The Renin-Angiotensin System

Le, Thu H.; Crowley, Steven D.; Gurley, Susan B.; Coffman, Thomas M.

doi:10.1016/b978-012088488-9.50016-4

Cited by 7 publications

(10 citation statements)

References 254 publications

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“…Normally a reduced Na intake will lead to extracellular volume depletion that will stimulate levels of renin, angiotensin II, and aldosterone (23). The appearance of Na ϩ channel activity in the CCD and CNT in response to Na depletion is mimicked by treatment with aldosterone (28), which interacts directly with principal cells in these segments (42).…”

Section: Resultsmentioning

confidence: 99%

“…In the K-replete state, dietary Na restriction leads to large rates of aldosterone secretion by glomerulosa cells secondary to increased levels of circulating angiotensin II (23). Increases in plasma K ϩ can also elicit aldosterone secretion by the adrenals directly (31).…”

Section: Discussionmentioning

confidence: 99%

“…The two systems share at least one common signaling factor-the adrenocortical steroid aldosterone. This hormone is secreted in response to both a reduction in plasma volume via the renin-angiotensin system and also directly in response to hyperkalemia (15,23,31). It interacts with distal segments of the nephron, called the aldosterone-sensitive distal nephron or ASDN, to promote both Na retention and K excretion by the kidney (42).…”

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confidence: 98%

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Conservation of Na⁺vs. K⁺by the rat cortical collecting duct

Frindt

Houde

Palmer

2011

American Journal of Physiology-Renal Physiology

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Regulation of transport by principal cells of the distal nephron contributes to maintenance of Na(+) and K(+) homeostasis. To assess which of these ions is given a higher priority by these cells, we investigated the upregulation of epithelial Na(+) channels (ENaC) in the rat cortical collecting duct (CCD) during Na depletion with and without simultaneous K depletion. ENaC activity, assessed as whole cell amiloride-sensitive current in split-open tubules, was 260 ± 40 pA/cell in K-repleted but virtually undetectable (3 ± 1 pA/cell) in K-depleted animals. This difference was confirmed biochemically by the reduced amounts of the cleaved forms of both the α-ENaC and γ-ENaC subunits measured in immunoblots. In contrast, in K-depleted rats, simultaneously reducing Na intake did not affect the activity of ROMK channels, assessed as tertiapin-Q-sensitive whole cell currents, in the CCDs. The lack of Na current in K-depleted animals was the result of reduced levels of aldosterone in plasma, rather than a reduced sensitivity to the hormone. However, rats on a low-Na, low-K diet for 1 wk did not excrete more Na than those on a low-Na, control-K diet for the same period of time. Immunoblot analysis indicated increased levels of the thiazide-sensitive NaCl cotransporter and the apical Na-H exchanger NHE3. This suggests that with reduced K intake, Na balance is maintained despite reduced aldosterone and Na(+) channel activity by upregulation of Na(+) transport in upstream segments. Under these conditions, Na(+) transport by the aldosterone-sensitive distal nephron is reduced, despite the low-Na intake to minimize K(+) secretion and urinary K losses.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 98%

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Conservation of Na⁺vs. K⁺by the rat cortical collecting duct

Frindt

Houde

Palmer

2011

American Journal of Physiology-Renal Physiology

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“…THE RENIN-ANGIOTENSIN SYSTEM (RAS) modulates many physiological processes and plays a central role in mechanisms of chronic renal disease (20). The major peptide mediator of the RAS, angiotensin II (Ang II), affects function of cells through specific, seven-transmembrane spanning receptors that can be divided into two pharmacological classes: AT 1 and AT 2 .…”

