PubMed Health⌕ Search

Biomedical subjects

V C Zammit

Publications and source records attributed to V C Zammit.

11 recordsLinked to original sources
PubMed1996

Preeclampsia: the effects of serum on endothelial cell prostacyclin, endothelin, and cell membrane integrity.

OBJECTIVE: Our purpose was to determine whether serum from women with preeclampsia or gestational hypertension (1) decreased endothelial cell prostacyclin, (2) increased endothelial cell endothelin, and (3) caused endothelial cell damage. STUDY DESIGN: Production of 6-keto-prostaglandin F1 alpha and endothelin by cultured endothelial cells was measured after 48 hours' incubation with sera from 23 nonpregnant women, 23 normal pregnant women, 12 women with preeclampsia, and 11 women with gestational hypertension. Structure damage of endothelial cells was assessed by a chromium release assay. RESULTS: Serum from normal pregnant women induced more endothelial prostacyclin but less endothelin than did serum form nonpregnant women (p<0.05). No difference was found between normal pregnant and hypertensive pregnant women for prostacyclin production, but serum of preeclamptic women induced less endothelin production than did that of normal pregnant women (p<0.05). Chromium 51 release by endothelial cells was similar between normal pregnant and hypertensive pregnant groups. CONCLUSIONS: Serum from preeclamptic women stimulates less endothelin production than does serum from normal pregnant women but does not alter prostacyclin production and is not cytotoxic to endothelial cells after short-term incubation.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Primary hyperaldosteronism: a missed diagnosis in 'essential hypertensives'?

BACKGROUND: It has been recognised recently that primary hyperaldosteronism may be more common than previously thought, the frequency of diagnosis being improved by screening using a plasma aldosterone concentration to renin activity ratio. AIMS: To determine the frequency of primary hyperaldosteronism, screening with both plasma aldosterone to renin concentration (PRC) and activity (PRA) ratios, in normokalaemic subjects previously diagnosed as having essential hypertension. METHODS: Plasma potassium, aldosterone and PRCs and PRA and blood pressure (BP) were measured in 74 hypertensive subjects previously diagnosed by one physician as having essential hypertension. A normal range for plasma aldosterone/renin ratios was determined in 147 control subjects. Hypertensive subjects with elevated aldosterone/renin ratios were further assessed for primary hyperaldosteronism using saline loading and fludrocortisone suppression. Those in whom plasma aldosterone concentration exceeded 140 pmol/L after suppression tests underwent adrenal vein sampling for measurement of aldosterone and cortisol concentrations as well as adrenal CT scanning to diagnose the cause of primary hyperaldosteronism. The main outcome measures were a diagnosis of aldosterone producing adenoma or bilateral adrenal hyperplasia based upon adrenal vein sampling. RESULTS: Four subjects (5%) had an elevated plasma aldosterone to renin ratio using PRC and six (8%) using PRA. Two subjects (2.7%) in this selected population had primary hyperaldosteronism, both of whom had BP > 160/110 mmHg at the time of testing. CONCLUSIONS: The frequency of normokalaemic primary hyperaldosteronism appears to be greater than previously thought, though the true incidence in the general population of hypertensive subjects remains unknown. The sensitivity of diagnosis (but not specificity) may be improved by measurement of the plasma aldosterone/renin ratio and PRC is at least as adequate as PRA for this process.

Adult↗
PubMed1994

Albumin excretory rate in normal and hypertensive pregnancy.

1. The purpose of this study was to determine whether the 24 h urinary albumin excretory rate was increased in the third trimester of normal pregnancy or in pregnant women with hypertension who had 24 h urinary total protein excretion within the normal range. 2. Twenty-four hour urinary creatinine and albumin excretions were determined prospectively in 26 non-pregnant and 115 pregnant women in their third trimester (40 in normal pregnancy, 38 with mild pre-eclampsia, 20 with severe pre-eclampsia, 17 with essential hypertension) in whom urinary total protein excretion was normal. Both the urinary albumin excretion rate and the urinary albumin/creatinine ratio were compared among the groups. The clearance of albumin relative to that of creatinine was also calculated in the hypertensive women and in 14 of the non-pregnant women and nine of the normal pregnant women. 3. The twenty-four hour urinary albumin excretion rate was similar in non-pregnant [8(5-10) mg/day; median (interquartile range)] and normal pregnant [7(6-10) mg/day] women. Women with essential hypertension [6(4-16) mg/day] and mild pre-eclampsia [7(4-10) mg/day] had a urinary albumin excretion rate similar to that of normal pregnant women. Women with severe pre-eclampsia had an urinary albumin excretion rate increased [13(7-32) mg/day] compared with other groups (P < 0.05). The clearance of albumin relative to that of creatinine was elevated significantly only in women with severe pre-eclampsia compared with normal pregnant women (0.00054 versus 0.00012; P < 0.05). Blood pressures were similar among all hypertensive groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effects of cortisol on blood pressure and salt preference in normal humans.

