Renin and Aldosterone Measurements in the Management of Arterial Hypertension

Viola, Andrea; Monticone, Silvia; Burrello, Jacopo; Buffolo, Fabrizio; Lucchiari, Manuela; Rabbia, Franco; Williams, Tracy Ann; Veglio, Franco; Mengozzi, Giulio; Mulatero, Paolo

doi:10.1055/s-0035-1548868

Cited by 28 publications

(26 citation statements)

References 87 publications

(109 reference statements)

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“…High‐renin hypertension is characterized by a disproportionate and persistent increase in peripheral vascular resistance, whereas low‐renin hypertension may be secondary to an increase in total body sodium concentration. In normal renin hypertension, renin and sodium remain within a normal range and fail to compensate appropriately . In addition to exhibiting tendencies toward hypertension and proteinuria, Greyhounds have also been documented to have disparities in the concentration of serum electrolytes regulated by the RAAS.…”

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confidence: 84%

“…In hypertensive states, the presence of either hyperreninemia or primary total body sodium excess is inappropriate and provides the basis for elevated blood pressure. In humans, hypertension is further characterized by high, low, or normal plasma renin activity (PRA) . High‐renin hypertension is characterized by a disproportionate and persistent increase in peripheral vascular resistance, whereas low‐renin hypertension may be secondary to an increase in total body sodium concentration.…”

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confidence: 99%

“…In humans, hypertension is further characterized by high, low, or normal plasma renin activity (PRA). 12 High-renin hypertension is characterized by a disproportionate and persistent increase in peripheral vascular resistance, whereas lowrenin hypertension may be secondary to an increase in total body sodium concentration. In normal renin hypertension, renin and sodium remain within a normal range and fail to compensate appropriately.…”

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confidence: 99%

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The Renin‐Angiotensin‐Aldosterone System in Greyhounds and Non‐Greyhound Dogs

Martinez

Kellogg

Iazbik

et al. 2017

Veterinary Internal Medicne

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BackgroundThe renin‐angiotensin‐aldosterone system (RAAS) regulates blood pressure, electrolyte homeostasis, and renal function. Blood pressure, serum sodium concentrations, and urinary albumin excretion are higher in Greyhounds than other purebred and mixed‐breed dogs.HypothesisAlterations in the RAAS in Greyhounds are associated with hemodynamic and clinicopathologic differences observed in the breed.AnimalsClinically healthy Greyhound and non‐Greyhound dogs consecutively enrolled as blood donors (n = 20/group).MethodsProspective study. Standard chemical analysis was performed on serum and urine. Serum angiotensin‐converting enzyme (ACE) activity was determined by fluorometric assay. All other RAAS hormones were determined by radioimmunoassay. Symmetric dimethylarginine (SDMA) was measured by immunoassay. Measurements were compared to blood pressure and urine albumin concentration. Data are presented as mean ± SD or median, range.ResultsSerum creatinine (1.5 ± 0.2 vs 1.0 ± 0.1 mg/dL, P < .001), sodium (149, 147–152 vs 148, 146–150 mEq/L, P = .017), and SDMA (16.1 ± 2.9 vs 12.2 ± 1.8 μg/dL, P < .001) were significantly higher in Greyhounds versus non‐Greyhounds, respectively. Plasma renin activity (0.69, 0.10–1.93 vs 0.65, 0.27–2.93 ng/mL/h, P = .60) and ACE activity (4.5, 2.1–8.5 vs 4.6, 2.1–11.4 activity/mL; P = .77) were similar between groups and did not correlate with higher systolic pressures and albuminuria in Greyhounds. Plasma aldosterone concentration was significantly lower in Greyhounds versus non‐Greyhounds (11, 11–52 vs 15, 11–56 pg/mL, respectively, P = .002).Conclusions and clinical importanceBasal RAAS activation did not differ between healthy Greyhounds and non‐Greyhounds. Lower aldosterone concentration in Greyhounds is an appropriate physiologic response to higher serum sodium concentration and blood pressure, suggesting that angiotensin II effects in the renal tubule predominate over those of aldosterone.

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confidence: 99%

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The Renin‐Angiotensin‐Aldosterone System in Greyhounds and Non‐Greyhound Dogs

Martinez

Kellogg

Iazbik

et al. 2017

Veterinary Internal Medicne

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“…Na + /K + -ATPase, located in the basolateral membrane of the kidney tubule cells, is responsible for the reabsorption of large amounts of Na + principally in the proximal tubule cells, where the electrochemical Na + gradient generated by the pump drives the majority of the water and solutes reabsorption in that nephron segment either by transcellular and paracellular pathways [6]. Different hormones and autacoids modulate the ion pumps involved in Na + homeostasis, and this includes DA (natriuretic) and the classic anti-natriuretic renin/ angiotensin/aldosterone system (RAAS) [7]. …”

Section: Introductionmentioning

confidence: 99%

L-Tyr-Induced Phosphorylation of Tyrosine Hydroxylase at Ser40: An Alternative Route for Dopamine Synthesis and Modulation of Na+/K+-ATPase in Kidney Cells

Taveira-da-Silva

Sampaio

Vieyra

et al. 2019

Kidney Blood Press Res

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Background/Aims: Dopamine (DA) is a natriuretic hormone that inhibits renal sodium reabsorption, being Angiotensin II (Ang II) its powerful counterpart. These two systems work together to maintain sodium homeostasis and consequently, the blood pressure (BP) within normal limits. We hypothesized that L-tyrosine (L-tyr) or L-dihydroxyphenylalanine (L-dopa) could inhibit the Na⁺/K⁺-ATPase activity. We also evaluated whether L-tyr treatment modulates Tyrosine Hydroxylase (TH). Methods: Experiments involved cultured LLCPK₁ cells treated with L-tyr or L-dopa for 30 minutes a 37°C. In experiments on the effect of Dopa Descarboxylase (DDC) inhibition, cells were pre incubated for 15 minutes with 3-Hydroxybenzylhydrazine dihydrochloride (HBH), and them L-dopa was added for 30 minutes. Na⁺/K⁺-ATPase activity was quantified colorimetrically. We used immunoblotting and immunocytochemistry to identify the enzymes TH, DDC and the dopamine receptor D₁R in LLCPK₁ cells. TH activity was accessed by immunoblotting (increase in the phosphorylation). TH and DDC activities were also evaluated by the modulation of the Na⁺/K⁺-ATPase activity, which can be ascribed to the synthesis of dopamine. Results: LLCPK₁ cells express the required machinery for DA synthesis: the enzymes TH, and (DDC) as well as its receptor D₁R, were detected in control steady state cells. Cells treated with L-tyr or L-dopa showed an inhibition of the basolateral Na⁺/K⁺-ATPase activity. We can assume that DA formed in the cytoplasm from L-tyr or L-dopa led to inhibition of the Na⁺/K⁺-ATPase activity compared to control. L-tyr treatment increases TH phosphorylation at Ser⁴⁰ by 100%. HBH, a specific DDC inhibitor; BCH, a LAT2 inhibitor; and Sch 23397, a specific D₁R antagonist, totally suppressed the inhibition of Na⁺/K⁺-ATPase activity due to L-dopa or L-tyr administration, as indicated in the figures. Conclusion: The results indicate that DA formed mainly from luminal L-tyr or L-dopa uptake by LAT2, can inhibit the Na⁺/K⁺-ATPase. In addition, our results showed for the very first time that TH activity is also significantly increased when the cells were exposed to L-tyr.

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“…The first enzymatic reaction, converting angiotensinogen into angiotensin I, is catalysed by the aspartyl‐protease renin, which is produced by the juxtaglomerular cells in response to a drop in renal perfusion pressure and/or the activation of the sympathetic nervous system . Since the first reports aiming at measuring plasma renin activity (PRA) in 1964, significant knowledge has been gained on the importance and clinical impact of assessing renin status in the management of arterial hypertension . Traditionally, the evaluation of the renin profiling was based on plasma renin activity (PRA), a radioimmuno assay (RIA) that measures the quantity of angiotensin I generated as a function of time .…”

Section: Introductionmentioning

confidence: 99%

Diagnostic approach to low‐renin hypertension

Monticone

Losano

Tetti

et al. 2018

Clinical Endocrinology

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Renin-angiotensin-aldosterone system (RAAS) plays a crucial role in maintaining water and electrolytes homoeostasis, and its deregulation contributes to the development of arterial hypertension. Since the historical description of the "classical" RAAS, a dramatic increase in our understanding of the molecular mechanisms underlying the development of both essential and secondary hypertension has occurred. Approximatively 25% of the patients affected by arterial hypertension display low-renin levels, a definition that is largely arbitrary and depends on the investigated population and the specific characteristics of the assay. Most often, low-renin levels are expression of a physiological response to sodium-volume overload, but also a significant number of secondary hereditary or acquired conditions falls within this category. In a context of suppressed renin status, the concomitant examination of plasma aldosterone levels (which can be inappropriately elevated, within the normal range or suppressed) and plasma potassium are essential to formulate a differential diagnosis. To distinguish between the different forms of low-renin hypertension is of fundamental importance to address the patient to the proper clinical management, as each subtype requires a specific and targeted therapy. The present review will discuss the differential diagnosis of the most common medical conditions manifesting with a clinical phenotype of low-renin hypertension, enlightening the novelties in genetics of the familial forms.

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Renin and Aldosterone Measurements in the Management of Arterial Hypertension

Cited by 28 publications

References 87 publications

The Renin‐Angiotensin‐Aldosterone System in Greyhounds and Non‐Greyhound Dogs

The Renin‐Angiotensin‐Aldosterone System in Greyhounds and Non‐Greyhound Dogs

L-Tyr-Induced Phosphorylation of Tyrosine Hydroxylase at Ser<sup>40</sup>: An Alternative Route for Dopamine Synthesis and Modulation of Na<sup>+</sup>/K<sup>+</sup>-ATPase in Kidney Cells

Diagnostic approach to low‐renin hypertension

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