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  • Title: Effect of sodium restriction and corticosteroids on glandular kallikrein in plasma and in the submandibular gland.
    Author: Seto S, Rabito SF, Maitra SR, Wu JN, Carretero OA.
    Journal: Adv Exp Med Biol; 1986; 198 Pt A():255-63. PubMed ID: 3643711.
    Abstract:
    We investigated whether sodium restriction or mineralocorticoid influence the release of submandibular 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 less than 0.05; 0.40 +/- 0.09 ng/min/100 g bw vs 0.18 +/- 0.02, p less than 0.05, and 81.6 +/- 5.5 micrograms/mg protein vs 65.1 +/- 4.0, p less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)
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