Circulating kallikreins in normotensive and hypertensive humans: effects of mineralocorticoid administration. 1997

K P Ohman
Department of Medicine and Care, Faculty of Health Sciences, Linköping, Sweden.

The aim of the study was to evaluate if short-term mineralocorticoid administration activates the circulating kallikrein-kinin systems in normotensive humans and patients with hypertension. Fludrocortisone was given daily for 1 week and circulating components of the plasma and tissue kallikrein-kinin systems and renin-angiotensin-aldosterone system were measured repeatedly. Fludrocortisone increased blood pressure in the normotensive group. A significant reduction in circulating pre-kallikrein and increase in tissue kallikrein occurred only in the normotensive group. Changes in blood pressure in the normotensive group correlated negatively with changes in plasma pre-kallikrein and positively with changes in circulating tissue kallikrein. In the hypertensive group the correlation with pre-kallikrein was non-significant and with tissue kallikrein negative. We conclude that short-term administration of fludrocortisone in moderate doses to normotensive humans induces changes compatible with increased activity in the circulating plasma and tissue kallikrein-kinin systems and that this activation may be abnormal in subjects with primary hypertension.

UI MeSH Term Description Entries
D006973 Hypertension Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more. Blood Pressure, High,Blood Pressures, High,High Blood Pressure,High Blood Pressures
D007610 Kallikreins Proteolytic enzymes from the serine endopeptidase family found in normal blood and urine. Specifically, Kallikreins are potent vasodilators and hypotensives and increase vascular permeability and affect smooth muscle. They act as infertility agents in men. Three forms are recognized, PLASMA KALLIKREIN (EC 3.4.21.34), TISSUE KALLIKREIN (EC 3.4.21.35), and PROSTATE-SPECIFIC ANTIGEN (EC 3.4.21.77). Kallikrein,Kininogenase,Callicrein,Dilminal,Kallidinogenase,Kalliginogenase,Kallikrein A,Kallikrein B',Kallikrein Light Chain,Kinin-Forming Enzyme,Padutin,alpha-Kallikrein,beta-Kallikrein,beta-Kallikrein B,Enzyme, Kinin-Forming,Kinin Forming Enzyme,Light Chain, Kallikrein,alpha Kallikrein,beta Kallikrein,beta Kallikrein B
D007705 Kinins A generic term used to describe a group of polypeptides with related chemical structures and pharmacological properties that are widely distributed in nature. These peptides are AUTACOIDS that act locally to produce pain, vasodilatation, increased vascular permeability, and the synthesis of prostaglandins. Thus, they comprise a subset of the large number of mediators that contribute to the inflammatory response. (From Goodman and Gilman's The Pharmacologic Basis of Therapeutics, 8th ed, p588) Kinin
D008297 Male Males
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D008901 Mineralocorticoids A group of CORTICOSTEROIDS primarily associated with water and electrolyte balance. This is accomplished through the effect on ION TRANSPORT in renal tubules, resulting in retention of sodium and loss of potassium. Mineralocorticoid secretion is itself regulated by PLASMA VOLUME, serum potassium, and ANGIOTENSIN II. Mineralocorticoid,Mineralocorticoid Effect,Mineralocorticoid Effects,Effect, Mineralocorticoid,Effects, Mineralocorticoid
D012084 Renin-Angiotensin System A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM. Renin-Angiotensin-Aldosterone System,Renin Angiotensin Aldosterone System,Renin Angiotensin System,System, Renin-Angiotensin,System, Renin-Angiotensin-Aldosterone
D001794 Blood Pressure PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS. Systolic Pressure,Diastolic Pressure,Pulse Pressure,Pressure, Blood,Pressure, Diastolic,Pressure, Pulse,Pressure, Systolic,Pressures, Systolic
D005260 Female Females
D005438 Fludrocortisone A synthetic mineralocorticoid with anti-inflammatory activity. 9-Fluorocortisol,9 alpha Fludrohydrocortisone,9 alpha-Fluoro-17-Hydroxycorticosterone,9 alpha-Fluorohydrocortisone,9-Fluoro-17-Hydroxycortisone,9-Fluorohydrocortisone,Astonin,Astonin Merck,Astonin-H,FCOL,9 Fluoro 17 Hydroxycortisone,9 Fluorocortisol,9 Fluorohydrocortisone,9 alpha Fluoro 17 Hydroxycorticosterone,9 alpha Fluorohydrocortisone,Astonin H,Merck, Astonin

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