Renin-angiotensin system generates Angiotensin II that decreases the afferent arteriolar radius. The effect of angiotensin is mediated by calcium mobilization. To compensate for decreased afferent diameter, efferent arteriolar diameters is decreased to a greater extent so that GFR remains almost unaltered. Nor-epinephrine also decreases the afferent arteriolar diameter. A number of physiological conditions like increased potassium concentration constricts (decreases radius) the afferent arterioles – this also happens in diabetic patients. The vasodilation of the afferent arterioles, on the other hand, occurs in response to nitric oxide (NO) secreted by the endothelium.
2. How could you adjust the afferent or efferent radius to compensate for the effect of the reduced pressure on glomerular filtration rate and urine volume? Use the simulation to determine your answer.
Due to the urinary obstruction (closed valve) the intra-glomerular pressure (back pressure) prevents any filtration to occur. There is no difference in the blood pressure and the intra-glomerular pressure and hence no urinary output.
Filtration function of kidney is zero so kidney is non-functional. It may however be noted that other (endocrine) functions of kidney like synthesis of erythropoietin and metabolism in the renal parenchyma would not stop.
Increasing the interstitial concentration of solutes, the reabsorption of solutes decreases as the movement of the solutes is dependent upon the concentration gradient between the interstitial fluid and the lumen of nephrons. In the presence of ADH water moves from the region of low concentration (lumen) to that with higher conetration (interstitial fluid) and hence urine becomes concentrated.
The diabetic patient’s urine contains a lot of glucose. It is due to the higher plasma concentration of glucose (because cells are not able to take up glucose in