investing one way functions of the kidney
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Investing one way functions of the kidney forex sharpe ratio

Investing one way functions of the kidney

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A role for the actions of angiotensin II in the kidney to influence blood pressure is well established. For example, studies by John Hall and associates in the s showed that chronic infusion of low doses of angiotensin II directly into the kidney caused hypertension with impaired natriuresis due to a shift of the pressure-natriuresis relationship In addition, Navar and associates have posited the existence of local and independent control of RAS activity within the kidney influencing sodium excretion and blood pressure regulation ref.

In this hypothetical construct, elevated circulating levels of angiotensin II are associated with accumulation of angiotensin peptides in the kidney, upregulated expression of angiotensinogen, the primary RAS substrate, in proximal tubule epithelium, and increased excretion of angiotensinogen and angiotensin peptides in urine In this feed-forward pathway, angiotensin II acting via type 1 angiotensin AT1 receptors in the kidney induces local activation of the RAS inside the kidney and increases generation of angiotensin II in the lumen of renal tubules, resulting in autocrine and paracrine stimulation of epithelial transporters 24 , Consistent with this idea, recent studies have verified the critical requirement of ACE within the kidney to fully manifest stimulation of sodium transporter expression, renal sodium reabsorption, and hypertension in the setting of RAS activation 26 , A model for local control of RAS activity within the kidney.

Within the kidney circulation and the tubule lumen, ANGII binds to AT1 receptors AT1Rs stimulating AGT transcription in renal epithelial cells and influencing the synthesis and activity of epithelial solute transporters with critical actions to influence body fluid volume and blood pressure. Recent work by Matsusaka and Ichikawa using mice with cell-specific deletion of angiotensinogen from the kidney or liver have called into question some features of this scheme Their study indicated that most of the angiotensinogen and angiotensin II within the kidney arise from angiotensinogen produced by the liver.

Subsequent work by Peti-Peterdi using intravital microscopy is consistent with the idea that the major source of angiotensinogen in the urine is, indeed, the renal epithelium To assess the capacity of RAS activation in the kidney to affect blood pressure, we turned to the strategy of kidney cross transplantation discussed above.

In this case, we carried out transplants between mice with genetic deletion of the AT1A angiotensin receptor and congenic wild-type controls AT1 receptors mediate the classical actions of the RAS including vasoconstriction and stimulation of aldosterone release; the AT1A receptor is the major murine AT1 receptor representing the homologue to the human AT1 receptor. In our cross-transplantation studies, we found that expression of AT1 receptors in the kidney is both necessary and sufficient for induction of angiotensin II-dependent hypertension To further dissect the specific cellular targets of angiotensin II driving the development of hypertension, we subsequently generated mice with cell-specific deletion of AT1 receptors in key cell lineages in the kidney These studies identified the population of AT1 receptors in the proximal tubular epithelium as critical mediators of angiotensin II-dependent hypertension.

Specifically, conditional deletion of AT1A receptors from the proximal tubule provided robust protection from hypertension and facilitated natriuresis by reducing the accumulation of key epithelial sodium transporters In addition, recent studies have suggested that direct actions of angiotensin II on AT1 receptors in the collecting duct can directly stimulate the activity of the epithelial sodium channel ENaC 33 and Figure 1.

Moreover, relative to aldosterone, these direct effects of angiotensin II in the collecting duct have a predominant effect on ENaC abundance and activity in angiotensin II-dependent hypertension. In aggregate, these studies indicate that the powerful RAS mediates its effects on blood pressure through direct effects on the kidney.

Furthermore, there is compartmentalized control of the RAS along the nephron contributing to hypertension pathogenesis. AT1 receptors in the zona glomerulosa of the adrenal gland stimulate aldosterone release, making aldosterone a downstream effector of the RAS.

Classically, activation of the mineralocorticoid receptor MR in aldosterone-sensitive nephron segments stimulates assembly and translocation of the subunits of the ENaC. Similarly, activating mutations in the gene encoding the MR also cause hypertension that is exacerbated by steroid hormone alterations during pregnancy In addition to stimulation of sodium reabsorption as discussed above, aldosterone also has important actions to promote secretion of potassium into urine.

Until recently, it has not been clear how the kidney distinguishes between the need for these distinct functions. Recent studies from Shibata et al. They showed that phosphorylation of S on the MR prevents ligand binding. In the kidney, this form of the MR is present only in intercalated cells of the collecting duct where its phosphorylation is differentially regulated by volume depletion and hyperkalemia. For example, in volume depletion, the MR in intercalated cells is dephosphorylated, resulting in potentiation of chloride and sodium reabsorption, allowing a distinct response to volume depletion Although the MR is classically activated by aldosterone, recent studies suggest that the small GTPase Rac1 may promote hypertension through an MR-dependent pathway, even in the setting of suppressed aldosterone levels 38 and Figure 1.

