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Urinary kallikrein was measured in normal pregnant women stages of gestation and in women who developed hypertension in late pregnancy. Mean urinary kallikrein was highest in the first trimester and fell significantly in the third trimester to nonpregnosterone system. A negative correlation was observed between urinary kallikrein and the length of gestation in normal pregnancy. Urinary kallikrein fell significantly below nonpregnant levels in patients with hypertension while the renal excretion of sodium and water was not different from that in normal pregnancy of the same dy is discussed in the light of factors known to increase kallikrein excretion. It is considered unlikely that this elevation is due to the escape from the sodium-retaining effect of the high aldosterone of pregnancy. It may be due in part to the stimulating effect of raised angiotensin II levels but it is considered most likely to be the effect of a circulating renal vasodilator. The reduced kallikrein in hypertension of pregnancy may play a part in the development of the hypertension and resembles the reduced kallikrein excretion in essential hypertension.
O A Elebute, and
I H Mills
November 1973,
Experientia,
O A Elebute, and
I H Mills
October 1999,
Immunopharmacology,
O A Elebute, and
I H Mills
January 1986,
Annals of clinical research,
O A Elebute, and
I H Mills
January 1989,
Archives of gynecology and obstetrics,
O A Elebute, and
I H Mills
January 1974,
Acta physiologica latino americana,
O A Elebute, and
I H Mills
September 1976,
Biomedicine / [publiee pour l'A.A.I.C.I.G.],
O A Elebute, and
I H Mills
February 1976,
Federation proceedings,
O A Elebute, and
I H Mills
February 1991,
Prostaglandins, leukotrienes, and essential fatty acids,
O A Elebute, and
I H Mills
January 1973,
Acta physiologica latino americana,
O A Elebute, and
I H Mills
January 1978,
Seminars in perinatology,
