The vasorelaxant effect of pituitary adenylate cyclase activating polypeptide and vasoactive intestinal polypeptide in isolated rat basilar arteries is partially mediated by activation of nitrergic neurons

Seebeck, Jörg; Löwe, Marcus; Kruse, Marie Luise; Schmidt, Wolfgang E.; Mehdorn, H. M.; Ziegler, Albrecht; Hempelmann, R. G.

doi:10.1016/s0167-0115(02)00072-1

Cited by 18 publications

(21 citation statements)

References 25 publications

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“…PACAP and VIP peptides regulate smooth muscle function, either directly or by facilitating cholinergic and nitric oxide mechanisms in a tissue-and species-specific manner (Mizumoto et al 1992;Fox-Threlkeld et al 1999;Onaga et al 1998;Seebeck et al 2002;Zizzo et al 2004). A number of studies have implicated PACAP in LUT function (Vizzard 2000c;Braas et al 2006;Herrera et al 2006;Zvara et al 2006).…”

Section: Discussionmentioning

confidence: 99%

PACAP-Mediated ATP Release from Rat Urothelium and Regulation of PACAP/VIP and Receptor mRNA in Micturition Pathways after Cyclophosphamide (CYP)-Induced Cystitis

et al. 2008

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Pituitary adenylate cyclase-activating peptide (PACAP) peptides are expressed in micturition pathways, and PACAP expression is regulated by urinary bladder inflammation. Previous physiological studies have demonstrated roles for PACAP27 and PACAP38 in detrusor smooth muscle (DSM) contraction and a PAC1 receptor antagonist reduced cyclophosphamide (CYP)-induced bladder hyperreflexia. To gain insight into PACAP signaling in micturition and regulation with cystitis, receptor characterization by real-time quantitative polymerase chain reaction and physiological assays were performed. PACAP receptors were identified in tissues of rat micturition pathway, including DSM, urothelium (U), and dorsal root ganglia (DRG) after acute (4 h), intermediate (48 h) or chronic (8 days) CYP-induced cystitis. PAC1 messenger RNA expression significantly (p < or = 0.05) increased in U and DSM after 48 h and chronic CYP-induced cystitis after an initial decrease at 4 h. VPAC1 and VPAC2 transcripts increased in U and DSM after acute and intermediate CYP-induced cystitis followed by a decrease in VPAC2 expression with chronic cystitis. Application of PACAP27 (100 nM) to cultured urothelial cells evoked adenosine triphosphate (ATP) release that was blocked by the PAC1 specific antagonist, M65 (1 microM). PACAP38 (100 nM) also evoked ATP release from cultured urothelial cells, but ATP release was less than that observed with PACAP27. PACAP transcripts were increased in the U with intermediate and chronic cystitis, whereas vasoactive intestinal polypeptide (VIP) expression in both tissues was very low and showed no regulation with cystitis. Regulation of PACAP, galanin, and substance P transcripts expression was observed in lumbosacral DRG, but no regulation for VIP was observed. The current data demonstrate PACAP and PAC1 regulation in micturition pathways with inflammation and PACAP-mediated ATP release from urothelium.

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Section: Discussionmentioning

confidence: 99%

PACAP-Mediated ATP Release from Rat Urothelium and Regulation of PACAP/VIP and Receptor mRNA in Micturition Pathways after Cyclophosphamide (CYP)-Induced Cystitis

et al. 2008

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“…By contrast, bladder VIP-IR fibers exhibited distribution patterns that were different from PACAP and were not sensitive to capsaicin, suggesting that they may have been derived from pelvic autonomic ganglia (17). There is good evidence that PACAP and VIP peptides regulate smooth muscle function, either directly or by facilitating cholinergic and nitric oxide mechanisms, in a tissue-and species-specific manner (20,40,48,57,78). PACAP and VIP peptides have been shown to be relaxants in bronchi, gut, oviduct, and vascular smooth muscle human, rat, and porcine tissues (19,37,56,60).…”

Section: Discussionmentioning

confidence: 99%

Role for pituitary adenylate cyclase activating polypeptide in cystitis-induced plasticity of micturition reflexes

