Effect of spironolactone on urinary kallikrein excretion in patients with essential hypertension and in primary aldosteronism.

Seino, Masahide; Abe, Keishi; Sakurai, Yoshinori; Irokawa, Nobuo; Yasujima, Minoru; Chiba, Satoru; Utsuka, Yoichi; Yoshinaga, Kaoru

doi:10.1620/tjem.121.111

Cited by 28 publications

(9 citation statements)

References 30 publications

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“…Urinary excretion of kallikrein is increased 1) in patients with primary aldosteronism (48), 2) in normal volunteers or patients with essential hypertension on a diet of low sodium or high potassium (121), 3) after treatment with 9α-fluorohydrocortisone (126), and 4) in Bartter's syndrome (hypertrophy and hyperplasia of the juxtaglomerular cells, producing hypokalemic alkalosis and hyperaldosteronism) (127). In addition, treatment of patients affected by primary aldosteronism and treatment of normal volunteers with spironolactone, a selective antagonist of aldosterone, markedly reduced urinary kallikrein excretion (121,128). The removal of aldosterone-producing tumors also reversed the increased excretion of urinary kallikrein (129).…”

Section: ) Sodium-retaining Steroid Hormonesmentioning

confidence: 99%

A Missing Link Between a High Salt Intake and Blood Pressure Increase

Katori

Murakami

2006

J Pharmacol Sci

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Abstract. It is widely accepted that a high sodium intake triggers blood pressure rise. However, only one-third of the normotensive subjects were reported to show salt-sensitivity in their blood pressure. Many factors have been proposed as causes of salt-sensitive hypertension, but none of them provides a satisfactory explanation. We propose, on the basis of accumulated data, that the reduced activity of the kallikrein-kinin system in the kidney may provide this link. Renal kallikrein is secreted by the distal connecting tubular cells and all kallikrein-kinin system components are distributed along the collecting ducts in the distal nephron. Bradykinin generated is immediately destroyed by carboxypeptidase Y-like exopeptidase and neutral endopeptidase, both quite independent from the kininases in plasma, such as angiotensin converting enzyme. The salt-sensitivity of the blood pressure depends largely upon ethnicity and potassium intake. Interestingly, potassium and ATP-sensitive potassium (K ATP ) channel blockers accelerate renal kallikrein secretion and suppress blood pressure rises in animal hypertension models. Measurement of urinary kallikrein may become necessary in salt-sensitive normotensive and hypertensive subjects. Furthermore, pharmaceutical development of renal kallikrein releasers, such as K ATP channel blockers, and renal kininase inhibitors, such as ebelactone B, may lead to the development of novel antihypertensive drugs.

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Section: ) Sodium-retaining Steroid Hormonesmentioning

confidence: 99%

A Missing Link Between a High Salt Intake and Blood Pressure Increase

Katori

Murakami

2006

J Pharmacol Sci

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“…On the other hand, very high levels of sodium intake do not markedly affect kallikrein levels (Margolius et al, 1974a; Levy et al, 1978). These effects and those of certain drugs are best explained by a direct response of kallikrein excretion to effect the level of aldosterone; i.e., aldosterone regulates kallikrein excretion (Margolius et al, 1974a(Margolius et al, ,b, 1976Seino et al, 1977). However, not all data support this hypothesis (Lawton and Fitz, 1980; Holland et aI., 1980).…”

Section: Kallikreinmentioning

confidence: 99%

“…Urinary kallikrein levels, measured by activity and by enzyme quantity, are below normal in individuals with essential hypertension and elevated in those with primary aldosteronism (Margolius et al, 1971;Miyashita, 1971;Margolius et al, 1972;Shimamoto et al, 1981). In "normal subjects," sodium intake shows an inverse relationship with kallikrein level; i.e., a sustained low sodium intake causes a progressive increase in kallikrein excretion (Margolius et al, 1974a;Seino et al, 1977). On the other hand, very high levels of sodium intake do not markedly affect kallikrein levels (Margolius et al, 1974a;Levy et al, 1978).…”