1. Adrenocorticotrophic hormone (ACTH) and corticosteroids stimulate salt appetite in laboratory animals. The hypothesis tested was that cortisol administration increases salt preference in humans. 2. Sodium taste studies (detection and recognition thresholds, taste intensity and preference tests) were conducted before, during and after cortisol administration (200 mg/day for 5 days) in normal men on a free diet. 3. Cortisol significantly increased systolic blood pressure (SBP), 113 +/- 3 - 130 +/- 4 mmHg, P < 0.05; diastolic blood pressure (DBP), 65 +/- 3 - 81 +/- 2 mmHg, P < 0.05; mean arterial pressure (MAP), 81 +/- 2 - 97 +/- 3 mmHg, P < 0.05; and bodyweight, 72.9 +/- 3.0 - 75.4 +/- 3.3 kg, P < 0.05. 4. Salt detection and recognition thresholds, taste intensity and preference for sodium chloride were unchanged following cortisol.

Adult↗
PubMed1992

Endothelium-derived prostacyclin: effect of serum from women with normal and hypertensive pregnancy.

1. Pregnancy-induced hypertension (or pre-eclampsia) is characterized by vasoconstriction, platelet aggregation and altered capillary permeability, implying disordered endothelial function and/or structure. Serum from women with pregnancy-induced hypertension has been reported by others to be cytotoxic to endothelial cells in vitro. We hypothesized that such serum contains a factor that limits the ability of endothelial cells to produce and/or release prostacyclin. 2. Prostacyclin production by intact and damaged cultured human umbilical vein endothelial cells was measured after incubating these cells with serum from non-pregnant and normal pregnant women and women with pregnancy-induced hypertension. Confluent human umbilical vein endothelial cell monolayers (intact and damaged) were incubated with sera for 24 h at 37 degrees C followed by 1 h of incubation with added thrombin (stimulated production) or media (basal production). Supernatants were then collected for measurement of 6-keto-prostaglandin F1 alpha by radioimmunoassay. 3. Basal production of 6-keto-prostaglandin F1 alpha was greater in response to serum from non-pregnant women than to that from pregnant women. Within each group, sub-lethally damaged cells had a similar basal production of 6-keto-prostaglandin F1 alpha to that of intact cells. 4. Basal production of 6-keto-prostaglandin F1 alpha by intact or damaged cells incubated with sera from normal pregnant women and from women with pregnancy-induced hypertension was similar. 5. In all groups the addition of thrombin to intact endothelial cells increased 6-keto-prostaglandin F1 alpha production approximately 15-30-fold over basal levels, but only three- to five-fold in damaged endothelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Renin-aldosterone relationships in pregnancy-induced hypertension.

The relationship between plasma renin (PRC) and aldosterone (PAC) concentrations was determined in 83 normal third trimester pregnant women (P), 50 women with pregnancy-induced hypertension (PIH), and 80 age-matched nonpregnant women not taking oral contraceptives (NP). Normal pregnant women had a slightly higher 24-h urine sodium: creatinine ratio than the other groups (P less than .001) (NP: 10 +/- 4 v P: 15 +/- 8 v PIH: 12 +/- 7; mean +/- SD). Both PRC and PAC were higher in normal pregnant women as was the ratio PAC:PRC [normal pregnant 195 (158 to 337) v nonpregnant 130 (101 to 209), median (interquartile range); P less than .001]. This was accompanied by a slightly reduced slope (sensitivity) of the logPRC-logPAC relationship in normal pregnant women (P less than .05). Women with PIH had reduced PRC and PAC compared with normal pregnant women but a two-fold greater increase in PAC:PRC ratio [PIH 411 (277 to 598) v normal pregnancy 195 (158 to 337), P less than .001], with a rise in the slope (sensitivity) of the logPRC-logPAC relationship in women with PIH (P less than .001). Thus there is proportionately greater aldosterone release in the third trimester of normal pregnancy than in nonpregnant women. This preferential increase in aldosterone may be due to altered adrenal sensitivity to angiotensin II or may reflect enhanced nonangiotensin stimulation of aldosterone during pregnancy. Women with PIH have reduced PRC and PAC but relatively greater stimulation of aldosterone than normal pregnant women, possibly due to enhanced sensitivity of the adrenal glands to angiotensin II.

Aldosterone↗
PubMed1992

Extracellular fluid volumes in pregnancy-induced hypertension.

