Pressure natriuresis and the renal control of arterial blood pressure
Insights from Studies of the Renal Regulation of Arterial Blood Pressure .. A renal pressure-natriuresis line (sometimes called a “renal function curve”) was .. We should bear in mind, as we interpret the results of the renal function tests for all. Pressure natriuresis is impaired in hypertension and mechanistic insight into Indeed, the relationship between renal perfusion and sodium. Circadian rhythm of natriuresis is disturbed in nondipper type of essential hypertension Relationships between night-day ratios of either UNa V (top; in millimoles 10% reduction in mean arterial pressure (MAP) from daytime to nighttime on a These findings showed that the circadian rhythm of renal sodium excretion.
Pressure—natriuresis lines for eight hypertensive adult patients before open circles and after closed circles administration of a thiazide diuretic mefruside 25 mg daily. Urinary sodium excretion rate was measured after several periods of 7 days of constant daily sodium intake of between 1 and 18 g NaCl and systemic mean arterial pressure plotted as a function of sodium excretion. Data from Saito and Kimura Note that the untreated hypertensive patients showed a marked dependence of mean arterial pressure MAP on sodium excretion, whilst thiazide administration reduced this dependence and also lowered MAP.
We have already noted the concept that this intercept gives information about the net filtration pressure at the glomerulus, implying that, if the intercept were to remain unchanged during administration of a drug, then for any given value of MAP the value of Pglom would be the same with or without the drug.
Figure 2 contains data obtained from the same patients under the condition of taking the antihypertensive thiazide-like diuretic mefruside. Mefruside moved the line toward the horizontal and lowered MAP over the range of sodium intakes. It is interesting to consider what the significance would have been were a drug like mefruside able to render the line completely horizontal so that MAP became independent of sodium intake.
If the imaginary drug were capable of inhibiting all active reabsorption of solutes from the renal tubule, we would then have a situation where the filtered sodium load entering the renal tubule from the glomerulus in a very low GFR requiring only a small net glomerular filtration pressure was all lost in the urine!
In this light, it may seem surprising that the normal healthy pressure-natriuresis line is indeed fairly flat, as has been seen in four-data-point plots obtained from dogs Hall et al.
Regulation of GFR
Indeed, the flatness of the relationship in health is a remarkable reflection of how the neural, humoral, or intrinsic regulation of the kidney is capable of permitting large changes in the renal elimination of salt without there being a large change in MAP. Bie has noted that modest acute body loading with sodium over 2—3 h can lead to a rapid substantial change in renal sodium excretion rate without a change in MAP, and that this phenomenon is strong evidence either for a vigorous macular densa tubulo-glomerular feedback mechanism, or for a further, as yet unidentified, regulator of renal function Bie, Whether the mechanisms regulating these short-term responses are also those acting in the longer term remains to be seen.
After analyzing the effects of different families of drugs on renal hemodynamics in the sections below, we shall be in a position to assess this apparent inconsistency of mefruside yielding a fairly flat pressure-natriuresis line, and also explore those situations in which antihypertensive drugs leave the gradient of the pressure-natriuresis line unchanged, and when they can make it steeper. We shall see that the pressure natriuresis line provides information that could usefully guide therapy if it were to be more widely available and its significance better understood.
The net glomerular filtration pressure is the sum of these forces. Measures of GFR see lab 7A on Testing Renal Function In a single nephron, the rate of filtration is a function of the net filtration pressure, the permeability of the filtration membrane, and the surface area available for filtration.
The measured GFR reflects these factors, and of course, the total number of functioning nephrons.
As well, GFR is usually normalized to body surface area to account for individuals of different sizes. GFR can be directly measured by measuring the renal clearance of inulin.
Inulin is a plant carbohydrate that is neither reabsorbed nor secreted, thus the renal clearance of inulin volume of blood per unit time from which inulin is removed is completely due to filtration. However, because inulin must be infused, in practice it is simpler to gauge kidney function by looking at an endogenous substance, namely creatinine, a metabolic breakdown product of skeletal muscle creatine.
The renal clearance of creatinine can be used to estimate the GFR.
Mechanisms of pressure natriuresis.
Alternatively, just the serum creatinine plasma concentration of creatinine may be measured to monitor kidney function. In general, any factor that reduces the number of nephrons can over time reduce the GFR. GFR normally declines with age, but this decline occurs much more rapidly in individuals with chronic kidney disease. Hypertension is the major modifiable risk factor for cardiovascular and renal disease and there is no cut off for risk, which doubles with every 20 mmHg increase in systolic blood pressure SBP; Lewington et al.
The prevalence of both diseases is increasing. One hundred years ago, cardiovascular disease was a minor cause of death, but now causes one-third of deaths worldwide Lim et al.ADH effects on blood pressure - Renal system physiology - NCLEX-RN - Khan Academy
Clearly, hypertension presents a global health challenge and exerts a large societal and economic burden. This quantitative threshold has reduced over the years and even those in the pre-hypertensive range SBP — mmHg have an increased risk profile Toprak et al.
The benefits of treating high blood pressure are strongly evidenced by clinical trial but at a population level, control rates are poor Chobanian, Part of the challenge is identifying affected individuals since they often do not feel unwell and routine blood pressure BP screening in the clinic is an unreliable indicator of the steady state.
Research can bridge this knowledge gap but there is no silver bullet: