title: Physiology and pharmacology of the human ureter: basis for current and future treatments.
abstract: BACKGROUND
  This article sets out to be a review regarding agents that affect contraction and relaxation of the ureter in order to establish a basis for current and future treatments for upper urinary tract obstruction.
  
  
  METHODS
  A complete review of the English literature using MEDLINE was performed between 1960 and 2007 on ureter physiology and pharmacology with special emphasis on signal transduction mechanisms involved in the contractile regulation of the human ureter.
  
  
  RESULTS
  Activation of muscarinic and adrenergic receptors increases the amplitude of ureteral contractions. The sympathetic nerves modulate the contractions by alpha-adrenoceptors and relaxation by beta-adrenoceptors. The purinergic system is important in sensory/motor functions and ATP is an important non-adrenergic non-cholinergic (NANC) agent causing contraction. Nitric oxide (NO) is a major inhibitory NANC neurotransmitter causing relaxation. Serotonin causes contraction. Prostaglandin-F(2)alpha contracts whereas prostaglandin-E(1)/E(2) relaxes the ureter. Phosphodiesterases (PDE) and the Rho-kinase pathway have recently been identified in the human ureter. PDE-IV inhibitors, K(+) channel openers, calcium antagonists, alpha(1)-adrenoceptor antagonists and NO donors seem to be promising drugs in relieving obstruction and facilitating stone passage.
  
  
  CONCLUSIONS
  Further understanding of the ureteral function and pharmacology may lead to the discovery of promising new drugs that could be useful in relieving ureteral colic, facilitating spontaneous stone passage, preparing the ureter for ureteroscopy as well as acting adjunctive to extracorporeal shock-wave lithotripsy.
authors.affiliation: Manisa State Hospital, Urology Clinic, Manisa, Turkey.
authors.forename: A Erdem
authors.initials: AE
authors.lastname: Canda
authors.forename: Burak
authors.initials: B
authors.lastname: Turna
authors.forename: G Mehtap
authors.initials: GM
authors.lastname: Cinar
authors.forename: Oktay
authors.initials: O
authors.lastname: Nazli
mesh_terms: D000322:Adrenergic Agonists / Q000494:pharmacology; D000527:Alprostadil / Q000378:metabolism; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects; D015237:Dinoprost / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects; D011941:Receptors, Adrenergic / Q000187:drug effects / Q000378:metabolism; D011976:Receptors, Muscarinic / Q000378:metabolism; D011983:Receptors, Purinergic / Q000378:metabolism; D012701:Serotonin / Q000378:metabolism; D014513:Ureter / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology*; D052878:Urolithiasis / Q000188:drug therapy / Q000503:physiopathology*
chemical_list: D000322:Adrenergic Agonists; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D011941:Receptors, Adrenergic; D011976:Receptors, Muscarinic; D011983:Receptors, Purinergic; D009569:Nitric Oxide; D012701:Serotonin; D015237:Dinoprost; D000527:Alprostadil; D015232:Dinoprostone