Chronic hypokalemia and the left ventricular responses to epinephrine and preload

Fitzovich, Douglas E; Hamaguchi, Masaaki; Tull, William Bailey; Young, David B.

doi:10.1016/0735-1097(91)90774-4

Cited by 40 publications

(30 citation statements)

References 21 publications

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“…13 Furthermore, the cardiac hypertrophy was improved by potassium supplementation in deoxycorticosterone acetate/Na mice independent of blood pressure (BP). 14 Consistent with these data, modest potassium depletion impaired LV contractile and relaxation responses to epinephrine or to preload alteration in the dog model, 15 and potassium repletion improved the LV relaxation, which was enfeebled by the restriction of potassium intake in the normal volunteers. 16 But the precise mechanism of cardiac functional improvement by potassium has not been fully elucidated.…”

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confidence: 73%

Protective Effect of Potassium Against the Hypertensive Cardiac Dysfunction

et al. 2006

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Abstract-Potassium supplementation has a potent protective effect against cardiovascular disease, but the precise mechanism of it against left ventricular abnormal relaxation, relatively early functional cardiac alteration in hypertensive subjects, has not been fully elucidated. In the present study, we investigated the effect of potassium against salt-induced cardiac dysfunction and the involved mechanism. Seven-to 8-week-old Dahl salt sensitive rats were fed normal diet (0.3% NaCl) or high-salt diet (8% NaCl) with or without high potassium (8% KCl) for 8 weeks. Left ventricular relaxation was evaluated by the deceleration time of early diastolic filling obtained from Doppler transmitral inflow, the slope of the pressure curve, and the time constant at the isovolumic relaxation phase. High-salt loading induced a significant elevation of blood pressure and impaired left ventricular relaxation, accompanied by augmentation of reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase activity in the cardiac tissue, measured by the lucigenin chemiluminescence method. Blood pressure lowering by hydralazine could not ameliorate NADPH oxidase activity and resulted in no improvement of left ventricular relaxation. Interestingly, although the blood pressure remained high, potassium supplementation as well as treatment with 4-hydroxy-2,2,6,6-tetramethyl-piperidine-N-oxyl, a superoxide dismutase mimetic, not only reduced the elevated NADPH oxidase activity but also improved the left ventricular relaxation. In conclusion, a high-potassium diet has a potent protective effect on left ventricular active relaxation independent of blood pressure, partly through the inhibition of cardiac NADPH oxidase activity. Sufficient potassium supplementation might be an attractive strategy for cardiac protection, especially in the salt-sensitive hypertensive subjects. Key Words: sodium Ⅲ blood pressure monitoring Ⅲ cardiac function Ⅲ heart failure Ⅲ oxidative stress Ⅲ potassium H igh-salt loading on the salt-sensitive subjects results in hypertension, left ventricular (LV) hypertrophy, and hypertensive heart failure. [1][2][3][4] The hypertensive heart failure is characterized by the LV diastolic dysfunction composed of the LV abnormal relaxation and the increased LV chamber stiffness. 5 The impaired LV active relaxation, which is observed in the patients with hypertension or diabetes, 6 has been reported recently to predict a poor prognosis, 7 thus, the preservation of the LV active relaxation from early stage may be a reasonable concept.High-salt loading on the salt-sensitive model also induces overproduction of reactive oxygen species (ROS) through activation of NADPH oxidase, 8 and ROS level had a significant positive correlation with the severity of heart failure. 9,10 In the pressure overload model by aortic banding, the impaired LV relaxation was improved effectively by antioxidant treatment, such as vitamin C or deferoxamine, indicating that excess ROS can induce LV abnormal relaxation. 11,12 To reduce ROS for cardioprotec...

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Protective Effect of Potassium Against the Hypertensive Cardiac Dysfunction

et al. 2006

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“…Experimental studies in dogs, 26 mice, 27 and human healthy volunteers 28,29 showed that hypokalemia induced LV hypertrophy and impaired LV function. Correction of hypokalemia by potassium supplementation prevented these adverse effects.…”

Section: He Et Al Effects Of Potassium Salts On Cvd Risk Factorsmentioning

confidence: 99%

Effects of Potassium Chloride and Potassium Bicarbonate on Endothelial Function, Cardiovascular Risk Factors, and Bone Turnover in Mild Hypertensives

