Diuretic-induced hypokalaemia: an updated review

2021 ◽  
pp. postgradmedj-2020-139701
Author(s):  
Ziying Lin ◽  
Louisa Y. F. Wong ◽  
Bernard M. Y. Cheung
Keyword(s):  
Black People ◽  
Salt Intake ◽  
Clinical Manifestations ◽  
Renin Angiotensin System ◽  
Reduce Blood Pressure ◽  
Potassium Depletion ◽  
Angiotensin System ◽  
Fatal Arrhythmia ◽  
Life Threatening ◽  
Vegetables And Fruits

Diuretic-induced hypokalaemia is a common and potentially life-threatening adverse drug reaction in clinical practice. Previous studies revealed a prevalence of 7%–56% of hypokalaemia in patients taking thiazide diuretics. The clinical manifestations of hypokalaemia due to diuretics are non-specific, varying from asymptomatic to fatal arrhythmia. Diagnosis of hypokalaemia is based on the level of serum potassium. ECG is useful in identifying the more severe consequences. A high dosage of diuretics and concomitant use of other drugs that increase the risk of potassium depletion or cardiac arrhythmias can increase the risk of cardiovascular events and mortality. Thiazide-induced potassium depletion may cause dysglycaemia. The risk of thiazide-induced hypokalaemia is higher in women and in black people. Reducing diuretic dose and potassium supplementation are the most direct and effective therapies for hypokalaemia. Combining with a potassium-sparing diuretic or blocker of the renin–angiotensin system also reduces the risk of hypokalaemia. Lowering salt intake and increasing intake of vegetables and fruits help to reduce blood pressure as well as prevent hypokalaemia.

scholarly journals Activation of the Renin-Angiotensin System Mediates the Effects of Dietary Salt Intake on Atherogenesis in the Apolipoprotein E Knockout Mouse

Hypertension ◽  
2012 ◽  
Vol 60 (1) ◽  
pp. 98-105 ◽  
Author(s):  
Chris Tikellis ◽  
Raelene J. Pickering ◽  
Despina Tsorotes ◽  
Olivier Huet ◽  
Jaye Chin-Dusting ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Knockout Mouse ◽  
Salt Intake ◽  
Renin Angiotensin System ◽  
Dietary Salt ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Dietary Salt Intake

Atrial Natriuretic Peptide: Regulator of Chronic Arterial Blood Pressure

Physiology ◽  
2000 ◽  
Vol 15 (3) ◽  
pp. 143-149 ◽  
Author(s):  
Luis Gabriel Melo ◽  
Stephen C. Pang ◽  
Uwe Ackermann
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Salt Intake ◽  
Gene Knockout ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Arterial Blood ◽  
Gene Knockout Mouse ◽  
Atrial Natriuretic

Recent findings in atrial natriuretic peptide (ANP) transgenic and gene knockout mouse models uncovered a tonic vasodilatory effect of this hormone that contributes to chronic blood pressure homeostasis. With elevated salt intake, ANP-mediated antagonism of the renin-angiotensin system is essential for blood pressure constancy, suggesting that a deficiency in ANP activity may underlie the etiology of sodium-retaining disorders.

Compensatory response to hemorrhage in conscious dogs on normal and low salt intake

1983 ◽  
Vol 244 (3) ◽  
pp. H351-H356 ◽  
Author(s):  
R. I. Kopelman ◽  
V. J. Dzau ◽  
S. Shimabukuro ◽  
A. C. Barger
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Salt Intake ◽  
Renin Angiotensin System ◽  
Conscious Dogs ◽  
Converting Enzyme ◽  
Compensatory Response ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Low Salt

The compensatory response to moderately severe hemorrhage (30 ml/kg) was studied in chronically catheterized conscious dogs maintained on normal and low salt intake. Although the fall in blood pressure and the increase in heart rate were similar in the two salt states, the salt-restricted animals had significantly greater rises in plasma renin activity and plasma catecholamines following hemorrhage than did the normal salt dogs. To compare further the relative roles of the alpha-adrenergic system and the renin-angiotensin system in the maintenance of blood pressure following hemorrhage, pharmacologic blockade with either phentolamine or converting enzyme inhibitor was performed 20 min after the completion of the hemorrhage. These latter experiments demonstrated that salt restriction resulted in a significantly greater role for the renin-angiotensin system. Moreover, interruption of the renin-angiotensin system blunted the anticipated rise in catecholamines and heart rate during the additional hypotension induced by converting enzyme blockade after hemorrhage.

High salt intake and the brain renin–angiotensin system in Dahl salt-sensitive rats

2001 ◽  
Vol 19 (1) ◽  
pp. 89-98 ◽  
Author(s):  
Xigeng Zhao ◽  
Roselyn White ◽  
Bing S. Huang ◽  
James Van Huysse ◽  
Frans H. H. Leenen
Keyword(s):  
Salt Intake ◽  
Renin Angiotensin System ◽  
High Salt ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
High Salt Intake ◽  
The Brain

scholarly journals Uric Acid and Hypertension: An Update With Recommendations

2020 ◽  
Vol 33 (7) ◽  
pp. 583-594 ◽  
Author(s):  
Laura G Sanchez-Lozada ◽  
Bernardo Rodriguez-Iturbe ◽  
Eric E Kelley ◽  
Takahiko Nakagawa ◽  
Magdalena Madero ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Uric Acid ◽  
Large Scale ◽  
Salt Intake ◽  
Renin Angiotensin System ◽  
Serum Urate ◽  
Primary Hypertension ◽  
Angiotensin System ◽  
Xanthine Oxidase Inhibitors ◽  
Key Factor

Abstract The association between increased serum urate and hypertension has been a subject of intense controversy. Extracellular uric acid drives uric acid deposition in gout, kidney stones, and possibly vascular calcification. Mendelian randomization studies, however, indicate that serum urate is likely not the causal factor in hypertension although it does increase the risk for sudden cardiac death and diabetic vascular disease. Nevertheless, experimental evidence strongly suggests that an increase in intracellular urate is a key factor in the pathogenesis of primary hypertension. Pilot clinical trials show beneficial effect of lowering serum urate in hyperuricemic individuals who are young, hypertensive, and have preserved kidney function. Some evidence suggest that activation of the renin–angiotensin system (RAS) occurs in hyperuricemia and blocking the RAS may mimic the effects of xanthine oxidase inhibitors. A reduction in intracellular urate may be achieved by lowering serum urate concentration or by suppressing intracellular urate production with dietary measures that include reducing sugar, fructose, and salt intake. We suggest that these elements in the western diet may play a major role in the pathogenesis of primary hypertension. Studies are necessary to better define the interrelation between uric acid concentrations inside and outside the cell. In addition, large-scale clinical trials are needed to determine if extracellular and intracellular urate reduction can provide benefit hypertension and cardiometabolic disease.

Drug-Induced Electrolyte Disorders

1983 ◽  
Vol 17 (3) ◽  
pp. 175-185 ◽  
Author(s):  
Amin A. Nanji
Keyword(s):  
Parathyroid Hormone ◽  
Renin Angiotensin System ◽  
Renal Tubules ◽  
Electrolyte Disorders ◽  
Drug Induced ◽  
Sodium Potassium ◽  
Angiotensin System ◽  
Life Threatening ◽  
Calcium Magnesium ◽  
Pharmacologic Agents

A wide variety of pharmacologic agents have been implicated in a number of electrolyte disorders. The present review focuses on abnormalities of sodium, potassium, calcium, magnesium, and phosphate. Several mechanisms are involved in the pathogenesis of these disorders. These involve stimulation and modulation of other hormones (e.g., antidiuretic hormone, renin-angiotensin system, parathyroid hormone), damage to renal tubules, and, in some cases, a combination of factors. Recognition of these abnormalities is important because their presence may be life threatening or may aggravate the side effects of the drug itself.

scholarly journals ERAP1 and ERAP2 Enzymes: A Protective Shield for RAS against COVID-19?

2021 ◽  
Vol 22 (4) ◽  
pp. 1705
Author(s):  
Silvia D’Amico ◽  
Patrizia Tempora ◽  
Valeria Lucarini ◽  
Ombretta Melaiu ◽  
Stefania Gaspari ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Prognostic Factors ◽  
Mhc Class I ◽  
Antigen Processing ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Inflammatory Conditions ◽  
Protective Shield ◽  
Life Threatening ◽  
Mhc Class I Antigen

Patients with coronavirus disease 2019 (COVID-19) have a wide variety of clinical outcomes ranging from asymptomatic to severe respiratory syndrome that can progress to life-threatening lung lesions. The identification of prognostic factors can help to improve the risk stratification of patients by promptly defining for each the most effective therapy to resolve the disease. The etiological agent causing COVID-19 is a new coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that enters cells via the ACE2 receptor. SARS-CoV-2 infection causes a reduction in ACE2 levels, leading to an imbalance in the renin-angiotensin system (RAS), and consequently, in blood pressure and systemic vascular resistance. ERAP1 and ERAP2 are two RAS regulators and key components of MHC class I antigen processing. Their polymorphisms have been associated with autoimmune and inflammatory conditions, hypertension, and cancer. Based on their involvement in the RAS, we believe that the dysfunctional status of ERAP1 and ERAP2 enzymes may exacerbate the effect of SARS-CoV-2 infection, aggravating the symptomatology and clinical outcome of the disease. In this review, we discuss this hypothesis.

Renal arterial 20-hydroxyeicosatetraenoic acid levels: regulation by cyclooxygenase

2003 ◽  
Vol 284 (3) ◽  
pp. F474-F479 ◽  
Author(s):  
Monica K. Cheng ◽  
John C. McGiff ◽  
Mairead A. Carroll
Keyword(s):  
Salt Intake ◽  
Renin Angiotensin System ◽  
Renal Arteries ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Sprague Dawley Rats ◽  
Cox 2 ◽  
Potent Vasoconstrictor ◽  
Cytochrome P 450 ◽  
Cox 1

20-HETE, a potent vasoconstrictor, is generated by cytochrome P-450 ω-hydroxylases and is the principal eicosanoid produced by preglomerular microvessels. It is released from preglomerular microvessels by ANG II and is subject to metabolism by cyclooxygenase (COX). Because low-salt (LS) intake stimulates the renin-angiotensin system and induces renal cortical COX-2 expression, we examined 20-HETE release from renal arteries (interlobar and arcuate and interlobular arteries) obtained from 6- to 7-wk-old male Sprague-Dawley rats fed either normal salt (0.4% NaCl) or LS (0.05% NaCl) diets for 10 days. With normal salt intake, the levels of 20-HETE recovered were similar in arcuate and interlobular arteries and interlobar arteries: 30.1 ± 8.5 vs. 24.6 ± 5.3 ng · mg protein−1 · 30 min−1, respectively. An LS diet increased 20-HETE levels in the incubate of either arcuate and interlobular or interlobar renal arteries only when COX was inhibited. Addition of indomethacin (10 μM) to the incubate of arteries obtained from rats fed an LS diet resulted in a two- to threefold increase in 20-HETE release from arcuate and interlobular arteries, from 39.1 ± 13.2 to 101.8 ± 42.6 ng · mg protein−1 · 30 min−1( P < 0.03), and interlobar arteries, from 31.7 ± 15.1 to 61.9 ± 29.4 ng · mg protein−1 · 30 min−1( P < 0.05) compared with release of 20-HETE when COX was not inhibited. An LS diet enhanced vascular expression of cytochrome P-4504A and COX-2 in arcuate and interlobular arteries; COX-1 was unaffected. Metabolism of 20-HETE by COX is proposed to represent an important regulatory mechanism in setting preglomerular microvascular tone.

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