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A missing link between a high salt intake and blood pressure increase.
Makoto Katori1, Masataka Majima
1Department of Pharmacology, Kitasato University School of Medicine, Kanagawa, Japan. hy3m_ktr@asahi-net.or.jp
Journal of Pharmacological Sciences
|May 3, 2006
Summary
Reduced kidney kallikrein-kinin system activity may explain salt-sensitive hypertension. This finding suggests measuring urinary kallikrein and developing new drugs targeting this system could help manage blood pressure.
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Pharmacology
Background:
- High sodium intake is linked to increased blood pressure, but the reasons for salt-sensitivity remain unclear in many individuals.
- Existing explanations for salt-sensitive hypertension are insufficient, necessitating further investigation into underlying mechanisms.
Purpose of the Study:
- To propose and investigate the role of reduced renal kallikrein-kinin system activity as a potential link to salt-sensitive hypertension.
- To explore the influence of ethnicity and potassium intake on blood pressure salt-sensitivity.
Main Methods:
- Review and synthesis of accumulated data on the kallikrein-kinin system in the kidney.
- Examination of the effects of potassium and ATP-sensitive potassium (K(ATP)) channel blockers in animal hypertension models.
- Discussion of the enzymatic pathways involved in bradykinin degradation within the nephron.
Main Results:
- Reduced activity of the renal kallikrein-kinin system is proposed as a key factor in salt-sensitivity.
- Ethnicity and potassium intake significantly influence blood pressure salt-sensitivity.
- K(ATP) channel blockers enhance renal kallikrein secretion and reduce blood pressure in animal models.
Conclusions:
- Measurement of urinary kallikrein may be valuable for identifying salt-sensitive individuals.
- Targeting the renal kallikrein-kinin system, via kallikrein releasers or kininase inhibitors, offers potential for novel antihypertensive therapies.