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Effects of Acute Water Load, Hypertonic Saline Infusion, and Furosemide Administration on Atrial Natriuretic Peptide and Vasopressin Release in Humans^*

TOKIHISA KIMURA, KEISHI ABE, KOZO OTA, KEN OMATA, MASARU SHOJI, KEI KUDO, KUNIAKI MATSUI, MINORU INOUE, MINORU YASUJIMA and YOSHINAGA KAORU

Second Department of Internal Medicine, Tohoku University School of Medicine Seiryo-cho 1-1 Sendai 980 Japan

Address requests for reprints to: Tokihisa Kimura, M.D., Second Department of Internal Medicine, Tohoku University School of Medicine,Seiryo-cho 1-1, Sendai 980, Japan.

A new specific RIA for a-human atrial natriuretic hormone (ahANP) was used to determine whether changes in plasma volume elicited by acute water loading, hypertonic saline infusion, and furosemide administration caused changes in ANP release and resultant changes in renal and cardiovascular function in normal subjects. In addition, changes in plasma arginine vasopressin (AVP), PRA, and aldosterone concentrations were studied simultaneously. Mean plasma ahANP and AVP levels were 51.3 ± 16.0 (±SE) and 3.1 ± 0.6 pg/ml, respectively, in the basal state. Plasma ahANP rose to 77.8 ± 27.6 in response to a 4.5% increase in plasma volume induced by water loading, increased further to 134.1 ± 28.9 in response to a 23% volume increase induced by hypertonic saline, and fell to 70.2 ± 15.8 pg/ml in response to a decrease in plasma volume after furosemide treatment (P 0.01–0.05). On the other hand, plasma AVP fell to 1.8 ± 0.1 pg/ml after the water load, rose to 4.1 ± 0.6 after hypertonic saline, and rose further to 5.8 ± 0.8 pg/ml after furosemide (P 0.01–0.05). Water and hypertonic saline loading decreased PRA, but plasma aldosterone concentrations did not change; subsequent furosemide administration increased both (P 0.01–0.05). Arterial pressure and heart rate did not change significantly. Increases in urinary Na excretion and osmolar clearances were associated with a rise in plasma ahANP after water loading and hypertonic saline infusion (P 0.01–0.05), but changes in urine flow were mainly associated with alterations in AVP release.

^* This work was supported by a research grant (60570380) from the Ministry of Education, Science, and Culture, Japan.

Address requests for reprints to: Tokihisa Kimura, M.D., Second Department of Internal Medicine, Tohoku University School of Medicine, Seiryo-cho 1-1, Sendai 980, Japan.

Received September 11, 1985.

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