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Details for anatomical structure: Goormaghtighs cell

EndoNet ID: ENC00457

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Synonyms

Goormaghtighs cell, juxtaglomerular cell,

General information

located at the vascular pole of the renal corpuscle; they are modified smooth muscle cells primarily of the afferent arteriole of the renal glomerulus.

Links to other resources

Cytomer cy0011519

Larger structures

  • juxtaglomerular_apparatus
  • parts_of_human_body
  • mesangium

Substructures

    Secreted hormones

    • Hormone: renin

      Influenced by:

      • CaSR
        in Goormaghtighs_cell
        • CaSRs modulate renin release both in vitro and in vivo. CaSRs play a role as a regulatory pathway of renin release. [1]
        • Activation of CaSR significantly decreases both JG cell cAMP formation and renin release by ~45%. Juxtaglomerular cells express CaSR, and CaSR respond to changes in extracellular calcium to modify or activate calcium-mediated intracellular signaling. [2]
        • While calcium does not directly control renin secretion, increased calcium inhibits and decreased calcium amplifies cAMP-stimulated renin secretion. [3]
      • beta-1 adrenoreceptor
        in kidney
        • renin secretion from juxtaglomerular cells is mediated by the action on β1-adrenoreceptors of norepinephrine released from renal sympathetic nerve terminals as a result of renal nerve activity [4]
      • angiotensin II type 1 receptor
        in Goormaghtighs_cell
        • Activation of AT1 receptors at the juxtaglomerular apparatus suppresses renin release through the so-called short-loop feedback mechanism. [5]
      • NPR1
        in kidney
        • In humans and experimental animals, administration of atrial natriuretic peptide (ANP) decreases plasma aldosterone levels by inhibiting renin secretion. [6]
        • ANP decreases renin secretion from the juxtaglomerular cells via a PKGII-dependent process (NPR1-involved). [7]

    Receptors

    • Receptor: CaSR

      Influences:

      • renin
        • CaSRs modulate renin release both in vitro and in vivo. CaSRs play a role as a regulatory pathway of renin release. [1]
        • Activation of CaSR significantly decreases both JG cell cAMP formation and renin release by ~45%. Juxtaglomerular cells express CaSR, and CaSR respond to changes in extracellular calcium to modify or activate calcium-mediated intracellular signaling. [2]
        • While calcium does not directly control renin secretion, increased calcium inhibits and decreased calcium amplifies cAMP-stimulated renin secretion. [3]

    • Receptor: angiotensin II type 1 receptor

      Influences:

      • renin
        • Activation of AT1 receptors at the juxtaglomerular apparatus suppresses renin release through the so-called short-loop feedback mechanism. [5]
    Reference