ArticleExperimental neurology2008
Effects of intrathecal administration of pituitary adenylate cyclase activating polypeptide on lower urinary tract functions in rats with intact or transected spinal cords.
Article in Experimental neurology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Standardization of an experimental model of intradural injection after spinal cord injury in rats.Clinics (Sao Paulo, Brazil) · 2021Article
- Sympathetic β-adrenergic mechanism in pudendal inhibition of nociceptive and non-nociceptive reflex bladder activity.American journal of physiology. Renal physiology · 2016Article
- Neurochemical plasticity of nitric oxide synthase isoforms in neurogenic detrusor overactivity after spinal cord injury.Neurochemical research · 2011Article
- Neuropeptides in lower urinary tract function.Handbook of experimental pharmacology · 2011Review
- Changes in afferent activity after spinal cord injury.Neurourology and urodynamics · 2010Review
- Afferent nerve regulation of bladder function in health and disease.Handbook of experimental pharmacology · 2009Review
- The role of vasoactive intestinal polypeptide and pituitary adenylate cyclase-activating polypeptide in the neural pathways controlling the lower urinary tract.Journal of molecular neuroscience : MN · 2008Review
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Effects of intrathecally administered pituitary adenylate cyclase activating polypeptide-38 (PACAP-38, 0.1-30 microg) on lower urinary tract function were examined in unanesthetized, decerebrate rats with an intact spinal cord and after chronic spinal cord transection (SCT). PACAP-38 was also studied in rats with intact or bilaterally transected hypogastric nerves (HGNs), to determine if sympathetic pathways to the bladder influenced responses. In SCT rats with intact HGNs under isovolumetric conditions, 30 mug of PACAP-38 but not lower doses (0.1-10 microg) increased (mean 194%) bladder contraction amplitude (BCA). In SCT rats with sectioned HGNs, 10 microg and 30 microg of PACAP-38 increased BCA by 62% and 195%, respectively. On the other hand, during continuous infusion cystometrograms (CMGs) in SCT rats with intact or sectioned HGNs, PACAP-38 (10 microg and 30 microg) markedly reduced or completely suppressed BCA (60% and 90%, respectively) and reduced external urethral sphincter (EUS) EMG activity (58% and 91%, respectively). During CMGs in spinal cord intact rats, with intact HGNs PACAP-38 30 microg increased BCA (26%) but after HGN section PACAP-38 10 microg and 30 microg increased BCA by 21% and 35%. These results suggest that after SCT, PACAP-38 activates spinal circuitry to facilitate the parasympathetic outflow to the urinary bladder and that the elimination of sympathetic pathways enhances this effect. The decrease in BCA by PACAP-38 during CMGs in SCT rats is most reasonably attributed to a reduction in urethral outlet resistance due to suppression of excitatory EUS reflexes.
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