Mineralocorticoid Hypertension and Hypokalemia

Khosla, Neenoo; Hogan, Donn

doi:10.1016/j.semnephrol.2006.10.004

Cited by 14 publications

(8 citation statements)

References 57 publications

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“…Short periods of mild potassium depletion have been shown to be capable of inducing serious cardiac, renal and neurologic dysfunction (Reungjui et al, 2008). Prolonged potassium depletion of even modest proportion can provoke or exacerbate kidney injury or hypertension (Khosla and Hogan, 2006). Also, reduced plasma potassium has been shown to correlate directly with higher blood pressure in both normotensive and hypertensive individuals (Whelton et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Toxicity Evaluation of Yoyo 'Cleanser' Bitters and Fields Swedish Bitters Herbal Preparations following Sub-Chronic Administration in Rats

Ekor¹

2010

American Journal of Pharmacology and Toxicology

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Problem statement:Owing to numerous adverse effects of most orthodox pharmaceuticals, the use of herbal remedies in treatment and prevention of diseases is gaining much attention, especially in developing countries. The increase patronage of these remedies is often predicated on the assumption that they are harmless since they are prepared from natural sources. However, toxicity related to herbal medicines is becoming widely recognized. Yoyo 'Cleanser' Bitters (YB) and Fields Swedish Bitters (SB) are herbal preparations largely consumed in Nigeria because of their high publicity in the various national news media. This study evaluated their toxicity potentials following sub-chronic administration in rats. Approach: Thirty-five Wistar rats were divided into five groups of 7 rats/group. Control received normal saline while the experimental groups were treated separately with 15 and 30 mL kg −1 of YB and SB respectively. Treatment was given daily by gavage for 30 days. Body weights were measured weekly and rats were sacrificed 24 h after last treatment. Blood was collected by cardiac puncture for biochemical and haematological assessment. Vital organs were also excised and weighed. Results: YB and SB did not significantly affect creatinine, blood urea nitrogen, Na + ion but significantly (p<0.01) decreased K + ion concentration when compared with control. Both herbal preparations produced moderate increases in alanine and aspartate aminotransferase activities, with YB (30 mL kg −1 ) significantly (p<0.05) increasing the latter. YB and SB did not significantly alter total cholesterol, triglycerides and albumin but SB (30 mL kg −1 ) significantly (p<0.05) decreased total protein when compared with control. SB significantly (p<0.05) elevated white blood cell count while other haematological parameters, vital organs and body weights were not significantly affected by both herbal preparations. Conclusion: YB and SB possess the risk of inducing hypokalaemia. The potential to also increase markers of liver function calls for cautious use in conditions associated with liver impairment.

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Section: Discussionmentioning

confidence: 99%

Toxicity Evaluation of Yoyo 'Cleanser' Bitters and Fields Swedish Bitters Herbal Preparations following Sub-Chronic Administration in Rats

Ekor¹

2010

American Journal of Pharmacology and Toxicology

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“…Although short periods of mild potassium depletion are typically well tolerated in healthy individuals, severe potassium depletion can result in glucose intolerance (2) and serious cardiac (3), renal (4), and neurologic (5) dysfunction, including death. Prolonged potassium depletion of even modest proportion can provoke or exacerbate kidney injury or hypertension (6, 7). Indeed, reduced potassium intake correlates directly with higher blood pressure in both normotensive and hypertensive individuals (8).…”

mentioning

confidence: 99%

Narrative Review: Evolving Concepts in Potassium Homeostasis and Hypokalemia

et al. 2009

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Humans are intermittently exposed to large variations in potassium intake, which range from periods of fasting to ingestion of potassium-rich meals. These fluctuations would abruptly alter plasma potassium concentration if not for rapid mechanisms, primarily in skeletal muscle and the liver, that buffer the changes in plasma potassium concentration by means of transcellular potassium redistribution and feedback control of renal potassium excretion. However, buffers have capacity limits, and even robust feedback control mechanisms require that the perturbation occur before feedback can initiate corrective action. In contrast, feedforward control mechanisms sense the effect of disturbances on the system’s homeostasis. This review highlights recent experimental insights into the participation of feedback and feedforward control mechanisms in potassium homeostasis. New data make clear that feedforward homeostatic responses activate when decreased potassium intake is sensed, even when plasma potassium concentration is still within the normal range and before frank hypokalemia ensues, in addition to the classic feedback activation of renal potassium conservation when plasma potassium concentration decreases. Given the clinical importance of dyskalemias in patients, these novel experimental paradigms invite renewed clinical inquiry into this important area.

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“…Mineralocorticoid hypertension is a potentially reversible cause of hypertension that is characterized by the triad of hypertension, metabolic alkalosis, and hypokalemia (Table 2)5, 6).…”

Section: Primary Aldosteronism (Pa)mentioning

confidence: 99%

Hypertensive Hypokalemic Disorders

Choi

2007

Electrolyte Blood Press

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Hypokalemia is a common clinical problem. The kidney is responsible for long term potassium homoeostasis, as well as the serum potassium concentration. The main nephron site where K secretion is regulated is the cortical collecting duct, mainly via the effects of aldosterone. Aldosterone interacts with the mineralocorticoid receptor to increase sodium reabsorption and potassium secretion; the removal of cationic sodium makes the lumen relatively electronegative, thereby promoting passive potassium secretion from the tubular cell into the lumen through apical potassium channels. As a result, any condition that decreases the activity of renal potassium channels results in hyperkalemia (for example, amiloride intake or aldosterone deficiency) whereas their increased activity results in hypokalemia (for example, primary aldosteronism or Liddle's syndrome). The cause of hypokalemia can usually be determined from the history. If there is no apparent cause, the initial step is to see if hypokalemia is in associated with systemic hypertension or not. In the former group hypokalaemia is associated with a high mineralocorticoid effect or hyperactive sodium channel as in Liddle's syndrome. In hypertensive hypokalemic patients, measurement of the renin, aldosterone, and cortisol concentrations would be of help in differential diagnosis.

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Mineralocorticoid Hypertension and Hypokalemia

Cited by 14 publications

References 57 publications

Toxicity Evaluation of Yoyo 'Cleanser' Bitters and Fields Swedish Bitters Herbal Preparations following Sub-Chronic Administration in Rats

Toxicity Evaluation of Yoyo 'Cleanser' Bitters and Fields Swedish Bitters Herbal Preparations following Sub-Chronic Administration in Rats

Narrative Review: Evolving Concepts in Potassium Homeostasis and Hypokalemia

Hypertensive Hypokalemic Disorders

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