Abstract
Prostacyclin (PGI2) may act physiologically as an antihypertensive hormone generated in vessel walls. It remains uncertain, however, whether or not PGI2 may be involved in the etiology of primary hypertension.
As an index of PGI2 production, we measured the levels of venous plasma 6-keto-PGF1α by specific radioimmunoassay after silicic acid column chromatographic purification in 64 normotensive and 48 essential hypertensive males. The subjects were grouped according to the presence or absence of a family history of hypertension in three age groups : young (24-39 years), middle-aged (40-55 years) and elderly (over 56 years) and were matched for age and blood pressure.
Mean levels of plasma 6-keto-PGF1α were 13.9±2.0pg/ml in the normotensive males and 15.5±2.2pg/ml in the hypertensive males. The levels of 6-keto-PGF1α in the hyper-tensive males were not significantly different from the levels in the normotensive males in the young, middle-aged and elderly groups, with or without a family history.
The levels of 6-keto-PGF1α in normotensive young males with a family history (12.2±2.1pg/ml; n=14) were lower than in normotensive young males without a family history (18.0±3.0pg/ml; n=9) (p<0.01). The levels of 6-keto-PGF1α in young hypertensive males with a family history (14.0±1.5pg/ml; n=9) were lower than in young hypertensive males without a family history (23.5±2.3pg/ml; n=8) (p<0.005). The levels of 6-keto-PGF1α in middle-aged hypertensive males with a family history (10.5±2.3pg/ml; n=12) however were lower than in middle-aged hypertensive males without a family history (18.0±2.0pg/ ml; n=9) (p<0.005).
But the levels of 6-keto-PGF1α in middle-aged normotensive males without a family history (15.0 ± 2.9pg/ml; n=11) were not significantly different from the levels in middle-aged normotensive males with a family history (12.5 ± 2.3pg/ml; n=11). The levels of 6-keto-PGF1α in elderly normotensive males without a family history (10.6 ± 1.9pg/ml; n=5) were not significantly different from the levels in elderly normotensive males with a family history (10.5 ± 1.9pg/ml; n=7). The levels of 6-keto-PGF1α in elderly hyper-tensive males without a family history (11.2 ± 2.5pg/ml; n=4) were not different from the levels in elderly hypertensive males with a family history (9.4 ± 2.3pg/ml; n=6).
And the levels of 6-keto-PGF1α in elderly males without a family history were significantly lower than in young or middle-aged males without a family history.
Consequently the levels of plasma 6-keto-PGF1α in males with, a family history may be decreased genetically. The decrease in production of PGI2 in young males with a family history may be a factor in the etiology of hypertension. And PGI2 production may decrease with age in males with a family history.
