Comprehensive Studies on the Renal Kallikrein-Kinin System in Essential Hypertension

Nakahashi, Yasuyuki; Shimamoto, Kazuaki; Ura, Nobuyuki; Tanaka, Shigemichi; Nishitani, Takahiro; Ishida, Hiroyuki; Yokoyama, Takahiro; Ando, Toshiaki; Ito, Osamu

doi:10.1007/978-1-4757-0154-8_44

Cited by 8 publications

(2 citation statements)

References 12 publications

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“…The report that a low kallikrein excretion rate may be accompanied by low plasma renin activity was not confirmed by another report (Holland et al, 1980), which stated that there is no significant difference between the urinary kallikrein excretion of either Black or white patients with low-renin essential hypertension and that of those with normal-renin essential hypertension. However, Japanese patients with low-renin hypertension, who are a relatively homogeneous population, show significant reductions in both active urinary kallikrein and kinin excretion together with increased levels of a kallikrein-inhibiting substance and kininase in the urine and with reduced levels of kininogen (Nakahashi et al, 1983). This controversy may be due to the heterogeneity of the subjects used in population studies.…”

Section: I77mentioning

confidence: 99%

Harmful algal blooms in Sodus Bay, Lake Ontario: A comparison of nutrients, marina presence, and cyanobacterial toxins

Perri

Sullivan

Boyer

2015

Journal of Great Lakes Research

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Section: I77mentioning

confidence: 99%

Harmful algal blooms in Sodus Bay, Lake Ontario: A comparison of nutrients, marina presence, and cyanobacterial toxins

Perri

Sullivan

Boyer

2015

Journal of Great Lakes Research

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“…Among Japanese patients with low-renin hypertension, there are significant reductions in both active urinary kallikrein and kinin excretion together with increased levels of a kallikrein-inhibiting substance and kininase in the urine accompanied by reduced levels of kininogen (151).…”

Section: Urinary Kallikrein In Hypertensivesmentioning

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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Kandidatengene der arteriellen Hypertonie und ihre klinische Bedeutung

Schunkert¹

1998

Herz-Kreislauf-Erkrankungen

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Comprehensive Studies on the Renal Kallikrein-Kinin System in Essential Hypertension

Cited by 8 publications

References 12 publications

Harmful algal blooms in Sodus Bay, Lake Ontario: A comparison of nutrients, marina presence, and cyanobacterial toxins

Harmful algal blooms in Sodus Bay, Lake Ontario: A comparison of nutrients, marina presence, and cyanobacterial toxins

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

Kandidatengene der arteriellen Hypertonie und ihre klinische Bedeutung

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