Urine storage mechanisms

Vaughan, Christopher W.

doi:10.1016/0301-0082(95)00004-f

Cited by 50 publications

(54 citation statements)

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“…Stimulation of sympathetic nerves has also been shown to have profound effects on NVA 25 , 26 , 62 . Thus, the output of the motor-sensory system appears to be under direct CNS control.…”

Section: “Afferent Noise” and The Concept Of The Peripheral Regulatiomentioning

confidence: 99%

The concept of peripheral modulation of bladder sensation

Eastham

Gillespie

2013

Organogenesis

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It is recognized that, as the bladder fills, there is a corresponding increase in sensation. This awareness of the volume in the bladder is then used in a complex decision making process to determine if there is a need to void. It is also part of everyday experience that, when the bladder is full and sensations strong, these sensations can be suppressed and the desire to void postponed. The obvious explanation for such altered perceptions is that they occur centrally. However, this may not be the only mechanism. There are data to suggest that descending neural influences and local factors might regulate the sensitivity of the systems within the bladder wall generating afferent activity. Specifically, evidence is accumulating to suggest that the motor-sensory system within the bladder wall is influenced in this way. The motor-sensory system, first described over 100 years ago, appears to be a key component in the afferent outflow, the afferent “noise,” generated within the bladder wall. However, the presence and possible importance of this complex system in the generation of bladder sensation has been overlooked in recent years. As the bladder fills the motor activity increases, driven by cholinergic inputs and modulated, possibly, by sympathetic inputs. In this way information on bladder volume can be transmitted to the CNS. It can be argued that the ability to alter the sensitivity of the mechanisms generating the motor component of this motor-sensory system represents a possible indirect way to influence afferent activity and so the perception of bladder volume centrally. Furthermore, it is emerging that the apparent modulation of sensation by drugs to alleviate the symptoms of overactive bladder (OAB), the anti-cholinergics and the new generation of drugs the β3 sympathomimetics, may be the result of their ability to modulate the motor component of the motor sensory system. The possibility of controlling sensation, physiologically and pharmacologically, by influencing afferent firing at its point of origin is a “new” concept in bladder physiology. It is one that deserves careful consideration as it might have wider implications for our understanding of bladder pathology and in the development of new therapeutic drugs. In this overview, evidence for the concept peripheral modulation of bladder afferent outflow is explored.

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“…Stimulation of sympathetic nerves has also been shown to have profound effects on NVA 25 , 26 , 62 . Thus, the output of the motor-sensory system appears to be under direct CNS control.…”

Section: “Afferent Noise” and The Concept Of The Peripheral Regulatiomentioning

confidence: 99%

The concept of peripheral modulation of bladder sensation

Eastham

Gillespie

2013

Organogenesis

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“…The mechanisms underlying the possible inhibitory events are not known. Inhibitory mechanisms have been postulated to be present in the bladder (Koley et al 1984;Vaughan & Satchell, 1995) but their existence and role is controversial.…”

Section: Figure 11mentioning

confidence: 99%

Agonist‐ and Nerve‐Induced Phasic Activity in the Isolated Whole Bladder of the Guinea Pig: Evidence for Two types of Bladder Activity

