Influence of the sympathetic nervous system on lower urinary tract in man

Nordling, Jørgen

doi:10.1002/nau.1930020103

Cited by 35 publications

(17 citation statements)

References 95 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Supporting the importance of this finding, Maggi et al (1985) provided evidence for a sympathetic inhibition of the reflex activation of the rat detrusor in response to physiological filling. On the other hand, no influence on the bladder function, at rest or during voiding, could be demonstrated in human patients with various lesions of the sympathetic nervous system (Nordling, 1983). Klevmark (1977) found no support for an inhibitory reflex via the sympathetic nervous system and suggested that accommodation of the bladder to increasing amount of fluid depends almost completely upon the viscoelastic properties of the detrusor muscle.…”

Section: Discussionmentioning

confidence: 97%

See 1 more Smart Citation

Effects of inhibition of the l‐arginine/nitric oxide pathway in the rat lower urinary tract in vivo and in vitro

Persson

Igawa

Mattiasson

et al. 1992

British J Pharmacology

178

107

View full text Add to dashboard Cite

1 The present study was performed to investigate how blockade of the L-arginine/nitric oxide (NO) pathway influences the function of the lower urinary tract in vivo, as studied by cystometry in conscious rats and in vitro, in isolated muscle preparations from the rat detrusor and urethra. 2 L-N0-nitro arginine methyl ester (L-NAME), 10 and 20 mg kg-, administered intra-arterially, decreased micturition volume and bladder capacity, and increased spontaneous bladder contractions. D-NAME (20mgkg-') had no effect. No changes in the urodynamic parameters were recorded if L-NAME (20mgkg-') was administered in combination with L-arginine (200mgkg-'). 3 Cystometries performed after intra-arterial administration of sodium nitroprusside (SNP) (3mg kg-') and 3-morpholino-sydnonimin hydrochloride (SIN-1, 2mgkg-') showed a decrease in bladder capacity, micturition volume and threshold pressure. SIN-1, but not SNP, induced spontaneous bladder contractions. 4 Isolated precontracted urethral preparations responded to electrical stimulation with a frequencydependent tetrodotoxin-sensitive relaxation. L-NAME (10-4 M), but not D-NAME, reduced the maximal relaxation to 31 ± 8% (n = 8) of the response prior to drug administration. The inhibition induced by L-NAME was completely reversed by L-arginine (10-3 M). SNP (10-1 10-4 M), SIN-1 (10-6-3 x l0-4 M) and NO (10-5-10-3M; present in acidified solution of NaNO2), caused relaxation (93-100%) of urethral preparations. L-NAME did not affect these relaxations.5 Detrusor strips contracted by carbachol or K' showed contractions in response to electrical stimulation, even when pretreated with a,p-methylene ATP and/or atropine. Small relaxations (14-41%) of detrusor strips were evoked by SNP (10-6-10-4M), SIN-1 (10-5-3 x 10-4M) and NO (10-5-10-3 M). Electrically (20 Hz) induced contractions of the detrusor muscle were unaffected by addition of L-NAME (10-6_10-4 M) or L-arginine (10-3 M).6 The present results suggest that the L-arginine/NO pathway is of functional importance for the bladder outlet region, but that its role in the detrusor is questionable. They also suggest that the site of action of L-NAME for inducing bladder hyperactivity in the rat is the outlet region rather than the detrusor muscle.

show abstract

Section: Discussionmentioning

confidence: 97%

“…Such a factor may be increased sympathetic activity and release of noradrenaline acting on the P-adrenoceptors of the detrusor (Edvardsen, 1968). However, the importance of f3-adrenoceptors in human detrusor relaxation has been questioned (Klevmark, 1977;Nordling, 1983), and is not clarified.…”

Section: Introductionmentioning

confidence: 99%

Effects of inhibition of the l‐arginine/nitric oxide pathway in the rat lower urinary tract in vivo and in vitro

Persson

Igawa

Mattiasson

et al. 1992

British J Pharmacology

178

107

View full text Add to dashboard Cite

show abstract

“…The submucosal vascular plexus has also been claimed to contribute to pressure generation [48,50,55,56]. From a theoretical point of view the contribution of a vascular plexus to pressure generation will be dependent on a surrounding firm sheath.…”

Section: Anatomy and Physiologymentioning

confidence: 99%

An analysis of urethral viscoelasticity with particular reference to the sphincter function in healthy women

Thind

1995

Int Urogynecol J

View full text Add to dashboard Cite

Urine ingression into the urethra involves stretching of the fibers, resulting in a pressure increase. This study describes the pressure response following a rapid urethral dilatation. A probe for simultaneous recording of cross-sectional area (dilatation) and pressure was used. The urethral dilatations were induced by a gravitationally operated pump. Fifteen healthy women were studied. The pressure response (viscoelastic reaction) is a steep increase with the maximum at the end of dilatation. The maximum pressure is followed by a pressure decay (stress relaxation) over the next few seconds. The pressure response was highly dependent on the size and rate of dilatation but not on the urethral site of measurement. The median pressure response to a dilatation of 10 mm 2 at a rate of 150 mm2/s (chosen arbitrarily within the physiological range) is 45 cmH20. The pressure response may account for 25% of the urethral resistance to dilatation.

show abstract

“…A relaxing effect on the detrusor musculature during ß-receptor stimulation has been demonstrated both in vi tro and in vivo [10,14], a-Receptor-stimulating drugs increase the intraurethral pressure [15], whereas a-block ing agents reduce the intraurethral pressure [13,16]. ß-Receptor-stimulating drugs have been reported to reduce the intraurethral pressure [17,18], whereas ß-blocking agents seem to have less effect on the intraurethral pres sure [16,17], studies have demonstrated minimal effect of both parasympathomimetics and parasympatholytics on the ure thra [6,7]; others have observed an increase in urethral closure pressure after parenteral administration of parasympathomimetics [8]. Thus, it is generally agreed, that the coordinated con traction of the detrusor muscle is parasympathetically induced, whereas the significance of the parasympathetic innervation of the bladder neck and the urethra remains controversial.…”

Section: Sympathetic Innervationmentioning

confidence: 99%