Kinins pp 361-373 | Cite as

The Effect of Water, Sodium Overloading and Diuretics upon Urinary Kallikrein

  • H. R. Croxatto
  • F. Huidobro
  • M. Rojas
  • J. Roblero
  • R. Albertini
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 70)


Urinary kallikrein is significantly decreased in different types of experimental (Croxatto and San Martin, 1970; Margolius et al., 1972), clinical (Margolius. et al., 1972; Adetuyibi and Mills, 1972; Greco et al., 1974) and spontaneous hypertension (Porcelli et al., 1975). In contrast to the numerous reports dealing with alterations in kallikrein excretion, there is still meager information concerning the physiological role of the kallikrein-kinin system in the kidney. Although renal kallikrein appear to be directly related to sodium excretion (Marin-Grez and Carretero, 1972; Adetuyibi and Mills, 1972), other data have been published suggesting that not Na, but mineralocorticoids are the primary factor regulating kallikrein excretion (Geller et al., 1972; Pisano et al., 1974; Margolius, et al., 1974). Other results indicate a functional relationship between kallikrein and water excretion (Mills and Ward, 1975). In addition it has been proposed that renal kallikrein, acting either locally in the kidney (Pisano et al., 1974), and/or systemically (Croxatto, 1972 a,b) can be part of the vasodilator system.


Sodium Excretion Water Excretion Spontaneous Hypertension Urinary Kallikrein Enzyme Excretion 
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Copyright information

© Plenum Press, New York 1976

Authors and Affiliations

  • H. R. Croxatto
    • 1
  • F. Huidobro
    • 1
  • M. Rojas
    • 1
  • J. Roblero
    • 1
  • R. Albertini
    • 1
  1. 1.Laboratorio de Fisiologia, Instituto de Ciencias BiologicasUniversidad Catolica de ChileSantiagoChile

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