et al. 2010

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Abstract-To determine the effects of potassium supplementation on endothelial function, cardiovascular risk factors, and bone turnover and to compare potassium chloride with potassium bicarbonate, we carried out a 12-week randomized, double-blind, placebo-controlled crossover trial in 42 individuals with untreated mildly raised blood pressure. Urinary potassium was 77Ϯ16, 122Ϯ25, and 125Ϯ27 mmol/24 hours after 4 weeks on placebo, potassium chloride, and potassium bicarbonate, respectively. There were no significant differences in office blood pressure among the 3 treatment periods, and only 24-hour and daytime systolic blood pressures were slightly lower with potassium chloride. Compared with placebo, both potassium chloride and potassium bicarbonate significantly improved endothelial function as measured by brachial artery flow-mediated dilatation, increased arterial compliance as assessed by carotid-femoral pulse wave velocity, decreased left ventricular mass, and improved left ventricular diastolic function. There was no significant difference between the 2 potassium salts in these measurements. The study also showed that potassium chloride reduced 24-hour urinary albumin and albumin:creatinine ratio, and potassium bicarbonate decreased 24-hour urinary calcium, calcium:creatinine ratio, and plasma C-terminal cross-linking telopeptide of type 1 collagen significantly. These results demonstrated that an increase in potassium intake had beneficial effects on the cardiovascular system, and potassium bicarbonate may improve bone health. Importantly, these effects were found in individuals who already had a relatively low-salt and high-potassium intake. (Hypertension. 2010;55:681-688.)Key Words: potassium chloride Ⅲ potassium bicarbonate Ⅲ endothelial function Ⅲ cardiovascular risk factors Ⅲ bone turnover Ⅲ randomized trial M any randomized trials have shown that an increase in potassium intake lowers blood pressure (BP), particularly in individuals with raised BP. 1 Increasing evidence also suggests that a higher potassium intake may have beneficial effects on endothelial function, renal disease, arterial compliance, left ventricular (LV) mass and function, and bone mineral density. 2 The evidence for many of these effects is mainly from experimental studies in animals, and few wellcontrolled trials have studied such effects in humans.Most previous studies on potassium have used potassium chloride, which is convenient for making the study double blinded by using slow-release potassium chloride versus slow-release potassium chloride placebo. 1 These studies have demonstrated clear benefits of potassium chloride, particularly on BP. Increasing potassium intake has been recommended as an important approach to lowering BP not only in individuals with raised BP but also in those with normal BP. However, no one is suggesting that the whole population take potassium chloride supplements. The best way to increase potassium intake is to increase the consumption of foods that are high in potassium, for example, fruit and ve...

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“…[1][2][3][4][5][6][7] Thus, even mild potassium depletion has been shown to produce a substantial impairment of cardiac function in dogs and healthy human subjects. 8,9 Several studies have also demonstrated that hypokalemia or mineralocorticoids that induce hypokalemia can affect cardiac structure, leading to cardiac necrosis and fibrosis in experimental animals and humans. 8,10 -13 Conversely, potassium supplementation appears to be rather cardioprotective and nephroprotective.…”

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Potassium Supplementation Reduces Cardiac and Renal Hypertrophy Independent of Blood Pressure in DOCA/Salt Mice

Wang¹,

Domenighetti²,

Pedrazzini³

et al. 2005

Hypertension

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Abstract-We have demonstrated previously that deoxycorticosterone acetate (DOCA)/salt induces cardiac hypertrophy and left ventricular dysfunction independent of blood pressure (BP) in 1-renin gene mice. Because these mice also develop hypokalemia and metabolic alkalosis caused by mineralocorticoid excess, we investigated whether correcting hypokalemia by dietary potassium supplementation would prevent the DOCA/salt-induced cardiac hypertrophy, cardiac dysfunction, and electrocardiographic changes in normotensive, 1-renin gene and hypertensive, 2-renin gene mice. All mice were studied after 5 weeks of DOCA and salt administration. Potassium was given by adding 0.4 or 0.6% KCl to the drinking water. Our results show that correction of hypokalemia and metabolic alkalosis prevents cardiac hypertrophy and normalizes cardiac function without affecting BP in normotensive, 1-renin gene mice. In hypertensive, 2-renin gene mice, potassium supplementation induces a significant decrease in BP. The decrease in BP and correction of kalemia are associated with a significant but partial correction of cardiac hypertrophy. In both group of mice, electrocardiographic alterations were measured after administration of DOCA/salt, which could be corrected by potassium supplementation. Thus, these results show that correction of hypokalemia and metabolic alkalosis does prevent the development of cardiac hypertrophy and normalizes cardiac function independent of BP in normotensive, 1-renin gene mice that receive excess mineralocorticoid and salt. In 2-renin gene, hypertensive mice, potassium supplementation also prevents the development of cardiac hypertrophy, but the effect cannot be separated from the decrease in BP. Key Words: hypokalemia Ⅲ metabolism Ⅲ hypertrophy Ⅲ heart failure Ⅲ deoxycorticosterone Ⅲ mouse T here is substantial clinical and experimental evidence that potassium depletion, or hypokalemia, has a negative impact on the cardiovascular system as well as on the kidney and contributes to the pathogenesis of hypertension, stroke, ventricular arrhythmias, and renal injury. 1-7 Thus, even mild potassium depletion has been shown to produce a substantial impairment of cardiac function in dogs and healthy human subjects. 8,9 Several studies have also demonstrated that hypokalemia or mineralocorticoids that induce hypokalemia can affect cardiac structure, leading to cardiac necrosis and fibrosis in experimental animals and humans. 8,10 -13 Conversely, potassium supplementation appears to be rather cardioprotective and nephroprotective. Indeed, a high potassium intake and prevention of hypokalemia have been associated with a decrease in blood pressure (BP) in hypertensive animals and humans. 14 -19 Potassium supplementation has also been shown to prevent stroke; to reduce mortality in stroke-prone spontaneously hypertensive and Dahl saltsensitive rats; and to prevent renal glomerular, tubular, and vascular lesions in rats. 14,17,20,21 Together with systemic hypertension and metabolic alkalosis, hypokalemia is the clinical hallm...

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Chronic hypokalemia and the left ventricular responses to epinephrine and preload

Cited by 40 publications

References 21 publications

Protective Effect of Potassium Against the Hypertensive Cardiac Dysfunction

Protective Effect of Potassium Against the Hypertensive Cardiac Dysfunction

Effects of Potassium Chloride and Potassium Bicarbonate on Endothelial Function, Cardiovascular Risk Factors, and Bone Turnover in Mild Hypertensives

Potassium Supplementation Reduces Cardiac and Renal Hypertrophy Independent of Blood Pressure in DOCA/Salt Mice

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