Acute volume expansion was produced in 9 dogs by infusing a lactated Ringer's solution at 1 ml/kg/min in a volume estimated to increase blood volume by 20%. Volume expansion was maintained by replacing urinary fluid losses with equal volumes of the Ringer’s solution. Following volume expansion, the effects of a slow, nonhypotensive hemorrhage on plasma antidiuretic hormone concentration (PADH) were determined and compared to a group of 9 normovolemic dogs subjected to the same hemorrhage procedure, in order to determine if volume receptor control of ADH release would adapt t o acute increases in blood volume. Ringer’s infusion significantly increased blood volume to 95.2 ± 3.1 ml/kg (mean ± SE; P < 0.01) when compared to a mean normovolemic blood volume of 77.6 ± 3.4 ml/kg. Volume expansion was associated with a significantly lower (P)ADH (3.2 ± 1.6 μU/ml) than that i n normovolemic dogs (5.7 ± 1.2 μU/ml; p < 0.05). Significant increases in PADH (P < 0.05) occurred in both groups of dogs after 20 and 40 minutes of a continuous, nonhypotensive hemorrhage (0.40 to 0.45 mg/kg/min. Hemorrhage was also associated with significant decreases in effective left atrial pressure in both groups of dogs after 5, 10, 20, and 40 minutes of hemorrhage (P < 0.01). There were no significant differences between the two groups of dogs nor were there any significant changes during the experiment within each group for mean arterial blood pressure, arterial pulse pressure, plasma osmolality, plasma sodium concentration and plasma potassium concentration. Effective left atrial pressure and PADH were found to be exponentially correlated with blood volume in both hypervolemic and normovolemic dogs. Analysis of covariance of these correlations suggested that the hypervolemic dogs exhibited the same exponential changes in PADH and effective left atrial pressure with decreased blood volume as in the normovolemic dogs. It is concluded that acute volume expansion does not alter volume control of plasma ADH concentration.
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