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Kinins IV pp 255-263 | Cite as

Effect of Sodium Restriction and Corticosteroids on Glandular Kallikrein in Plasma and in the Submandibular Gland

  • Shinji Seto
  • Sara F. Rabito
  • Subir R. Maitra
  • Jonathan N. Wu
  • Oscar A. Carretero
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 198A)

Summary

We investigated whether sodium restriction or mineralocorticoid influence the release of submandibulary kallikrein into the blood and/or the concentration of kallikrein in glandular tissue. For this we measured submandibular gland blood flow, arterial and submandibular gland venous kallikrein, and kallikrein in glandular homogenates of male Sprague-Dawley rats after one week of either low sodium or deoxycorticosterone acetate (DOCA) treatment. We also studied the effect of dexamethasone on the concentration of kallikrein in gland tissue and peripheral plasma. Kallikrein in plasma and in homogenates was measured by radioimmunoassay. Blood flow was determined by timed collections of venous outflow. Kallikrein release was calculated as the arteriovenous difference in kallikrein times the rate of submandibular gland plasma flow. The concentration of kallikrein in arterial plasma, the basal submandibular kallikrein release into blood, and the concentration of kallikrein in submandibular gland tissue were all higher during low sodium than during normal sodium intake (20.1 ± 3.6 ng/ml vs 10.7 ± 0.5, p< 0.05; 0.40 ± 0.09 ng/min/100 g bw vs 0.18 ± 0.02, p< 0.05, and 81.6 ± 5.5 lig/mg protein vs 65.1 ± 4.0, p< 0.05, respectively). In contrast, DOCA treatment did not affect the concentration of kallikrein in arterial plasma, the basal release of kallikrein from the submandibular gland into blood, or the concentration of kallikrein in the gland. Dexamethasone in doses that did not affect the normal growth of the animals had no significant effect on the concentration of kallikrein either in submandibular gland tissue or in peripheral plasma. We concluded that sodium restriction increases the kallikrein content of the submandibular gland and its release into blood, but this effect is probably not caused by increases in mineralocorticoid levels. The increased release of submandibular gland kallikrein into blood may explain, in part, the increased plasma levels of kallikrein observed during sodium restriction.

Keywords

Sodium Intake Sodium Restriction Arterial Plasma Peripheral Plasma Parotid Saliva 
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Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • Shinji Seto
    • 1
  • Sara F. Rabito
    • 1
  • Subir R. Maitra
    • 1
  • Jonathan N. Wu
    • 1
  • Oscar A. Carretero
    • 1
  1. 1.Hypertension Research DivisionHenry Ford HospitalDetroitUSA

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