Role of pressure natriuresis in long-term control of renal electrolyte excretion.

Abstract

If pressure natriuresis is to play an important role in arterial pressure control, renal perfusion pressure must have a long-term effect on urinary sodium excretion. The aim of this study was to quantitate the importance of renal perfusion pressure per se in controlling renal hemodynamics and electrolyte excretion chronically. Female mongrel dogs (n=6) were instrumented with bilateral renal artery catheters for measurement of renal perfusion pressure and occluders on both renal arteries for servo-control of renal perfusion pressure at different levels; the urinary bladder was split for determination of renal clearances and electrolyte excretion from each kidney separately. Because both kidneys were exposed to the same neurohumoral influences, any changes in renal function could be attributed to differences in renal perfusion pressure between the two kidneys. After 5 days of control, renal perfusion pressure to one kidney was reduced from 86.7 ±0.2 to 74.2 ±0.6 mm Hg for 12 days, and pressure in the contralateral kidney increased to 91.5±0.4 mm Hg. Sodium excretion decreased from 41±2 to 25±1 mmol/d in the servo-controlled kidney and increased from 41 ±1 to 55 ±1 mmol/d in the contralateral kidney during 12 days of servo-control. Urine volume, chloride excretion, and potassium excretion exhibited similar patterns during servo-control. In addition, autoregulation of effective renal plasma flow and glomerular filtration rate was relatively well maintained; however, in the low-pressure kidney, glomerular filtration rate was slightly but significantly lower (-8%) than in the contralateral kidney. In summary, long-term changes in renal perfusion pressure caused sustained alterations in renal electrolyte excretion. These results suggest that renal perfusion pressure is an important long-term controller of sodium and water excretion. over the long-term by complex interactions J~ A . between the various neurohumoral control systems and the ability of the kidneys to excrete salt and water. Guyton and colleagues 1 (see References 2 through 5 for review) have emphasized renal-body fluid feedback as the dominant control system for long-term blood pressure control. A key component of this feedback is the effect of arterial pressure on renal excretion of sodium, often referred to as pressure natriuresis. In most instances, this mechanism is believed to stabilize blood pressure in response to various perturbations that would tend to cause hypertension or hypotension.The validity of this concept depends on the assumption that arterial pressure has a long-term influence on renal excretion of sodium and water, a premise that has been difficult to test experimentally. Numerous investigators have demonstrated that acute changes in arterial pressure markedly alter sodium and water excretion, 69 but the long-term effects of pressure per se on renal excretion are largely unknown. Long-term pressurenatriuresis curves are usually determined indirectly by

Louis K. Dahl Memorial Lecture. Renal and cardiovascular mechanisms of hypertension in obesity.

“…Moreover, weight reduction lowered plasma renin activity and aldosterone concentration in obese subjects. 34 In our study of obese dogs, plasma renin activity was elevated more than twofold after 5 weeks of a high-fat diet despite marked sodium retention and increased extracellular fluid volume. 45 The failure to suppress Ang II levels despite volume expansion and hypertension suggests that there may be a powerful underlying stimulus for renin secretion in the development of obesity.…”

“…34 Because both kidneys were exposed to the same neurohumoral influences, these studies were able to measure the effects of long-term changes in renal perfusion pressure per se on renal hemodynamics and electrolyte excretion. These studies indicated that relatively small changes in renal perfusion pressure caused large alterations in renal sodium and water excretion that persisted as long as renal artery pressure was altered.…”

Renal Denervation Does Not Abolish Sustained Baroreflex-Mediated Reductions in Arterial Pressure

“…8,11 Strong experimental support for this notion comes from a study in dogs in which the renal perfusion pressure to 1 kidney was servocontrolled at a reduction in pressure comparable to that achieved in the present study. 18 Throughout the duration of this study (12 days), there was a sustained reduction in sodium excretion in the kidney with the reduced renal perfusion pressure and an increase in sodium excretion in the high-pressure contralateral kidney. Because both kidneys were exposed to the same neurohumoral influences, this study supports a premise that has been difficult to test experimentally and one that is critical to the renal body fluid feedback mechanism: that renal perfusion pressure is an important long-term controller of sodium excretion.…”

The Kidney, Hypertension, and Obesity

“…21 Because the 2 kidneys in each animal were exposed to the same neurohumoral influences, these studies were able to quantitate the chronic effects of small changes in renal perfusion pressure per se on electrolyte excretion and renal hemodynamics. These studies demonstrated that relatively small changes in renal artery pressure cause large alterations in sodium and water excretions that persisted as long as renal artery pressure was altered (12 days).…”