Gillespie

Harvey

Drake

2003

Experimental Physiology

150

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Spontaneous localised propagating waves of contraction and localised stretches have been reported to occur in the isolated whole bladder of the guinea pig. The physiological role and the cellular processes underlying these events are unknown. In order to gain insight into the mechanisms generating this complex activity, experiments were performed to examine and compare the responses of the whole bladder preparation to (i) the muscarinic agonists carbachol and arecaidine, (ii) the nicotinic ligand lobeline and (iii) nerve stimulation. High concentrations of the muscarinic agonists (>3 μM) induced a slow rise in intra‐vesical pressure upon which were superimposed pressure transients, while low concentrations (< 300 nM) induced only phasic rises in pressure. One interpretation of these data is that there are two separate mechanisms activated by muscarinic agonists: one generating contracture and the other phasic activity. Immunocytochemical staining revealed M3 muscarinic receptors on smooth muscle cells within trabeculae and a second population of positive cells in the sub‐urothelial layer. This observation raises the possibility that the actions of muscarinic agonists are a consequence of activating different cell types. Lobeline (1‐60 μM) activated phasic contractions but did not cause a rise in basal pressure. Atropine did not inhibit the lobeline‐induced responses but abolished the muscarinic responses. Also, hexamethonium or tetrodotoxin did not affect the lobeline‐induced responses. These observations suggest that the mechanism generating phasic activity is activated by a nicotinic stimulus that does not involve ganglia, nerves or the neuromuscular junction. Stimulation of the bladder nerve at frequencies between 20 and 30 Hz for 5 s resulted in a rapid rise in intra‐vesical pressure. Prolonged nerve stimulation (10‐200 s) at frequencies between 1 and 10 Hz activated phasic rises in pressure. Low frequency nerve stimulation increased the frequency of agonist‐induced phasic activity. Thus, nerve stimulation can also produce two forms of activity and low frequency stimulation can augment the processes generating phasic activity. These observations suggest that there are two distinct types of bladder activity: global contractions involving most of the bladder wall and phasic contractions comprising propagating waves of contraction. The mechanisms generating these contractile events appear to be different and they may involve cells located in different regions of the bladder. The nature of these mechanisms and their possible physiological significance is discussed.

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“…The net effect of the adrenergic inhibitory system appears to be to prolong bladder filling time by reducing the level of bladder wall tension transduced by local mechanoreceptors (Vaughan and Satchell, 1995). Recent evidence shows that, in addition to expressing M 3 receptors that elevate Ca 2+ and cause contraction when stimulated by muscarinic receptor agonists, detrusor smooth muscle expresses M 2 muscarinic receptors that can inhibit β-adrenoceptor-induced relaxation (Hegde and Eglen, 1999; Ostrom and Ehlert, 1998).…”

Section: Introductionmentioning

confidence: 99%

Potentiation of carbachol-induced detrusor smooth muscle contractions by β-adrenoceptor activation

Klausner¹,

Rourke²,

Miner³

et al. 2009

European Journal of Pharmacology

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In strips of rabbit bladder free of urothelium, the β-adrenoceptor agonist, isoproterenol, significantly reduced basal detrusor smooth muscle tone and inhibited contractions produced by low concentrations of the muscarinic receptor agonist, carbachol. During a carbachol concentration-response curve, instead of inhibiting, isoproterenol strengthened contractions produced by high carbachol concentrations. Thus, the carbachol concentration-response curve was shifted by isoproterenol from a shallow, graded relationship, to a steep, switch-like relationship. The tyrosine kinase inhibitor, genistein, inhibited carbachol-induced contractions only in the presence of isoproterenol. Contraction produced by a single high carbachol concentration (1 µM) displayed 1 fast and 1 slow peak. In the presence of isoproterenol, the slow peak was not strengthened, but was delayed, and U-0126 (mitogen-activated protein kinase kinase inhibitor) selectively inhibited this delay concomitantly with inhibition of extracellular signal-regulated kinase (ERK) phosphorylation. Isoproterenol reduced ERK phosphorylation only in the absence of carbachol. These data support the concept that, by inhibiting weak contractions, potentiating strong contractions, and producing a more switch-like concentration-response curve, β-adrenoceptor stimulation enhanced the effectiveness of muscarinic receptor-induced detrusor smooth muscle contraction. Moreover, β-adrenoceptor stimulation changed the cellular mechanism by which carbachol produced contraction. The potential significance of multi-receptor and multi-cell crosstalk is discussed.

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Urine storage mechanisms

Cited by 50 publications

References 0 publications

The concept of peripheral modulation of bladder sensation

The concept of peripheral modulation of bladder sensation

Agonist‐ and Nerve‐Induced Phasic Activity in the Isolated Whole Bladder of the Guinea Pig: Evidence for Two types of Bladder Activity

Potentiation of carbachol-induced detrusor smooth muscle contractions by β-adrenoceptor activation

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