scholarly journals Systematic review of overactive bladder therapy in females

2013 ◽  
Vol 5 (5-S2) ◽  
pp. 139
Author(s):  
Linda Cardozo
Keyword(s):  
Overactive Bladder ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Beta Agonists ◽  
Bladder Retraining ◽  
Neurokinin Receptor ◽  
Calcium Channel Blocking Agents ◽  
Channel Blocking ◽  
Alternative Routes ◽  
Vasopressin Analogues

Although the prevalence of overactive bladder (OAB) is similarin both male and female populations, females have a greater tendencyto seek medical advice regarding their symptoms. A reviewof the evidence of therapy among women shows that a variety ofmodalities has been shown to be effective for symptom improvementin women with OAB. Bladder retraining/re-education shouldbe considered for all women with OAB. With respect to first-linepharmacotherapy with antimuscarinic agents, the development ofextended release preparations, bladder selective M3 antagonistsand alternative routes of delivery, have improved compliance andpersistence. Other pharmacotherapeutic options with potential forproviding benefit include antidepressants, vasopressin analogues,alpha-adrenoceptor antagonists and beta-adrenoceptor agonists.There are also a number of newer agents currently being investigated,including calcium channel blocking agents, potassium channelopening drugs, beta agonists and neurokinin receptor antagonists.Intravesical injections of botulinum toxin may be an alternative,while surgery can be considered for truly intractable cases.

scholarly journals Comparative Pharmacodynamics of Eight Calcium Channel Blocking Agents in Japanese Essential Hypertensive Patients.

1996 ◽  
Vol 19 (3) ◽  
pp. 430-437 ◽  
Author(s):  
Shuji SHIMADA ◽  
Yukiko NAKAJIMA ◽  
Koujirou YAMAMOTO ◽  
Yasufumi SAWADA ◽  
Tatsuji IGA
Keyword(s):  
Calcium Channel ◽  
Hypertensive Patients ◽  
Blocking Agents ◽  
Calcium Channel Blocking Agents ◽  
Channel Blocking

scholarly journals Pathogenesis of Arterial Lesions Induced by Dopaminergic Compounds in the Rat

1989 ◽  
Vol 17 (1_part_2) ◽  
pp. 203-213 ◽  
Author(s):  
William D. Kerns ◽  
Emanuel Arena ◽  
Richard A. Macia ◽  
Peter J. Bugelski ◽  
William D. Matthews ◽  
...  
Keyword(s):  
Arterial Injury ◽  
Mesenteric Arteries ◽  
Receptor Subtypes ◽  
Alpha Adrenoceptors ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Alpha Adrenoceptor Agonists ◽  
Arterial Lesions ◽  
Vascular Beds ◽  
Renal Vascular

Fenoldopam mesylate (FM), a selective post-junctional dopaminergic (DA1) vasodilator, causes lesions of large caliber splanchnic arteries (100–800 μm) in the rat characterized by necrosis of medial smooth muscle cells and hemorrhage. FM does not induce lesions in other vascular beds of the rat, or in dogs or monkeys. Dopamine, like FM, causes hemorrhagic lesions of large caliber splanchnic arteries in the rat, as well as fibrinoid necrosis of small caliber arteries (<100 μm) of the splanchnic, cerebral, coronary and renal vascular beds. Dopamine is an alpha- and beta-adrenoceptor and a dopaminergic receptor agonist. Because these arterial lesions are thought to result from the pharmacologic activity of these 2 compounds, we sought to ascertain the presence of DA1 receptors in mesenteric arteries of the rat and to determine the role of these or other vascular receptor subtypes in lesion induction. We also studied the process of repair after arterial injury caused by FM or dopamine. The presence of DA1 receptors was confirmed in isolated perfused mesenteric arteries by standard pharmacologic techniques; stimulation by FM resulted in vasodilation which was inhibited by the DA1 receptor antagonist SK&F 83566-C. Likewise, SK&F 83566-C prevented the induction of hemorrhagic lesions of large caliber arteries in rats upon infusion of FM or dopamine. In rats co-exposed to the alpha-adrenoreceptor antagonist phenoxybenzamine (PBZ) and either FM or dopamine, the incidence and severity of hemorrhagic lesions of large caliber arteries were increased, but PBZ prevented the formation of dopamine-induced fibrinoid lesions in arteries of small caliber. Rats exposed concurrently to dopamine, phenoxybenzamine, and SK&F 83566-C were free of all arterial lesions. Thus, the induction of splanchnic arterial lesions in the rat by dopamine and FM is caused by stimulation of, and interaction between, alpha-adrenoceptors and dopaminergic DA1 receptors. Fibrinoid lesions of small arteries (alpha-adrenoceptor-mediated) were repaired, as observed morphologically by 14 d after exposure to dopamine. Hemorrhagic lesions of large caliber arteries (DA1 receptor-mediated) had undergone significant repair by 28 d after exposure to FM but these arteries possessed a thicker media surrounded by adventitial fibrosis. Thus, morphologically distinct receptor-mediated splanchnic arterial lesions induced by dopaminergic and alpha-adrenoceptor agonists follow a markedly different course of repair. Arterial lesions induced by FM or dopamine by activation of post-junctional dopaminergic DA1 receptors may represent a model of polyarteritis nodosa.

