic Agonists stimulate fluid secretion in lacrimal gland ducts
Investigative Ophthalmology & Visual Science, 2020Co-Authors: Dora Szarka, Greta Elekes, Orsolya Berczeli, Eszter Vizvari, L Szalay, Chuanqing Ding, Laszlo Talosi, Edit TothmolnarAbstract:Purpose The role of adrenergic innervation in the regulation of lacrimal gland (LG) ductal fluid secretion is unknown. The Aim of the present study was to investigate the effect of adrenergic stimulation on fluid secretion in isolated LG duct segments and to study the underlying intracellular mechanisms. Methods Fluid secretion of isolated mouse LG ducts was measured using video-microscopy. Effect of various adrenergic Agonists (norepinephrine, phenylephrine, and isoproterenol) on fluid secretion as well as inhibitory effects of specific antAgonists on adrenergic agonist-stimulated secretory response were analyzed. Changes in intracellular Ca2+ level [Ca2+i] were investigated with microfluorometry. Results Both norepinephrine and phenylephrine initiated a rapid and robust fluid secretory response, whereas isoproterenol did not cause any secretion. Phenylephrine-induced secretion was completely blocked by α1D-adrenergic receptor blocker BMY-7378. The endothelial nitric oxide synthase (eNOS) inhibitor L-NAME or guanylyl cyclase inhibitor ODQ reduced but not completely abolished the phenylephrine-induced fluid secretion, whereas co-administration of Ca2+-chelator BAPTA-AM resulted in a complete blockade. Phenylephrine stimulation induced a small, but statistically significant elevation in [\(Ca_i^{2 + }\)]. Conclusions Our results prove the direct role of α1-adrenergic stimulation on LG ductal fluid secretion. Lack of isoproterenol-induced fluid secretory response suggests the absence of β-receptor mediated pathway in mouse LG ducts. Complete blockade of phenylephrine-induced fluid secretion by BMY-7378 and predominant inhibition of the secretory response either by L-NAME or ODQ suggest that α-adrenergic Agonists use the NO/cGMP pathway through α1D receptor. Ca2+ signaling independent from NO/cGMP pathway may also play an at least partial role in α-adrenergic induced ductal fluid secretion.