Abstract
BackgroundData on blood flow regulation, renal filtration, and urine output in salt-sensitive Dahl S rats fed on high-salt (hypertensive) and low-salt (prehypertensive) diets and salt-resistant Dahl R rats fed on high-salt diets were analyzed using a mathematical model of renal blood flow regulation, glomerular filtration, and solute transport in a nephron.ResultsThe mechanism of pressure-diuresis and pressure-natriuresis that emerges from simulation of the integrated systems is that relatively small increases in glomerular filtration that follow from increases in renal arterial pressure cause relatively large increases in urine and sodium output. Furthermore, analysis reveals the minimal differences between the experimental cases necessary to explain the observed data. It is determined that differences in renal afferent and efferent arterial resistances are able to explain all of the qualitative differences in observed flows, filtration rates, and glomerular pressure as well as the differences in the pressure-natriuresis and pressure-diuresis relationships in the three groups. The model is able to satisfactorily explain data from all three groups without varying parameters associated with glomerular filtration or solute transport in the nephron component of the model.ConclusionsThus the differences between the experimental groups are explained solely in terms of difference in blood flow regulation. This finding is consistent with the hypothesis that, if a shift in the pressure-natriuresis relationship is the primary cause of elevated arterial pressure in the Dahl S rat, then alternation in how renal afferent and efferent arterial resistances are regulated represents the primary cause of chronic hypertension in the Dahl S rat.
Highlights
Data on blood flow regulation, renal filtration, and urine output in salt-sensitive Dahl S rats fed on high-salt and low-salt diets and salt-resistant Dahl R rats fed on high-salt diets were analyzed using a mathematical model of renal blood flow regulation, glomerular filtration, and solute transport in a nephron
The 19 adjustable parameters invoked in this model are not identifiable for a given experimental group based on the six data sets represented in these figures
One school of thought maintains that because renal blood flow and glomerular filtration rate do not change over a wide range of arterial pressure, the observed decrease in sodium and water reabsorption associated with an increase in pressure could not be substantially impacted by an increase in the rate of filtrate delivery to nephrons
Summary
Data on blood flow regulation, renal filtration, and urine output in salt-sensitive Dahl S rats fed on high-salt (hypertensive) and low-salt (prehypertensive) diets and salt-resistant Dahl R rats fed on high-salt diets were analyzed using a mathematical model of renal blood flow regulation, glomerular filtration, and solute transport in a nephron. Other investigators suggest that angiotensin II- and saltinduced increases in sympathetic nervous activity in the vasculature may be a primary causal factor in saltsensitive hypertension while the shift in the renal pressure-natriuresis relationship may not [9,10,11]. Is it unclear whether and when the observed changes in the pressure-natriuresis relationship are causes or consequences of chronic hypertension (or in some way both), it remains unclear what specific aspects of renal physiology are altered in salt-sensitive hypertension, underlying the observed changes in the pressurenatriuresis and pressure-diuresis relationships
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