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Volume 121 (2003)
- Issue 6 Pages 377-
- Issue 5 Pages 290-
- Issue 4 Pages 203-
- Issue 3 Pages 143-
- Issue 2 Pages 85-
- Issue 1 Pages 4-
Volume 121, Issue 5
Displaying 1-9 of 9 articles from this issue
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Reviews:Current Progress in Studies on Lower Urinary Tract Function: From the Standpoint of Basic and Clinical Medicine
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Naoki YOSHIMURAArticle type: Reviews
2003 Volume 121 Issue 5 Pages 290-298
Published: 2003
Released on J-STAGE: April 26, 2003
JOURNAL FREE ACCESSThe functions of the lower urinary tract, to store and periodically release urine, are dependent on the activity of smooth and striated muscles in the bladder, urethra, and external urethral sphincter. This activity is in turn controlled by neural circuits in the brain, spinal cord, and peripheral ganglia. During urine storage, the outlet is closed and the bladder smooth muscle is quiescent. When bladder volume reaches the micturition threshold, activation of a micturition center in the dorsolateral pons (the pontine micturition center) induces a bladder contraction and a reciprocal relaxation of the urethra, leading to bladder emptying. During voiding, sacral parasympathetic (pelvic) nerves provide an excitatory input (cholinergic and purinergic) to the bladder and inhibitory input (nitrergic) to the urethra. The brain rostral to the pons (diencephalon and cerebral cortex) is also involved in excitatory and inhibitory regulation of the micturition reflex. Various transmitters including dopamine, serotonin, norepinephrine, GABA, excitatory and inhibitory amino acids, opioids, acetylcholine, and neuropeptides are implicated in the modulation of the micturition reflex in the central nervous system. Therefore, injury or diseases of the nervous system, as well as drugs and disorders of the peripheral organs, can produce bladder and urethral dysfunctions such as urinary frequency, urgency and incontinence, or inefficient bladder emptying.
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- mainly on inhibitory NANC nerves-Yojiro UKAI, Kumiko NODA, Noboru TODAArticle type: Reviews
2003 Volume 121 Issue 5 Pages 299-306
Published: 2003
Released on J-STAGE: April 26, 2003
JOURNAL FREE ACCESSThis article describes current information concerning analyses of contraction and relaxation associated with electrical stimulation of efferent nerves in isolated mammalian sphincter muscles. Contractile responses of sphincters are mediated by α1-adrenoceptors and muscarinic receptors stimulated by transmitters from adrenergic and cholinergic nerves, respectively, whereas those of the bladder body are almost exclusively mediated by transmitters from parasympathetic nerves. Relaxant responses to nerve stimulation are ascribed mainly to mechanisms that are sensitive and resistant to nitric oxide (NO) synthase inhibitors. Neurogenic calcitonin gene-related peptide and β-adrenoceptor activation by neurogenic norepinephrine may also be involved in some mammals. Stimulus frequency is an important determinant to distinguish NO synthase-sensitive and -resistant components; responses at low frequencies are abolished by the enzyme inhibitors, whereas those at high frequencies are inhibited only partially. High and low frequency stimulation increases the cyclic GMP content in muscles, suggesting the involvement of neurogenic NO, although relaxation at high frequencies is only partially due to such a mechanism. From pharmacological studies so far analyzed, including ours performed with porcine urinary tract sphincters, it is concluded that NO synthase resistant-relaxation is not mediated by peptides nor compounds that open K+ channels in muscle cell membrane and stimulate β-adrenoceptors. Contribution of NO and non-NO relaxing factor(s) in relaxant responses varies with animal species. Identification of this factor, determination of intracellular signaling processes and interaction with the NO/cyclic GMP system may give us a clue in developing new therapeutics to treat dysfunctions of the lower urinary tract sphincters.
