This study aimed to investigate the mechanism of gastrointestinal regulation of natriuresis. Sixteen subjects without (group I) and sixteen subjects with a truncal vagotomy (group II), were given a daily diet of 18mmol of sodium for 5days (D1-D5). The sodium deficit for this period was calculated for each subject and on the morning of day-6 (D6), their cumulative deficit (E) was given as 3% NaCl. In both groups the subjects were divided to receive the hypertonic saline either orally (Ior, IIor) or intravenously (Iiv, IIiv). During the period of low sodium diet when compared to group II subjects of group I (1) had a greater weight loss (p<0.005), (2) demonstrated a larger drop in pulse pressure (p<0.005), (3) achieved a positive sodium equilibrium later (D5 vs D4) and (4) developed a greater sodium deficit (p<0.005). During the two 12h periods of D6, both Ior and Iiv exhibited greater natriuresis during the first 12h period (p<0.0001) whereas both IIor and IIiv did so during the second 12h period (p<0.0001). On D6 Ior excreted the greatest percentage of E (E%; 35.63%±3.12%, p<0.0001) compared to Iiv (17.06%±1.78%), IIor (16.03%±3.54%) and IIiv (15.39%±2.77%) whereas E% was not different between the other subgroups. These results indicate that the differential natriuresis between oral and intravenous sodium loading in previously sodium deprived subjects, is due to a mechanism in which the vagal nerves play a significant role as part of neural reflex or via a natriuretic hormone.
Keywords: Blood pressure; Natriuresis; Renal; Sodium; Vagal nerve; Vagotomy.
Copyright © 2017 Elsevier B.V. All rights reserved.