Section: Kallikreinmentioning

confidence: 99%

Genetic and familial factors in essential hypertension and related traits

Siervogel

1983

American J Phys Anthropol

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The health significance of essential hypertension (high blood pressure of undefined origin) is well established. It is a major factor contributing to coronary heart disease, stroke, and kidney failure. It directly affects about one in five Americans. Factors which are known to be associated with blood pressure include: body composition as it relates to overall mass and fat mass; physiological variables involving the sympathetic and parasympathetic nervous systems; biochemical variables such as renin, aldosterone, kallikrein, lipids, and lipoproteins, etc.; environmental variables such as sodium intake, heavy metals, and noise; and psychological variables involving personality type and mental stress.There is a definite, well-established genetic involvement in hypertension, but specific genetic mechanisms remain a mystery. Familial aggregation occurs for many of the associated traits listed above. For some, specific polymorphic major genes have been identified, but for others genetic factors are unidentified. Essential hypertension is undoubtedly a heterogeneous group of diseases with the common end result of elevated blood pressure. Because of its health significance, there is considerable interest in identifying genetic mechanisms resulting in essential hypertension. One area that currently shows some potential for the identification of a specific genetic mechanism is related to the transmembrane transport of sodium and potassium cations.A genetic component has long been suspected in essential hypertension, but a clear and definitive genetic mechanism has yet to be identified. Since there are many variables that can affect blood pressure, this review of the genetics of essential hypertension necessarily involves a discussion of related traits. Before focusing on the genetic and familial aspects of hypertension a description of the normal course of human blood pressure is presented and some of the traits related to it are discussed. NATURAL HISTORY OF BLOOD PRESSUREUntil recently, reports describing blood pressure patterns during the neonatal period were relatively few, largely because of the difficulty of accurately measuring blood pressure in infants by noninvasive techniques. The ultrasonic technique utilizing the Doppler effect greatly facilitated noninvasive systolic blood pressure determination in infants (McLaughlin et al., 1971). Accurate automatic methods are currently available using the oscillometric principal coupled with a microcomputer and a standard limb blood presure cuff (Friesen and Lichtor, 1981). Even in adults newer methods are being developed (Wolthuis et al., 1981).© 1983 Alan R. Liss, Inc. [Vol.26,1983 Systolic blood pressure tends to increase sharply during the first two weeks of life from a mean of 70 mmHg at 2 days to 84 mmHg at 2 weeks. It continues to increase at a slightly slower rate over the next 4 weeks to a mean of about 93 mmHg at 6 weeks (Earley et aI., 1980); from 6 weeks to 1 year af age there is little change in systolic pressure (deSwiet et aI., 1975(deSwiet et ...

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“…They suggest that kallikrein excretion in hypertension may be correlated with plasma renin and that admixture of patients with low renin hypertension may account for reduced excretion in unclassified hypertensives in previous studies. However, patients with primary aldosteronism, whose plasma renin is suppressed, have greatly elevated urinary kallikrein (Lechi et al, 1976;Margolius et al, 1974b;Seino et al, 1975Seino et al, , 1977, an observation not consistent with any simple relation between plasma renin and kallikrein excretion in hypertension. Spironolactone decreases kallikrein excretion in primary aldosteronism (Margolius et al, 1974b, Seino et al, 1977 but not in essential hypertension (Seino et al, 1977).…”

Section: Hypertensionmentioning

confidence: 99%

“…Such methods are simple and, if the substrate is radiolabeled, quite sensitive (Margolius et al, 1974a;Beaven et al, 1971). Several groups have reported that urinary alkaline esterase activity correlates well with urokallikrein-related biological activities, as determined by bioassays (Levy et al, 1977;Margolius et al, 1974a, Seino et al, 1977. However, recent studies have demonstrated that urine contains non-kallikrein esterases which contribute significantly to measured activity Ole-MoiYoi et al, 1977a).…”

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confidence: 99%