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Bioartificial organs
Published in Ronald L. Fournier, Basic Transport Phenomena in Biomedical Engineering, 2017
The kidney not only provides a filtration and waste removal function but also provides several other important functions that are important to the metabolic, immune, and endocrine systems of the body. For example, erythropoietin is released by specialized cells found in the kidney in response to hypoxia. Erythropoietin is a major stimulus for the production of red blood cells in the bone marrow. Uremic patients therefore suffer from anemia. Low blood pressure causes the release of renin from the juxtaglomerular cells that are found in the kidney. Renin initiates the formation of angiotensin II, a potent vasoconstrictor, that results in an increase in blood pressure. Angiotensin II also acts on the kidneys, decreasing the excretion of both salt and water. This expands the extracellular fluid volume with the result that the blood pressure is increased. The kidneys are also responsible for the conversion of vitamin D into a substance* that promotes the absorption of calcium from the intestine. Without this substance, the bones become severely weakened because of the loss of calcium. These other very important functions that are performed by the healthy kidney are therefore compromised as a result of kidney failure.
Hormonal Regulation of Sodium, Potassium, Calcium, and Magnesium Ions
Published in Robert B. Northrop, Endogenous and Exogenous Regulation and Control of Physiological Systems, 2020
Guyton59 shows that the GFR is autoregulated. That is, the GFR normally remains constant at 125 ml/min over a MAP range of 75 to 160 mmHg, with PCO remaining constant. This autoregulation occurs through modulation of the blood pressure in the Bowman’s capsule by local hormonal control of the diameters of the efferent and afferent arterioles supplying the capsule. An optimum autoregulated GFR is necessary to optimally filter the blood in the capsule and reabsorb water, ions, glucose, etc. in the tubules at the normal rates. If the GFR is too high, there is not enough time for absorption in the tubules; if it is too low, there is excess absorption, urine output is too low, and the body cannot eliminate urea properly. The mechanism whereby each of the 2.4 million nephrons adjusts its GFR involves their juxtaglomerular complexes, which by local hormonal control modulate the hydraulic resistance of the afferent and efferent glomerular arterioles, thus adjusting Peff and hence the individual GFR. A portion of the thick ascending limb of the renal tubule passes in close contact with the glomerular arterioles. Specialized dense epithelial cells in the juxtaglomerular portion of the ascending tubule, forming the macula densa, lie against specialized smooth muscle cells in the arteriole walls called juxtaglomerular cells. Guyton states that a low GFR causes excessive absorption of Na+ and C1− over the tubule so that the tubular fluid at the region of the macula densa is hypotonic. This hypotonic fluid in some way causes the macula densa cells to secrete some hormone that causes the juxtaglomerular muscle cells to secrete the protein enzyme renin. Renin causes the local formation of angiotensin II. Angiotensin II causes the smooth muscle cells of the efferent arteriole to contract, decreasing the diameter of the efferent arteriole, which raises its hydraulic resistance and the Peff in the Bowman’s capsule. An increase in Peff of course raises the GFR. What we have described is a local type 0 regulator for GFR which operates on each individual glomerulus in the kidneys.
Device profile of the MobiusHD EVBA system for the treatment of resistant hypertension: overview of its mechanism of action, safety and efficacy
Published in Expert Review of Medical Devices, 2020
Mark C. Bates, Gregg W. Stone, Chao-Yin Chen, Wilko Spiering
Hemodynamic balance is maintained through a complex neurohumoral network of pressure, stretch, and volume sensing feedback loops (Figure 6). The signals impacting BP include local paracrine-driven changes in vessel tone and juxtaglomerular cell-mediated sodium retention, systemic modulation in enzymatic cascades including the renin-angiotensin system, and central – as well as peripheral-mediated changes in adrenergic tone. The complexity of these biochemical, neurologic, and cellular interactions, along with the heterogeneity of hypertensive patient phenotypes, may explain why no single feedback loop derangement has been consistently identified as the predominant cause of primary hypertension. It also may explain why the cure for hypertension has remained elusive.