Some of the most powerful lines of evidence implicating a predominant role for the kidney in the regulation of blood pressure are the classic studies from the Lifton laboratory, which have defined the genetic basis of virtually all of the known Mendelian disorders associated with abnormal blood pressure phenotypes in humans 36 , 39 , In each case, these mutations impact sodium and fluid reabsorption along the nephron This discovery triggered intense study of these unique kinases, identifying roles for WNK1 and WNK4 in the regulation of sodium and potassium flux in the distal nephron refs.

The NCC represents a major pathway for sodium reabsorption in the distal nephron and is the target for thiazide diuretics, which are effective and widely used antihypertensive agents Mechanisms regulating sodium and potassium flux in the distal nephron. Individual mutations in WNK1, WNK4, cullin 3, and KLHL3 generate a similar phenotype: the syndrome of pseudo-hypoaldosteronism type II PHAII , a Mendelian syndrome characterized by the unusual combination of hypertension and hyperkalemia, highlighting the continuity and importance of this pathway in the normal control of sodium and potassium handling in the distal nephron.

Enhanced activity of NCC through modulation of WNKs seems to be a final common pathway for the development of hypertension in a number of scenarios. In addition, calcineurin inhibitors, commonly used to treat autoimmune disease and prevent transplant rejection, frequently cause hypertension. Recent studies by Ellison and colleagues indicate that the mechanism of hypertension associated with calcineurin inhibitor use involves stimulation of NCC through upregulation of WNK3 Furthermore, abrogation of this pathway for ubiquitination resulted in intracellular accumulation of WNK4.

Finally, this alteration in WNK4 ubiquitination reduced levels of cell surface-associated ROMK, which, in kidney tubules, results in diminished excretion of potassium in urine, leading to hyperkalemia characteristic of PHAII These studies raise a number of interesting questions regarding the role of this pathway in regulating NCC, its role in global regulation of electrolyte excretion in the distal nephron and, perhaps most importantly, the relevance of these findings to more common forms of hypertension.

Salt sensitivity, defined as an exaggerated change in blood pressure in response to extremes in dietary salt intake, is relatively common and is associated with an increased risk for the development of hypertension. Classic Guytonian models suggest that a defect in sodium excretion by the kidney is the basis for salt sensitivity, with impaired elimination of sodium during high-salt feeding leading directly to expanded extracellular fluid volume, which promotes increased blood pressure 8.

This model presumes that the two major components of extracellular volume within the intravascular and interstitial spaces are in equilibrium. As such, accumulation of sodium would be accompanied by commensurate retention of water to maintain iso-osmolality and would thereby proportionally expand the intravascular volume. On the other hand, recent innovative studies by Titze and associates indicate that sodium handling is more complex than this classical two-compartment model; the interstitium of the skin may act as a sodium reservoir, buffering the impact of sodium accumulation on intravascular volume and blood pressure During high-salt feeding, sodium accumulates in the subdermal interstitium at hypertonic concentrations in complexes with proteoglycans 52 , Macrophages infiltrating the interstitial space sense hypertonicity caused by this accumulation of sodium in excess of water, triggering expression of TonEBP, a transcription factor regulating the expression of osmo-protective genes.

Depletion of macrophages, cell-specific deletion of TonEBP from macrophages, or specific blockade of VEGF-C prevented hyperplasia of lymphatic vessels and enhanced the level of sodium-dependent hypertension 52 — 54 , demonstrating that this pathway has a key role in the extrarenal control of sodium and fluid volumes.

The nature and regulation of proteoglycans mediating hypertonic storage of sodium in the skin, as well as mechanisms for control of macrophage gene expression by hypertonicity, remain unclear. The authors have found elevated plasma levels of VEGF-C in patients with refractory hypertension, indicating that this system might be perturbed in the human disorder. Consistent with this notion, a recent report showed that overexpression of VEGF-C lowered blood pressure in a model of salt-sensitive hypertension, whereas blocking VEGF-C activity exaggerated the severity of hypertension Nonetheless, chronic hypertension in humans is a complex disorder; it is possible that the observed elevation in VEGF-C levels may reflect tissue resistance to VEGF-C or even a compensatory response.

