scholarly journals Nitric oxide modulates bladder afferent nerve activity in the in vitro urinary bladder–pelvic nerve preparation from rats with cyclophosphamide induced cystitis

2013 ◽  
Vol 1490 ◽  
pp. 83-94 ◽  
Author(s):  
Yongbei Yu ◽  
William C. de Groat
Keyword(s):  
Nitric Oxide ◽  
Urinary Bladder ◽  
Afferent Nerve ◽  
Pelvic Nerve ◽  
Nerve Activity

scholarly journals Cystitis increases colorectal afferent sensitivity in the mouse

2009 ◽  
Vol 297 (6) ◽  
pp. G1250-G1258 ◽  
Author(s):  
Pablo Rodolfo Brumovsky ◽  
Bin Feng ◽  
Linjing Xu ◽  
Carly Jane McCarthy ◽  
G. F. Gebhart
Keyword(s):  
Urinary Bladder ◽  
Treated Group ◽  
Mechanical Sensitivity ◽  
Pelvic Nerve ◽  
Treatment Groups ◽  
Colon Inflammation ◽  
Afferent Fibers ◽  
Peripheral Mechanism ◽  
Inflammatory Soup

Studies in humans and rodents suggest that colon inflammation promotes urinary bladder hypersensitivity and, conversely, that cystitis contributes to colon hypersensitivity, events referred to as cross-organ sensitization. To investigate a potential peripheral mechanism, we examined whether cystitis alters the sensitivity of pelvic nerve colorectal afferents. Male C57BL/6 mice were treated with cyclophosphamide (CYP) or saline, and the mechanosensitive properties of single afferent fibers innervating the colorectum were studied with an in vitro preparation. In addition, mechanosensitive receptive endings were exposed to an inflammatory soup (IS) to study sensitization. Urinary bladder mechanosensitive afferents were also tested. We found that baseline responses of stretch-sensitive colorectal afferents did not differ between treatment groups. Whereas IS excited a proportion of colorectal afferents CYP treatment did not alter the magnitude of this response. However, the number of stretch-sensitive fibers excited by IS was increased relative to saline-treated mice. Responses to IS were not altered by CYP treatment, but the proportion of IS-responsive fibers was increased relative to saline-treated mice. In bladder, IS application increased responses of muscular afferents to stretch, although no differences were detected between saline- and CYP-treated mice. In contrast, their chemosensitivity to IS was decreased in the CYP-treated group. Histological examination revealed no changes in colorectum and modest edema and infiltration in the urinary bladder of CYP-treated mice. In conclusion, CYP treatment increased mechanical sensitivity of colorectal muscular afferents and increased the proportion of chemosensitive colorectal afferents. These data support a peripheral contribution to cross-organ sensitization of pelvic organs.

Involvement of nitric oxide in inhibitory innervation of urinary bladder of Atlantic cod, Gadus morhua

1996 ◽  
Vol 270 (6) ◽  
pp. R1380-R1385
Author(s):  
C. Olsson ◽  
S. Holmgren
Keyword(s):  
Nitric Oxide ◽  
Urinary Bladder ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Maximal Effect ◽  
No Donor ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Ly 83583

The aim of this study was to investigate the involvement of nitric oxide (NO) in the nonadrenergic, noncholinergic (NANC) relaxation of the urinary bladder of the Atlantic cod, Gadus morhua. NADPH diaphorase-reactive nerve cells, presumed to be able to produce NO, were found in the vesicular nerve. The cells occurred alone and in ganglia together with stained and unstained cells. The effect of inhibitors of NO synthesis on the relaxation was examined in vitro in isolated muscle preparations. NG-nitro-L-arginine methyl ester (10(-4) M) and NG-nitro-L-arginine (L-NNA; 10(-4) M) decreased the electrically induced relaxation to 32 +/- 6 (n = 8) and 28 +/- 6% (n = 8) of the control, respectively. L-Arginine (10(-3) M) increased the relaxation to 152 +/- 24% (n = 8), without affecting the inhibition by L-NNA. The beta-adrenoceptor antagonist propranolol together with L-arginine analogues abolished the relaxation in 7 of 11 preparations. The NO donor sodium nitroprusside (NaNP) caused a concentration-dependent relaxation of the bladder, with a maximal effect obtained at 10(-4) M. LY-83583 (10(-5) M), a guanylate cyclase inhibitor, decreased both the electrically (n = 8) and the NaNP (10(-6) M, n = 9)-induced relaxation to 69 +/- 5 and 20 +/- 4% of the control, respectively. Together these findings suggest that NO is involved in the NANC regulation of the motility of the urinary bladder of the Atlantic cod.

scholarly journals In Vitro Recording of Mesenteric Afferent Nerve Activity in Mouse Jejunal and Colonic Segments

10.3791/54576 ◽  
2016 ◽  
Author(s):  
Sara Nullens ◽  
Annemie Deiteren ◽  
Wen Jiang ◽  
Christopher Keating ◽  
Hannah Ceuleers ◽  
...  
Keyword(s):  
Afferent Nerve ◽  
Nerve Activity

scholarly journals Coupled Nitric Oxide and Autonomic Receptor Functional Responses in the Normal and Inflamed Urinary Bladder of the Rat

