Potassium balance and the control of renin secretion

Sealey, Jean E.; Clark, Irwin; Bull, Marcia B.; Laragh, John H.

doi:10.1172/jci106429

Cited by 156 publications

(54 citation statements)

References 20 publications

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“…Other possible mechanisms are a direct inhibiting effect of plasma potassium concentration on the enzyme renin or an effect of potassium administration on renin substrate concentration. However, as described above, studies in our laboratory have failed to demonstrate either of these effects (24). Changes in potassium metabolism might also operate to induce the release of an extrarenal hormone concerned with the control of renal renin secretion.…”

Section: Potassium Administration and Plasma Renin In Manmentioning

confidence: 88%

“…Control samples were collected on the last day of each control period and frequently during the subsequent experimental periods which lasted from 5 to 13 days. 24-hr urine samples were collected daily during the control and experimental periods and matching days were saved for the determination of aldosterone excretion or secretion rates. The samples collected on the last day of the experimental period were compared to the samples of the control period.…”

Section: Methodsmentioning

confidence: 99%

“…However, because this procedure often produces transient natriuresis, an increased sodium delivery to the macula densa might be involved, at least initially, in the renin suppression. Such a mechanism may not adequately explain the chronic suppression of renin caused by potassium loading, because this can obtain even after sodium depletion is established, at a time when the rate of urinary sodium excretion is very low (14,24).…”

Section: Potassium Administration and Plasma Renin In Manmentioning

confidence: 99%

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The influence of potassium administration and of potassium deprivation on plasma renin in normal and hypertensive subjects

Brunner¹,

Baer²,

Sealey³

et al. 1970

J. Clin. Invest.

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223

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A B S T R A C T The effect of potassium administration and of dietary potassium deprivation on plasma renin activity and aldosterone excretion has been studied in 10 normal subjects and in 12 hypertensive patients maintained on a constant dietary regimen.Potassium administration reduced plasma renin activity in 18 of 28 studies of both normal and hypertensive subjects. Suppression of renin often occurred despite sodium diuresis induced by potassium administration. The renin suppression was related to induced changes in plasma potassium concentration and urinary potassium excretion.The failure of suppression of plasma renin in 10 studies could be accounted for by the smaller amounts of potassium administered to these subjects, together with a possibly overriding influence of an induced sodium diuresis.In six studies potassium deprivation invariably increased plasma renin activity even though a tendency for sodium retention often accompanied this procedure.The data indicate that both the suppression of plasma renin activity induced by potassium administration and the stimulation of renin activity which follows potassium depletion occur independently of associated changes in either aldosterone secretion or in sodium balance. However, the results do suggest that in various situations, the influence of potassium on plasma renin activity may be either amplified or preempted by changes in sodium balance.These interactions between potassium and plasma renin could be mediated by an ill-defined extrarenal pathway. But the findings are more consistent with an

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Section: Potassium Administration and Plasma Renin In Manmentioning

confidence: 88%

Section: Methodsmentioning

confidence: 99%

Section: Potassium Administration and Plasma Renin In Manmentioning

confidence: 99%

See 1 more Smart Citation

The influence of potassium administration and of potassium deprivation on plasma renin in normal and hypertensive subjects

Brunner¹,

Baer²,

Sealey³

et al. 1970

J. Clin. Invest.

Self Cite

223

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“…9,10 Thus, it is possible that inhibition of the AngII signaling pathway may be involved in upregulation of CYP2C23. To test this hypothesis, we examined the expression of AngII type I receptor (AT1R) in the kidney (mixture of renal cortex and OM) of rats on a normal-K (1%), or an HK diet (2.5 and 10.0%).…”

Section: Hk Intake Enhances Aa and 1112-eet-mediated Inhibition Of Enacmentioning