Effect of epinephrine and norepinephrine on zinc thionein levels and induction in rat liver

1984 ◽  
Vol 247 (3) ◽  
pp. E318-E322 ◽  
Author(s):  
F. O. Brady ◽  
B. Helvig
Keyword(s):  
Protein Synthesis ◽  
Stress Response ◽  
De Novo ◽  
Zinc Metabolism ◽  
Multiple Injections ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Blocker ◽  
Glucocorticoid Induction ◽  
De Novo Protein Synthesis

Hepatic zinc metallothionein (MT) levels are increased in response to a variety of stresses. Glucocorticoid induction of zinc thionein is insufficient in accounting for the levels attained. The potential involvement of catecholamines in the modulation of rat hepatic zinc metabolism and zinc thionein levels has been systematically studied. Eleven hours after multiple injections (6) of epinephrine, norepinephrine, or isoproterenol, zinc thionein levels of 4.01 +/- 0.74, 6.83 +/- 0.67, and 11.75 +/- 0.96 micrograms Zn in MT/g liver, respectively, were attained (untreated, 1.04 +/- 0.14). The levels of hepatic zinc thionein thus reached the range of stress response-induced levels (4–10 micrograms Zn in MT/g liver), attained 11 h after the onset of the stress. Multiple injections of isoproterenol and norepinephrine induced the formation of isoforms MT-I and MT-II in roughly equal amounts. The alpha-adrenoceptor blocker phentolamine blocked the 11-h increase in norepinephrine-stimulated (6) zinc thionein levels by 88%. The beta-adrenoceptor blocker propranolol blocked the 11-h increase in isoproterenol-stimulated (6) zinc thionein levels by 55%. This inhibition could be increased to 72% by previous administration of both phentolamine and propranolol. Catecholamines stimulated increases in both the zinc and the protein of MT, the latter as assessed by [35S]cysteine incorporation. Both of these increases were blocked by cycloheximide, confirming the requirement for de novo protein synthesis in this induction response.

Adenosine inhibits beta-adrenoceptor but not DBcAMP-induced renin release

1987 ◽  
Vol 252 (1) ◽  
pp. F46-F52 ◽  
Author(s):  
G. Deray ◽  
R. A. Branch ◽  
W. A. Herzer ◽  
A. Ohnishi ◽  
E. K. Jackson
Keyword(s):  
Nerve Stimulation ◽  
Initial Study ◽  
Renin Release ◽  
Base Line ◽  
Renal Nerve ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Renal Nerve Stimulation ◽  
Canine Kidney

The purpose of these studies was to assess the direct effect of adenosine on the renin release response to beta-adrenoceptor activation in vivo in the canine kidney. In an initial study, innervated, intrarenal beta-adrenoceptors were activated selectively via renal nerve stimulation in kidneys in which the alpha-adrenoceptor response to renal nerve stimulation had been blocked with phentolamine. Adenosine, infused directly into the renal artery (10 and 30 micrograms/min), significantly blunted the renin release response to renal nerve stimulation. However, adenosine also caused significant reductions in base-line glomerular filtration rate, sodium excretion rate, and filtration fraction. To eliminate these confounding effects of adenosine on renal function and to prevent changes in norepinephrine release due to prejunctional inhibition by adenosine, we also studied the effect of intrarenal infusions of adenosine on norepinephrine-induced renin release in the nonfiltering, alpha-adrenoceptor-blocked, canine kidney. In this model of beta-adrenoceptor activation, adenosine abolished the renin release response to intrarenal infusions of norepinephrine. In a final series of experiments, the effect of adenosine on the renin response to dibutyryl-adenosine 3',5'-cyclic monophosphate (cAMP) was examined in the nonfiltering, beta-adrenoceptor-blocked, canine kidney. In this model of cAMP-induced renin release, adenosine was ineffective in attenuating the renin release response. These data demonstrate that in vivo adenosine directly inhibits beta-adrenoceptor-mediated renin release by a mechanism that does not involve a reduction in the ability of cAMP to activate intracellular mechanisms leading to renin release.

Calcium Channel Blocking Agents in CHF

1987 ◽  
Vol 21 (4) ◽  
pp. 337-338
Author(s):  
Carolyn M. Dinardo ◽  
Julio R. Lopez
Keyword(s):  
Calcium Channel ◽  
Blocking Agents ◽  
Calcium Channel Blocking Agents ◽  
Channel Blocking
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