Braas¹,

May²,

Zvara³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

118

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Pituitary adenylate cyclase activating polypeptide (PACAP) peptides are expressed and regulated in sensory afferents of the micturition pathway. Although these studies have implicated PACAP in bladder control, the physiological significance of these observations has not been firmly established. To clarify these issues, the roles of PACAP and PACAP signaling in micturition and cystitis were examined in receptor characterization and physiological assays. PACAP receptors were identified in various tissues of the micturition pathway, including bladder detrusor smooth muscle and urothelium. Bladder smooth muscle expressed heterogeneously PAC 1null, PAC1HOP1, and VPAC2 receptors; the urothelium was more restricted in expressing preferentially the PAC 1 receptor subtype only. Immunocytochemical studies for PAC 1 receptors were consistent with these tissue distributions. Furthermore, the addition of 50 -100 nM PACAP27 or PACAP38 to isolated bladder strips elicited transient contractions and sustained increases in the amplitude of spontaneous phasic contractions. Treatment of the bladder strips with tetrodotoxin (1 M) did not alter the spontaneous phasic contractions suggesting direct PACAP effects on bladder smooth muscle. PACAP also increased the amplitude of nerve-evoked contractions. By contrast, vasoactive intestinal polypeptide had no direct effects on bladder smooth muscle. In a rat cyclophosphamide (CYP)-induced cystitis paradigm, intrathecal or intravesical administration of PAC 1 receptor antagonist, PACAP6 -38, reduced cystitis-induced bladder overactivity. In summary, these studies support roles for PACAP in micturition and suggest that inflammation-induced plasticity in PACAP expression in peripheral and central micturition pathways contribute to bladder dysfunction with cystitis.neuropeptides; urinary bladder; bladder overactivity; dorsal root ganglia; spinal cord; inflammation THE STORAGE AND PERIODIC ELIMINATION of urine requires a complex neural control system that coordinates the activities of the smooth muscle of the urinary bladder and the smooth and striated muscle of the urethral sphincters (13,32,33). Coordination between these organs is mediated by a complex neural control system located in the brain, spinal cord, and peripheral ganglia (12). Experiments with a chemically (cyclophosphamide, CYP)-induced bladder inflammation (11, 34,38) rodent model have demonstrated alterations in neurochemical (52, 53, 66, 69), electrophysiological (29, 72), organizational (65, 68), and functional properties of the micturition reflex (24, 38, 39), suggesting dramatic reorganization of the micturition reflex pathways. Alterations in peripheral bladder afferent (sensory)/ efferent (autonomic and motor) and central interneuronal pathway functions may underlie detrusor overactivity that accompany CYP-induced cystitis.Pituitary adenylate cyclase activating polypeptide (PACAP) peptides have diverse functions in the endocrine, nervous, gastrointestinal, and cardiovascular systems (1, 6) through PAC 1 , VPAC 1 and VPAC ...

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“…The corresponding neuropeptide inhibitors (truncated peptides) were administered in 100-fold concentrations (VIP 6-28 10 Ϫ7 mol/L and PACAP ), as described in other studies. 21,[47][48][49] There was a weak to no cAMP response at various concentrations of the VPAC1R antagonists VIP or PACAP (100ϫ as concentrated as the corresponding agonist at the optimal concentration). Pretreatment with the antagonist occurred 3 minutes before agonist stimulation.…”

Section: Hdmec Express Functional Vpac1rmentioning

confidence: 99%

Pituitary Adenylate Cyclase Activating Polypeptide

Seeliger

Buddenkotte

Schmidt‐Choudhury

et al. 2010

The American Journal of Pathology

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The vasorelaxant effect of pituitary adenylate cyclase activating polypeptide and vasoactive intestinal polypeptide in isolated rat basilar arteries is partially mediated by activation of nitrergic neurons

Cited by 18 publications

References 25 publications

PACAP-Mediated ATP Release from Rat Urothelium and Regulation of PACAP/VIP and Receptor mRNA in Micturition Pathways after Cyclophosphamide (CYP)-Induced Cystitis

PACAP-Mediated ATP Release from Rat Urothelium and Regulation of PACAP/VIP and Receptor mRNA in Micturition Pathways after Cyclophosphamide (CYP)-Induced Cystitis

Role for pituitary adenylate cyclase activating polypeptide in cystitis-induced plasticity of micturition reflexes

Pituitary Adenylate Cyclase Activating Polypeptide

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