Abstract
The influence of acute intravascular volume expansion on salt gland secretion of conscious, adult geese was investigated. The intravenous administration of 5% dextran in Krebs-bicarbonate-Ringer solution in an amount equivalent to 30% of the estimated blood volume caused a transient but highly significant increase in salt gland secretion independent of changes in plasma osmolality or sodium concentration. Intravenous veratrine (60 microng) caused a similar increase in salt gland secretion only when administered after the volume load. Intravenous 5% NaCl always caused a prolonged and significant increase in salt gland secretion which was not potentiated by veratrine. Volume expansion and hypertonic saline caused a significant tachycardia while veratrine caused a significant bradycardia. It is concluded that a volume component may contribute to the initiation of salt gland secretion in the goose and that the peripheral receptor involved is most likely vascular in origin.
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