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Biomedical subjects

G Porcelli

Publications and source records attributed to G Porcelli.

At least 55 records · Page 3Linked to original sources
PubMed1979

Variation of urinary kallikrein excretion during pregnancy and the effects of hypertension.

In normal pregnant women the excretion of urinary kallikrein diminishes between the second and the third trimester and such reduction is maintained during the first ten days of puerperium. A comparison between normal women and those suffering from hypertension during the first, second and third trimester of pregnancy shows that, except for the first trimester, there exists a significant net reduction of enzyme excretion in the hypertensive cases. Dividing the patients according to the type of hypertension, it reveals that this phenomenon is unaltered for subjects having essential hypertension, while those affected by secondary hypertension or gestosis do not show any statistically significant variation in enzyme excretion from normal subjects.

Adolescent↗
PubMed1979

Altered urinary excretion of human kininase activity in hypertension.

This study describes the levels of urinary kininase activity in hypertension. Urinary kininase activity in essential and secondary hypertensive patients was higher than in controls (1010.2 +/- 102.7 versus 114.4 +/- 23.1 ng destroyed bradykinin/min.; p less than 0.001). In a group of hypertensive diabetics without nephropathy kininase activity in urine was decreased (46.0 +/- 12.7 ng destroyed bradykinin/min.). This investigation shows that in hypertension urinary kininase activity reaches higher levels. An inverse correlation was found between urinary kallikrein and urinary kininase activity from essential hypertensive patients.

Adolescent↗
PubMed1978

Urinary kallikrein excretion and plasma DBH activity in hypertension.

Many factors are to be considered in maintaining normal blood pressure. Authors study the behavior of urinary kallikrein (U.K.) and plasma dopamine-beta-hydroxylase (DBH) activity in various forms of hypertension. The values of U.K. excretion in normals were 20.5 +/- 1.8 E.U./24 h. In essential hypertensive patients (9.4 +/- 2.0 E.U./24 h) U.K. decreased, while in secondary hypertension it was significantly higher (33.8 +/- 3.0 E.U./24 h). Plasma DBH activity in essential hypertensive patients (17.72 +/- 2.33 I.U./ml) was similar to controls (20.22 +/- 1.39 I.U./ml); in secondary hypertension the mean values of plasma DBH were decreased (12.31 +/- 2.55 I.U./ml). No correlation between U.K. and plasma DBH activity was observed in normals and in various forms of hypertensive patients. U.K. seems a more reliable factor than plasma DBH in defining the different types of hypertension.

Adolescent↗
PubMed1978

Urinary kallikrein activity of workers exposed to lead.

Two groups of men of different age ranges and with the same period of lead exposure were selected for study in a recently opened car-battery factory. Two other groups of age-matched men, not exposed to heavy metals in their work, were used as controls. Morning urines were collected from control and exposed groups for determination of urinary kallikrein activity, urinary delta-amino-levulinic acid (ALA) and lead levels. The environmental lead levels and the urinary ALA and lead values indicated that exposure in the factory was not heavy. The older group of lead-exposed workers showed greatly reduced urinary kallikrein activity compared with that of the age-matched controls. In contrast, the younger group did not show any significant alteration in urinary kallikrein excretion.

Adult↗
PubMed1978

[Urinary kallikrein in cadmium-exposed workers].

The urinary kallikrein activity was determined in a group of 20 young workers exposed to cadmium and to lower concentrations of lead and other toxic agents. Two of them were suffering from labile hypertension. The urinary kallikrein activity of exposed workers was found to be reduced by more than 80% in comparison with a control group.

Adult↗
PubMed1977

[Urinary kallikrein and risk of lead poisoning].

Urinary kallikrein is an enzyme, probably originated in the kidney, which acts on plasma kininogen to produce kallidin, the decapeptide precursor of bradykinin, and appears to be implicated in various forms of arterial hypertension. It is significantly decreased in workers exposed to lead showing no hypertension or other clinical signs of lead poisoning. In respect to measurement of ALA or other heme precursors the determination of urinary kallikrein seems to be able to detect a different, and perhaps in certain cases earlier, effect of lead intoxication on enzyme functions.

Adult↗
PubMed1975

[Urinary kallikrein excretion in hepatic cirrhosis].

Measurements of urinary kallikrein using an esterolytic assay revealed higher levels in patients with liver cirrhosis than in a control population. The range of excretion in 33 patients with cirrhosis was from 18.68 to 85.20 E.U. per 24 hours with a mean excretion of 39.42 plus or minus 2.84 E.U. Kallikrein excretion in the control group ranged from 13.20 to 39.50 E.U. per 24 hours with a mean of 24.44 plus or minus 1.66 E.U.

Adult↗
PubMed1975

Urinary kallikrein excretion in a spontaneously hypertensive strain of rats.

Concentration and 24-hr excretion of urinary kallikrein in spontaneous hypertensive Wistar strain rats of both sexes obtained by selected inbreeding (25th generation) are significantly decreased as compared with the excretion in normotensive inbred rats (24th generation) descending from common ancestors. Apparently in these hypertensive rats there is an abnormal capacity of the kidneys to produce or release kallikrein, but more studies will be necessary to correlate this findings with blood pressure increase.

Animals↗