AJP - Heart and Circulatory Physiology, Vol 250, Issue 2 195-H201, Copyright © 1986 by American Physiological Society
Neurogenic antinatriuresis during development of acute cardiac tamponade
J. L. Osborn and M. T. Lawton
Renal function was measured during the development of cardiac tamponade in
anesthetized dogs. Tamponade was induced by infusion of isotonic saline (37
degrees C) into the pericardial space. Step increases in pericardial fluid
volume in 20-ml increments from 0 to 160 ml increased renal efferent nerve
activity by a total of 140 +/- 58% of control (from 205 +/- 70 microV/s).
Since renal nerve traffic was elevated by pericardial fluid volume infusion
prior to any changes in arterial pressure, renal function was determined
before and after increasing pericardial pressure (PCP) by approximately 5
and 10 mmHg. Increasing PCP by 5 mmHg decreased urinary sodium excretion
and increased renin secretion rate without changing mean arterial pressure,
renal blood flow, or glomerular filtration rate (GFR). Further elevation of
PCP to approximately 10 mmHg also decreased urinary sodium excretion as
well as arterial pressure and GFR. Renal denervation prevented both of
these antinatriuretic responses to elevated PCP. In a third group of dogs,
similar antinatriuresis was induced by increasing PCP by approximately 5
and 10 mmHg. Bilateral cervical vagotomy abolished the antinatriuretic
response to increased PCP by 5 mmHg but was ineffective when PCP was
increased by 10 mmHg, which was accompanied by decreased arterial pressure.
These results demonstrate that elevation of pericardial fluid volume, and
consequently PCP, reflexly decreases urinary sodium excretion via
activation of renal sympathetic outflow. Early reflex antinatriuresis
results primarily from activation of cardiopulmonary or splanchnic
receptors with vagal afferents, whereas, at larger PCP, reflex
antinatriuresis may result from hypotension and unloading of high pressure
baroreceptors.(ABSTRACT TRUNCATED AT 250 WORDS)