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Masaki YOSHIDA, Akito INADOME, Shigetaka MURAKAMIArticle type: Reviews
2003 Volume 121 Issue 5 Pages 307-316
Published: 2003
Released on J-STAGE: April 26, 2003
JOURNAL FREE ACCESSLower urinary tract function is controlled by the autonomic nervous system, which consists of adrenergic, cholinergic, and non-adrenergic, non-cholinergic (NANC) neurons. We have measured the amount of various neurotransmitters (acetylcholine, ACh; noradrenaline, NA; adenosine triphosphate, ATP; and nitric oxide, NO) released from human and rabbit urinary tract smooth muscles by the microdialysis method coupled with HPLC. Muscle strips are isolated from human or rabbit bladder, urethra, and prostate. A microdialysis probe was inserted into each smooth muscle strip. Each muscle strip was connected to an isometric transducer, and tension development was measured. We have evaluated the changes in electrical field stimulation-induced neurotransmitter releases and functional responses in physiological and pathological conditions and the interactions between neurotransmitters or neurons. In this review, we present several of our results: 1) interactions between adrenergic and nitrergic neurons in rabbit urethra, 2) effect of NO on human bladder function, 3) effect of NO on human prostate function, and 4) effects of aging on acetylcholine and ATP releases from human bladder smooth muscles. These data may reveal physiological or pathological neurotransmitter control of lower urinary tract function and give us useful information for clinical intervention to treat lower urinary tract symptoms.
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Noriyoshi TERAMOTOArticle type: Reviews
2003 Volume 121 Issue 5 Pages 317-324
Published: 2003
Released on J-STAGE: April 26, 2003
JOURNAL FREE ACCESSIt is a common sequelae of bladder outlet obstruction caused by benign prostatic hyperplasia in adult males and gives rise to significant bladder dysfunction such as frequency and urgency of micturition. The unstable detrusor contractions may lead to urge incontinence. Since it has been reported that experimentally-induced bladder instability can be abolished by ATP-sensitive K+ channel (KATP channel) openers, various types of detrusor-selective KATP channels have been newly synthesized, targeting KATP channels in urinary bladder. Thus, the significant differences in molecular and pharmacological properties of KATP channels between urinary bladder and urethra hold out some hope for the development of tissue-selective KATP channel openers for urge urinary incontinence, and detrusor-selective KATP channel openers should be screened against urethral as well as vascular smooth muscle. In functional expression experiments, pharmacological and electrophysiological studies have reported that SUR1/Kir6.2 represents the pancreatic β-cell KATP channel and that SUR2A/Kir6.2 is thought to represent the cardiac KATP channel, whereas SUR2B/Kir6.1 represents the smooth muscle-type KATP channel. In general, the smooth muscle type-KATP channel is (i) of a relatively small conductance (about 20 pS under quasi-physiological conditions, approximately 40 pS in symmetrical 140 mM K+ conditions), (ii) intracellular Ca2+-insensitive, (iii) inhibited by intracellular ATP, (iv) abolished by glibenclamide at a submicromolar concentration, and (v) reactivated by intracellular nucleoside diphosphates (NDPs). There has been no report concerning the properties of KATP channels in human detrusor by use of single-channel recordings. We would like to introduce our recent evidence of novel synthesized detrusor-selective KATP channel openers and properties of KATP channels in the lower urinary tract.
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Masayuki TAKEDA, Isao ARAKIArticle type: Reviews
2003 Volume 121 Issue 5 Pages 325-330
Published: 2003
Released on J-STAGE: April 26, 2003
JOURNAL FREE ACCESSAdrenergic alpha1 and beta receptors are present in the target organs of sympathetic nerve and they participate in the signal transduction mechanism of the lower urinary tract. Adrenergic alpha1 receptors are present in urethral and prostatic smooth muscles, and contract these muscles. Among these receptor subtypes, the alpha1-A receptor has the most important role, and mRNA expression of the corresponding alpha1-a subtype is predominant. In the human urinary bladder detrusor smooth muscle, the expression of adrenergic beta3 receptor subtype mRNA is predominant, and relaxation of detrusor smooth muscle is mediated mainly via beta3 receptor. Afferent nerve with lower threshold can easily transmit bladder sensation and takes an important role in the pathophysiology of urge urinary incontinence. Successful molecular cloning of vanilloid receptors, which are present in these afferent nerves, revealed that vanilloid receptors are ion-channels, sensitive for heat and pH, and termed VR1 and VRL1. Among purinergic receptors, ion channel type P2X3 receptor is found in afferent nerve fibers and plays some roles in the signal transduction of bladder sensation. In the near future, agonist for the adrenergic beta3 receptor and selective antagonists for VR1, VRL1, or P2X3 will possibly become drugs for pollakisuria and urge urinary incontinence.