mentioning

confidence: 99%

Gene expression profiles linked to AT₁angiotensin receptors in the kidney

Makhanova

Crowley

Griffiths

et al. 2010

Physiological Genomics

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To characterize gene expression networks linked to AT(1) angiotensin receptors in the kidney, we carried out genome-wide transcriptional analysis of RNA from kidneys of wild-type (WT) and AT(1A) receptor-deficient mice (KOs) at baseline and after 2 days of angiotensin II infusion (1,000 ng·kg(-1)·min(-1)). At baseline, 405 genes were differentially expressed (>1.5×) between WT and KO kidneys. Of these, >80% were upregulated in the KO group including genes involved in inflammation, oxidative stress, and cell proliferation. After 2 days of angiotensin II infusion in WT mice, expression of ≈805 genes was altered (18% upregulated, 82% repressed). Genes in metabolism and ion transport pathways were upregulated while there was attenuated expression of genes protective against oxidative stress including glutathione synthetase and mitochondrial superoxide dismutase 2. Angiotensin II infusion had little effect on blood pressure in KOs. Nonetheless, expression of >250 genes was altered in kidneys from KO mice during angiotensin II infusion; 14% were upregulated, while 86% were repressed including genes involved in immune responses, angiogenesis, and glutathione metabolism. Between WT and KO kidneys during angiotensin II infusion, 728 genes were differentially expressed; 10% were increased and 90% were decreased in the WT group. Differentially regulated pathways included those involved in ion transport, immune responses, metabolism, apoptosis, cell proliferation, and oxidative stress. This genome-wide assessment should facilitate identification of critical distal pathways linked to blood pressure regulation.

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“…In the presence of low perfusion or blood pressure (reduced cardiac output), the RAAS is activated to release renin from the juxtaglomerular apparatus of the kidneys. Renin cleaves angiotensinogen circulating from the liver to angiotensin I. Angiotensinconverting enzyme converts angiotensin I to the biologically active angiotensin II [ 55 ]. The effects of angiotensin II include direct vasoconstriction, sodium retention through a direct renal tubular effect and increased aldosterone secretion, and stimulation of water intake through the thirst center [ 56 ].…”

Section: Renal Dysfunction and Hfmentioning

confidence: 99%

Pathophysiology of Heart Failure

Capote

Nyakundi

Martinez

et al. 2015

Pathophysiology and Pharmacotherapy of Cardiovascular Disease

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Cardiac dysfunction precipitates changes in vascular function, blood volume, and neurohormonal status. These changes serve as compensatory mechanisms to help maintain cardiac output and arterial blood pressure. However, these compensatory changes over months and years can worsen cardiac function. Overall, the changes in cardiac function associated with heart failure (HF) result in a decrease in cardiac output. This results from a decline in stroke volume that is due to systolic dysfunction, diastolic dysfunction, or a combination of the two. Systolic dysfunction results from a loss of intrinsic inotropy (contractility), most likely due to alterations in signal transduction mechanisms responsible for regulating inotropy. Systolic dysfunction can also result from the loss of viable, contracting muscle as occurs following acute myocardial infarction (MI). Diastolic dysfunction refers to the diastolic properties of the ventricle and occurs when the ventricle becomes less compliant (i.e., "stiffer"), which impairs ventricular fi lling. Both systolic and diastolic dysfunctions result in a higher ventricular end-diastolic pressure, which serves as a compensatory mechanism by utilizing the Frank-Starling mechanism to augment stroke volume. In this chapter, we discuss the various types of cardiac insults and morbidities/conditions that can cause myocardial damage (directly or indirectly) in humans, thereby precipitating chronic systolic HF. Particular focus is given to the pathophysiological mechanisms by which they initiate or aggravate the development of clinical HF.

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The Renin-Angiotensin System

Cited by 7 publications

References 254 publications

Conservation of Na⁺vs. K⁺by the rat cortical collecting duct

Conservation of Na⁺vs. K⁺by the rat cortical collecting duct

Gene expression profiles linked to AT₁angiotensin receptors in the kidney

Pathophysiology of Heart Failure

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The Renin-Angiotensin System

Cited by 7 publications

References 254 publications

Conservation of Na+vs. K+by the rat cortical collecting duct

Conservation of Na+vs. K+by the rat cortical collecting duct

Gene expression profiles linked to AT1angiotensin receptors in the kidney

Pathophysiology of Heart Failure

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Conservation of Na⁺vs. K⁺by the rat cortical collecting duct

Conservation of Na⁺vs. K⁺by the rat cortical collecting duct

Gene expression profiles linked to AT₁angiotensin receptors in the kidney