title: Adrenergic regulation of the intracellular [Ca2+] and voltage-operated Ca2+ channel currents in the rat prostate neuroendocrine cells.
abstract: BACKGROUND
  The prostate gland contains numerous neuroendocrine cells (PNECs) innervated by adrenergic neurons. PNECs are believed to influence the growth and physiological function of the prostate gland via paracrine release of hormones.
  
  
  METHODS
  Using fura-2 fluorescence measurement and patch-clamp techniques, we investigated the effects of adrenergic stimulation on cytosolic concentration of Ca2+ ([Ca2+]c) and high voltage-activated Ca2+ channel currents (HVA-I(Ca)) of the putative rat prostate neuroendocrine cells (RPNECs) freshly isolated by an enzymic digestion.
  
  
  RESULTS
  Noradrenaline (NA, 1 microM) induced a sharp, transient increase of [Ca2+]c measured by the fura-2 fluorescence. Pharmacological studies showed that alpha1-adrenoceptors (alpha1-ARs) coupled with PLC/IP3 signaling pathway induce the release of stored Ca2+, which subsequently recruits store-operated Ca2+ entry pathways. In the whole-cell voltage clamp experiment, NA decreased the amplitude of HVA-I(Ca) by 40%, which was mimicked by an alpha2-AR agonist (UK14304) but not by an alpha1-AR agonist (phenyleprine). After selective blockade of N-type Ca2+ channels by omega-conotoxin GVIA, the addition of NA showed no further inhibition on the remaining L-type Ca2+ channel currents. The adrenergic inhibition of HVA-I(Ca) was partially prevented by the pretreatment with pertussis toxin (PTX) (5 microg/ml, 4 hr, 37 degrees C).
  
  
  CONCLUSIONS
  RPNECs express both alpha1- and alpha2-ARs, signaling the release of stored Ca2+ and the inhibition of N-type Ca2+ channels, respectively.
authors.affiliation: Department of Physiology, Sungkyunkwan University School of Medicine, Suwon, Korea.
authors.forename: Jun Hee
authors.initials: JH
authors.lastname: Kim
authors.forename: Sun Young
authors.initials: SY
authors.lastname: Shin
authors.forename: Joo Hyun
authors.initials: JH
authors.lastname: Nam
authors.forename: Eun-Kyung
authors.initials: EK
authors.lastname: Hong
authors.forename: Young-Shin
authors.initials: YS
authors.lastname: Chung
authors.forename: Jeong Yun
authors.initials: JY
authors.lastname: Jeong
authors.forename: Jeongyoon
authors.initials: J
authors.lastname: Kang
authors.forename: Dae-Yong
authors.initials: DY
authors.lastname: Uhm
authors.forename: Sung Joon
authors.initials: SJ
authors.lastname: Kim
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000502:physiology*; D004351:Drug Resistance; D004553:Electric Conductivity; D007424:Intracellular Fluid / Q000378:metabolism*; D008297:Male; D009490:Neurosecretory Systems / Q000166:cytology / Q000378:metabolism*; D009638:Norepinephrine / Q000494:pharmacology*; D009994:Osmolar Concentration; D011467:Prostate / Q000166:cytology / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology; D018341:Receptors, Adrenergic, alpha-2 / Q000502:physiology; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D015220:Calcium Channels; D011942:Receptors, Adrenergic, alpha; D018340:Receptors, Adrenergic, alpha-1; D018341:Receptors, Adrenergic, alpha-2; D015222:Sodium Channels; D013779:Tetrodotoxin; D002118:Calcium; D009638:Norepinephrine