2012 ◽  
pp. 371-380 ◽  
Author(s):  
R. VESELÁ ◽  
H. ASKLUND ◽  
P. ARONSSON ◽  
M. JOHNSSON ◽  
V. WSOL ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Urinary Bladder ◽  
The Body ◽  
Bladder Function ◽  
Detrusor Muscle ◽  
Functional Responses ◽  
Nitric Oxide Synthase Inhibitor ◽  
Parasympathetic Nerve ◽  
Contractile Responses

Both divisions of the autonomic nervous system are involved in regulation of urinary bladder function. Several substances, other than noradrenaline and acetylcholine, seem to play important roles in physiology and pathophysiology of lower urinary tract. In the current study, we aimed to examine if there exist interplays between nitric oxide (NO) and autonomic transmitters and if such interactions vary in different parts of the urinary bladder in healthy and cyclophosphamide (CYP)-induced cystitic rats; when administered to the animals (100 mg/kg; i.p.), the cytotoxic CYP metabolite acrolein induces bladder inflammation. In the current study a series of in vitro functional studies were performed on detrusor muscle strip preparations. Stimulation with electrical field stimulation (EFS), methacholine, adenosine 5´-triphosphate (ATP), and adrenaline evoked contractile responses in isolated bladder preparations that were significantly reduced in cyclophosphamide (CYP)-treated rats. While the nitric oxide synthase inhibitor Nω nitro-L-arginine (L-NNA; 10-4 M) did not affect contractile responses in normal, healthy strip preparations, it significantly increased the contractile responses to EFS, methacholine and adrenaline, but not to ATP, in the bladders from the CYP-treated rats. In the CYP-treated rats, the ATP-evoked relaxatory part of its dual response (an initial contraction followed by a relaxation) was 6-fold increased in comparison with that of normal preparations, whereas the isoprenaline relaxation was halved in the CYP-treated. While L-NNA (10-4 M) had no effect on the isoprenaline-evoked relaxations, it reduced the ATP-evoked relaxations in strip preparations from the bladder body of CYP-treated rats. Stimulation of β2- and β3 adrenoceptors evoked relaxations and both responses were reduced in cystitis, the latter to a larger extent. In the trigone, the reduced ATP-evoked contractile response in the inflamed strips was increased by L-NNA, while L NNA had no effect on the ATP-evoked relaxations, neither on the relaxations in healthy nor on the larger relaxations in the inflamed trigone. The study shows that both contractile and relaxatory functions are altered in the state of inflammation. The parasympathetic nerve-mediated contractions of the body of the bladder, evoked by the release of ATP and acetylcholine, were substantially reduced in cystitis. The relaxations to β-adrenoceptor and purinoceptor stimulation were also reduced but only the ATP-evoked relaxation involved NO.

scholarly journals Transient contractions of urinary bladder smooth muscle are drivers of afferent nerve activity during filling

2016 ◽  
Vol 147 (4) ◽  
pp. 323-335 ◽  
Author(s):  
Thomas J. Heppner ◽  
Nathan R. Tykocki ◽  
David Hill-Eubanks ◽  
Mark T. Nelson
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Sensory Nerve ◽  
Bk Channels ◽  
Filling Pressure ◽  
Afferent Nerve ◽  
Detrusor Muscle ◽  
Afferent Activity ◽  
Intravesical Pressure ◽  
Nerve Activity

Activation of afferent nerves during urinary bladder (UB) filling conveys the sensation of UB fullness to the central nervous system (CNS). Although this sensory outflow is presumed to reflect graded increases in pressure associated with filling, UBs also exhibit nonvoiding, transient contractions (TCs) that cause small, rapid increases in intravesical pressure. Here, using an ex vivo mouse bladder preparation, we explored the relative contributions of filling pressure and TC-induced pressure transients to sensory nerve stimulation. Continuous UB filling caused an increase in afferent nerve activity composed of a graded increase in baseline activity and activity associated with increases in intravesical pressure produced by TCs. For each ∼4-mmHg pressure increase, filling pressure increased baseline afferent activity by ∼60 action potentials per second. In contrast, a similar pressure elevation induced by a TC evoked an ∼10-fold greater increase in afferent activity. Filling pressure did not affect TC frequency but did increase the TC rate of rise, reflecting a change in the length-tension relationship of detrusor smooth muscle. The frequency of afferent bursts depended on the TC rate of rise and peaked before maximum pressure. Inhibition of small- and large-conductance Ca2+-activated K+ (SK and BK) channels increased TC amplitude and afferent nerve activity. After inhibiting detrusor muscle contractility, simulating the waveform of a TC by gently compressing the bladder evoked similar increases in afferent activity. Notably, afferent activity elicited by simulated TCs was augmented by SK channel inhibition. Our results show that afferent nerve activity evoked by TCs represents the majority of afferent outflow conveyed to the CNS during UB filling and suggest that the maximum TC rate of rise corresponds to an optimal length-tension relationship for efficient UB contraction. Furthermore, our findings implicate SK channels in controlling the gain of sensory outflow independent of UB contractility.

Sign in / Sign up

Export Citation Format

Share Document