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Osamu YAMAGUCHIArticle type: Reviews
2003 Volume 121 Issue 5 Pages 331-338
Published: 2003
Released on J-STAGE: April 26, 2003
JOURNAL FREE ACCESSThis paper reviews the possible mechanisms underlying bladder overactivity and discusses the targets for pharmacological treatment of this disorder. Damage to the brain (cerebrovascular disease, etc.) induces bladder overactivity by reducing suprapontine inhibition. Currently, attention has focused on C-fiber bladder afferents that may concern the mechanisms for bladder overactivity resulting from various etiologies such as spinal cord lesions, bladder outlet obstruction and bladder hypersensitivity disorders. With regard to the pathophysiology of idiopathic overactive bladder, both myogenic and neurogenic mechanisms may be involved in involuntary detrusor contraction. Since an intravesical capsaicin or resiniferatoxin was shown to have favorable therapeutic effects, afferent C-fiber neurons become a new target for pharmacological treatment. C-fiber neurons are known to contain tachykinins and other peptides as neurotransmitters. When released, tachykinins can influence via NK receptors bladder activity. In addition, evidences suggest that ATP receptors (P2X3) and prostaglandin receptors in afferent C-fiber neurons may play a role in mediating bladder overactivity. Thus, NK-antagonist, P2X3-antagonist and PG receptor-antagonist may be potential therapeutic drugs in the near future. β3-Adrenoceptor agonist is an another candidate drug for the treatment of the overactive bladder. Finally, it is important to notice that in any etiology including an idiopathic one, antimuscarinic drugs can improve bladder overactivity, although dry mouth and constipation are inevitable side- effects.
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Review
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Kouichi TANONAKA, Satoshi TAKEOArticle type: Review
2003 Volume 121 Issue 5 Pages 339-348
Published: 2003
Released on J-STAGE: April 26, 2003
JOURNAL FREE ACCESSAn accumulation of Na+ is induced in the ischemic myocardium, which is so-called “Na+ overload”. The exact role of Na+ overload in the genesis of myocardial ischemia/reperfusion injury remains unclear except for the role as a driving force of Ca2+ overload in the reperfused myocardium. Excessive activation of Na+/H+ exchanger (NHE) and Na+ channels may contribute to Na+ influx into the ischemic myocardium, resulting in sodium overload under ischemic conditions. A decrease in energy-producing ability of mitochondria in the ischemic myocardium is also observed in an ischemic duration-dependent manner. Attenuation of Na+ overload by an NHE inhibitor or a Na+ channel blocker preserved mitochondrial energy production in the ischemic myocardium and enhanced post-ischemic contractile recovery. To mimic Na+ overload in the ischemic myocardium, isolated mitochondria were incubated with sodium lactate, a possible end product of anaerobic glycolysis. Sodium lactate induced an irreversible reduction in the mitochondrial energy production. The mitochondrial damage induced by sodium lactate was not attenuated by the NHE inhibitor or the Na+ channel blocker, suggesting that these agents may indirectly preserve mitochondrial function in the ischemic myocardium. Taken together, Na+ overload in the ischemic myocardium may induce mitochondrial dysfunction, leading to contractile failure of the reperfused myocardium.
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Technical Note
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Keiichi TORIMITSU, Yuriko FURUKAWA, Nahoko KASAIArticle type: Technical Note
2003 Volume 121 Issue 5 Pages 349-356
Published: 2003
Released on J-STAGE: April 26, 2003
JOURNAL FREE ACCESSNeurotransmitters have been well known as information carriers for a long time. Recently, some of the research indicated their neurotoxicity, while some indicated their neurotrophic actions. It is very important to understand the role of neurotransmitters. Glutamate is one of the most important excitatory neurotransmitter in the brain. We developed a novel measurement method for glutamate. The method we describe here is based on the enzyme-mediated electrochemical detection. Glutamate oxidase and horseradish peroxidase were deposited together with polymer-mediator on the electrode. We applied this idea on ITO multi-array electrode and developed a 64 channel multi-array sensor. The sensor permits us to detect glutamate release from multiple regions simultaneously in real time. As it is possible to illustrate the distribution of glutamate release, the sensor could be used not only in the pharmacological field, but also in medical treatment in the near future.
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Takeshi NAKAMURAArticle type: Technical Note
2003 Volume 121 Issue 5 Pages 357-364
Published: 2003
Released on J-STAGE: April 26, 2003
JOURNAL FREE ACCESSIn addition to the multiple mechanisms of the intracellular calcium mobilizing pathways, neurons possess multiple functional compartments such as the soma, the axon, the dendrites, and the spines. In this article, technical procedures and tips are described to measure local calcium signaling in response to neuronal excitation in single neurons.
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