Premium
Studies on the role of platelet‐activating factor in blood pressure regulation
Author(s) -
Sakaguchi Katsuhiko,
Morimoto Shigeto,
Masugi Fuminori,
Saeki Shuichi,
Ogihara Toshio,
Yamada Kouji,
Yamatsu Isao
Publication year - 1991
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02536544
Subject(s) - chemistry , medicine , endocrinology , platelet activating factor , blood pressure , endogeny , platelet , clinical chemistry , creatinine , mean platelet volume
Circulating levels of 1‐ O ‐hexadecyl‐2‐acetyl‐ sn ‐glycero‐3‐phosphocholine (C 16 PAF) in human subjects were measured by gas chromatography/mass spectrometry using negative ion chemical ionization. The mean (±S.D.) circulating C 16 PAF levels in patients with essential hypertension (18.1±5.3 pg/mL, n=16) were not significantly different from those in normotensive subjects (17.2±7.2 pg/mL, n=14). During a salt balance study, high salt intake (20 g/day) significantly increased the circulating level of C 16 PAF, and changes in circulating C 16 PAF significantly and positively correlated with changes in mean arterial blood pressure (r=0.47, p<0.05). Changes in C 16 PAF also correlated with changes in creatinine clearance (r=0.55, p<0.05), but did not correlate with changes in plasma sodium concentration, plasma chloride concentration and plasma volume. An intravenous injection of 50 μg of human atrial natriuretic peptide (hANP) decreased circulating C 16 PAF levels from 20.0±2.7 to 13.9±2.4 pg/mL of blood (n=10, p<0.01) in healthy subjects. The data appear to indicate that C 16 PAF levels are changed by salt intake‐induced mild increase in blood pressure, and that hANP may be an endogenous factor which lowers circulating C 16 PAF.