The specific relevance of this pathway in human hypertension and its potential value as a therapeutic target are interesting questions for future studies. A subsequent study by Titze et al. In this enclosed, restricted environment, subjects were provided diets with scrupulously defined sodium content while undergoing continuous monitoring of a range of parameters including urinary sodium excretion, blood pressure, body weight, and steroid hormone levels.

Aspects of these findings are consistent with Guytonian principles whereby abrupt increases of salt intake caused expansion of total-body sodium and extracellular water, brisk suppression of aldosterone, and consequent increases in urinary sodium excretion. However, the authors unexpectedly found considerable day-to-day variability in 24 hour urinary sodium excretion, accompanied by fluctuations in excretion of aldosterone, cortisol, and cortisone, despite the fixed sodium content in the diet.

Power spectral analysis demonstrated a regular pattern, peaking with a period interval of about 6 days. Regular fluctuations of total body sodium TBNa , estimated using bioimpedance spectroscopy, were also observed but with much longer periodicity. This uncoupling of changes in TBNa from body weight and blood pressure may reflect this process of sodium storage in the subdermal interstitium Along with the endogenous rhythms of sodium balance, the authors also observed increases in blood pressure and urinary aldosterone excretion following night shift duty, reminiscent of mouse studies wherein disruption of the clock gene Cry is associated with hypertension caused by chronically enhanced aldosterone levels A prominent emerging area of hypertension research over the past decade suggests that the immune system may provide an independent cardiovascular control mechanism, whereby its cellular constituents and inflammatory mediators regulate blood pressure.

Moreover, we suggest below that immunological effector mechanisms impacting blood pressure can be mapped to the kidney. Although not rigorously controlled, small clinical studies indicate that broad immunosuppression lowers blood pressure in hypertensive patients with rheumatologic disorders 58 , pointing to a role for immune activation in human hypertension.

Within the innate immune system, adoptive transfer of monocytes, which are precursors to dendritic cells and macrophages, promotes the hypertensive response to angiotensin II Studies by Guzik and associates convincingly established a role for the adaptive immune response in hypertension pathogenesis, showing that mice with targeted disruption of the recombinase-activating gene-1 Rag1 , and thus lacking T and B cells, were resistant to the development of hypertension induced by chronic infusion of angiotensin II.

A modified diet for chronic kidney disease may include adjustments to your intake of the following food items:. Medications make up the next layer of both offense and defense in the treatment of low kidney function. They are frequently used to control common symptoms and related medical conditions of chronic kidney disease. Diet modification and medications can help delay the progression of chronic kidney disease, especially in the early stages. If the disease progresses, however, other forms of treatment may become necessary.

Research is ongoing to find new treatments and interventions that will someday soon render dialysis and kidney donation unnecessary. The Harvard Stem Cell Institute is just one of many institutions exploring a wide variety of options, such as experimental treatments.

Pirfenidone is an anti-scarring drug used to treat idiopathic pulmonary fibrosis. In this way, it could stabilize and preserve kidney function in kidney disease patients with either type 1 or type 2 diabetes. Living with kidney disease is complicated. Join hundreds of people with kidney disease who trust Responsum for CKD to provide vetted medical information, a space for community, and resources to help them live better.

A modified diet for chronic kidney disease may include adjustments to your intake of the following food items: Sodium: Sodium raises blood pressure, and high blood pressure hypertension is a primary cause and complication of CKD. Sodium is widely used as a preservative. Your intake can be reduced by eating fresh and minimally processed foods instead of canned or pre-packaged ones. Protein: When metabolized, protein creates wastes that the kidneys may no longer be able to process optimally.

Reducing your protein intake can decrease the burden on your kidneys. If and when you start dialysis, however, you may need to increase your protein intake again. Alcohol: Alcohol can raise your blood pressure and cause dehydration—both of which are especially dangerous for people with CKD.

As a liquid, alcohol must also be added to the equation when calculating your fluid intake. Too much phosphorus in your blood can leach calcium from your bones, leaving them weak and brittle. Dairy products are high in phosphorus, so your doctor may limit your dairy consumption. Calories: Dietary limitations, along with an often severe and prolonged loss of appetite, can lead to malnutrition.

Sugar: Sugar can help with your short-term energy, but it can also be dangerous if you have diabetes or are prediabetic. Like hypertension, diabetes is both a cause and a complication of chronic kidney disease. Your doctor may reduce your sugar intake. Dietary supplements: People with CKD often have insufficient amounts of vitamins and minerals in their blood. Do not attempt to supplement without consulting your physician.

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