confidence: 99%

High Potassium Intake Enhances the Inhibitory Effect of 11,12-EET on ENaC

Sun

Lin

Yue

et al. 2010

Journal of the American Society of Nephrology

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High dietary potassium stimulates the renal expression of cytochrome P450 (CYP) epoxygenase 2C23, which metabolizes arachidonic acid (AA). Because the AA metabolite 11,12-epoxyeicosatrienoic acid (11, can inhibit the epithelial sodium channel (ENaC) in the cortical collecting duct, we tested whether dietary potassium modulates ENaC function. High dietary potassium increased 11,12-EET in the isolated cortical collecting duct, an effect mimicked by inhibiting the angiotensin II type I receptor with valsartan. In patch-clamp experiments, a high potassium intake or treatment with valsartan enhanced AA-induced inhibition of ENaC, an effect mediated by a CYP-epoxygenase-dependent pathway. Moreover, high dietary potassium and valsartan each augmented the inhibitory effect of 11,12-EET on ENaC. Liquid chromatography/mass spectrometry showed that the rate of EET conversion to dihydroxyeicosatrienoic acids (DHET) was lower in renal tissue obtained from rats on a high-potassium diet than from those on a control diet, but this was not a result of altered expression of soluble epoxide hydrolase (sEH). Instead, suppression of sEH activity seemed to be responsible for the 11,12-EET-mediated enhanced inhibition of ENaC in animals on a high-potassium diet. Patch-clamp experiments demonstrated that 11,12-DHET was a weak inhibitor of ENaC compared with 11,12-EET, whereas 8,9-and 14,15-DHET were not. Furthermore, inhibition of sEH enhanced the 11,12-EET-induced inhibition of ENaC similar to high dietary potassium. In conclusion, high dietary potassium enhances the inhibitory effect of AA and 11,12-EET on ENaC by increasing CYP epoxygenase activity and decreasing sEH activity, respectively. 21: 166721: -167721: , 201021: . doi: 10.1681 We previously demonstrated that cytochrome P450 (CYP) epoxygenase-dependent arachidonic acid (AA) metabolism inhibited epithelial sodium channel (ENaC) in the cortical collecting duct (CCD) and that 11,12-epoxyeicosatrienoic acid (11,12-EET) was responsible for mediating the effect of AA on ENaC. 1 Furthermore, the observation that AA failed to inhibit ENaC in the CCD of the mice with a low expression of CYP2C44 suggests that CYP2C44 and its orthologs may be responsible for mediating the inhibitory effect of AA. 2 The expression of CYP2C44 or its orthologs has been shown to be regulated by dietary Na intake: A high Na intake stimulates 2 whereas a low Na intake suppresses the expression of CYP2C44 homologue. 3 A large body of evidence has suggested that EET plays a role in the regulation of renal Na transport and salt-sensitive hypertension. 1,2,4,5 Inhibition of CYP epoxygenase-dependent AA metabolism results in the development of salt-sensitive hypertension 5,6 ; however, the BP returned to normal after the removal of the epoxygenase inhibitor, even when the animals were still kept on a high-Na diet. The high Na intake-induced in- J Am Soc Nephrol

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“…Potassium might interfere with a number of mechanisms that have been implicated in the adverse effects of high sodium intake in SHRSP. Such mechanisms include changes in extracellular fluid volume, 7 activation of central or autonomic nervous system, 8 " 10 enhanced vascular reactivity to pressor agents, 11 Previous research from our laboratory has defined the effects of dietary potassium deprivation and administration on plasma renin activity (PRA) in both animals 18 and human subjects. 19 We also detected a positive correlation between PRA and the development of stroke and heart attack in humans.…”

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confidence: 99%

Relation of plasma renin to end organ damage and to protection of K+ feeding in stroke-prone hypertensive rats.

et al. 1990

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We studied the effects of regular diet (035% NaCl/1.1% potassium), high sodium diet (4% NaCl/0.75% potassium), or high sodium and high potassium diet (4% NaQ/2.11% potassium) on blood pressure, plasma renin activity, renal and cerebrovascular lesions, and incidence of stroke and mortality in male stroke-prone spontaneously hypertensive rats (SHRSP). In the first 4 weeks, the rise in blood pressure was higher hi high NaQ than in high NaCI/high potassium or regular diet groups. However, by 8 and 12 weeks, the blood pressure in all three groups was similar. After 4 weeks of diet, plasma renin activity was similar in the three groups (3.4±0.8, 4.1±0.9, and 52±1.6 ng/ml/hr, in high NaO, high NaCI/high potassium, and regular diet groups, respectively) and were not related to sodium excretion. After 8 weeks, plasma renin activity was significantly increased only in the high NaQ group (13.7±3.7 ng/ml/hr), and by 12 weeks plasma renin activity was significantly higher in the high NaCl group (253 ±3.6 ng/ml/hr) than in the high NaCI/high potassium (11.1±2.9 ng/ml/hr) or in the regular diet (7.8±4.6 ng/ml/hr) groups. Moderate to severe renal vascular lesions were first detected in the high NaQ group by 8 weeks of diet At 12 weeks, renal vascular damage index (RVDI), estimated hlstologically, was significantly higher in the high NaCl group (RVDI=79±14) than hi the high NaCI/high potassium (RVDI=40±ll) and regular diet (RVDI=7.8±4.6) groups. At this time, incidence of stroke was 81% in high NaCl, 24.5% in high NaCI/high potassium, and 7.7% in regular diet groups. Hie data demonstrate that: 1) the increase in mortality, stroke, and renal and cerebrovascular lesions in SHRSP fed a high sodium diet is associated with a paradoxical rise in plasma renin activity; 2) the protective effect of high potassium hi SHRSP fed a high potassium diet is related to a lower blood pressure at 2 -4 weeks and a lower plasma renin activity, but not a lower blood pressure at 8-12 weeks; 3) this rise in plasma renin activity demonstrates that a high potassium diet suppresses or delays a primary or secondary paradoxical rise hi plasma renin activity and thus, angiotensin JJ in the rats fed a high sodium diet This action together with possible direct effects of potassium hi the vasculature contributes to the protective effect on end organ damage and stroke hi SHRSP. {Hypertension 1990;15:318-326)

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Potassium balance and the control of renin secretion

Cited by 156 publications

References 20 publications

The influence of potassium administration and of potassium deprivation on plasma renin in normal and hypertensive subjects

The influence of potassium administration and of potassium deprivation on plasma renin in normal and hypertensive subjects

High Potassium Intake Enhances the Inhibitory Effect of 11,12-EET on ENaC

Relation of plasma renin to end organ damage and to protection of K+ feeding in stroke-prone hypertensive rats.

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