Neurogenic antinatriuresis during development of acute cardiac tamponade

Renal function was measured during the development of cardiac tamponade in anesthetized dogs. Tamponade was induced by infusion of isotonic saline (37°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 μV/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. We conclude that this reflex antinatriuresis may support overall cardiovascular function during the development of cardiac tamponade.