AJP - Regulatory, Integrative and Comparative Physiology, Vol 257, Issue 3 522-R527, Copyright © 1989 by American Physiological Society
Normal atrial natriuretic peptide release after acute and chronic stimuli in hypophysectomized rats
A. Hoffman and H. R. Keiser
National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892.
To test the hypothesis that the pituitary gland has a role in modulating
the release of atrial natriuretic peptide (ANP) from atrial myocytes, we
applied different stimuli of both acute and chronic nature to rats 8-10
days after hypophysectomy (Hypx). Acute rapid cardiac pacing at a rate of
500 beats/min in anesthetized rats caused a marked increase in plasma
levels of ANP (from 76 +/- 7 to 237 +/- 60 pg/ml, P less than 0.05) despite
a marked decrease of blood pressure. This response was similar to that of
paced control rats, but because the basal levels were lower in Hypx rats,
the relative increase in ANP was larger in the experimental group. Studies
were also done in a chronic model of high-output congestive heart failure
produced by an aortocaval fistula in hydrocortisone-supplemented rats.
Although these rats had low blood pressure 2-3 days after surgery, there
were marked increases in right atrial pressures associated with high plasma
levels of ANP (194 +/- 24 pg/ml) that were not significantly different from
controls (221 +/- 26 pg/ml, P greater than 0.05). These results indicate
that the role of the pituitary in ANP release is indirect, and no specific
hypophyseal factor is required for this response. Hemodynamic parameters
are the important determinants of ANP secretion, even in hypophysectomized
rats.