OBJECTIVES: Reduction in plasma volume (Pvol) of women with pregnancy-induced hypertension (PIH; preeclampsia) has both physiological and clinical implications. This study was undertaken to determine the following variables in women with PIH: (1) the incidence of reduced Pvol; (2) the distribution of total extracellular fluid volume (ECFV); (3) the relationship between Pvol and birth weight; and (4) whether any readily available clinical or laboratory parameters predict the presence of reduced Pvol. SETTING: Teaching hospital obstetric unit and antenatal clinic. PARTICIPANTS: Forty-nine primigravidae with PIH (28 mild, 21 severe), 54 normotensive primigravidae and 25 non-pregnant controls. DESIGN: Pvol was measured using Evans Blue dye and ECFV as the mannitol space. These measures were compared amongst groups, and also within groups for those with PIH, according to the severity of their disorder and the presence of proteinuria or oedema. Blood pressure, haematocrit, uric acid and serum albumin were also evaluated as predictive indices of reduced Pvol in women with PIH. RESULTS: Pvol, ECFV and the Pvol:ECFV ratio all increased during normal pregnancy. Pvol in women with PIH was reduced compared with normal pregnancy and correlated significantly with birth weight. Total ECFV was unchanged in women with PIH, but their Pvol:ECFV ratio was significantly reduced compared with normal pregnancy. Although there was a significant correlation between Pvol and haematocrit in women with PIH, haematocrit was a poor predictor for reduced Pvol. Diastolic blood pressure greater than 100 mmHg, persistent proteinuria and severe PIH were the only reliable positive predictors of a reduced Pvol. CONCLUSIONS: Pvol is related to birth weight, but is reduced in only approximately half of women with PIH. This reduced Pvol is the result of maldistribution, not loss, of total ECFV, and can be predicted by high diastolic blood pressure, proteinuria or other clinical signs of severity, but not by haematocrit.

Adult↗
PubMed1991

Atrial natriuretic peptide and plasma volume in pregnancy-induced hypertension.

Pregnancy-induced hypertension (PIH) is characterized by a relative decrease in plasma volume and renin and aldosterone concentrations as well as increased capillary permeability compared with normal pregnancy. As many of these features could be explained by the actions of atrial natriuretic peptide (ANP), we examined the relationship between plasma volume and plasma ANP in women with PIH and in normal third trimester pregnant women, and whether ANP responses to alterations in posture were intact in women with PIH. Basal plasma ANP measured after 20 min lateral recumbency in women with PIH was 24.0 (13.9, 33.1) pmol/L (median [25th, 75th percentile]), which was significantly greater than in normal pregnant women (9.9 [6.3, 16.0]), (P less than .05). Plasma ANP did not differ between those with and without proteinuria in the PIH group. Plasma volume was decreased in women with PIH (20.1 [19.0, 23.2] mL/cm) v 23.5 [21.4, 25.3], P less than .05). Plasma renin concentration but not plasma aldosterone concentration was also decreased significantly in women with PIH compared with normal pregnant women (P less than .001) and both were correlated negatively with plasma ANP. Following prolonged lateral recumbency, plasma ANP rose to 26.9 [19.1, 44.1] pmol/L in women with PIH (P less than .05), which was still significantly greater than in normal pregnant women (15.5 [6.7, 21.9] pmol/L) (P less than .05). In a subgroup of these subjects, 30 min head-up tilt decreased plasma ANP by 5.2 [0.9, 22.3] pmol/L in women with PIH and by 6.1 [2.2, 10.3] pmol/L in normal pregnant women, a nonsignificant difference.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Stimulation of active renin release in normal and hypertensive pregnancy.

1. Active plasma renin concentration but not total renin concentration is reduced in women with pregnancy-induced hypertension compared with normotensive pregnant women. This study was conducted to determine whether women with pregnancy-induced hypertension are able to stimulate release of active renin. 2. Active plasma renin concentration was measured as the generation of angiotensin I at physiological pH in the presence of excess renin substrate, and total renin concentration was determined in the same way after trypsin activation. Inactive plasma renin concentration was calculated as the difference between total renin and active plasma renin concentrations. 3. Resting active plasma renin concentration was significantly greater in third-trimester primigravidae compared with normotensive non-pregnant women and active plasma renin and total renin concentrations rose significantly without a fall in inactive plasma renin concentration in both groups after 2 h ambulation, suggesting increased release of active plasma renin and not conversion of circulating inactive to active renin. These responses were blunted in women taking oral contraceptives. 4. Although the active plasma renin concentration was significantly reduced in third-trimester primigravidae with pregnancy-induced hypertension, total renin concentration was not significantly different compared with normotensive women of similar gestation and in both groups 30 min 60 degrees head-up tilt increased active but not inactive plasma renin concentration. 5. These studies show that in normal pregnancy active plasma renin concentration can be stimulated to a similar extent as in non-pregnant women, despite a higher resting level. This appears to be due to increased secretion of active plasma renin rather than conversion of circulating inactive to active renin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Capillary permeability and extracellular fluid volumes in pregnancy-induced hypertension.

1. Capillary permeability was determined by the disappearance rate of Evans Blue dye from plasma in healthy non-pregnant women, normal third-trimester primigravidae and primigravidae with pregnancy-induced hypertension. 2. Extracellular fluid volume was determined from the disappearance curves of injected mannitol in the same subjects and the plasma volume was measured by the Evans Blue dye dilution technique. 3. In normal pregnancy capillary permeability was not altered from that of non-pregnant subjects. Although extracellular fluid volume and plasma volume were increased in normal pregnant compared with non-pregnant women, the distribution of fluid between plasma volume and interstitial fluid volume was unaltered. 4. Women with established pregnancy-induced hypertension had a more rapid Evans Blue disappearance rate and a lower plasma volume than normal pregnant women, independent of the presence of proteinuria. Maternal plasma volume correlated positively and significantly with fetal birth weight in women with pregnancy-induced hypertension, emphasizing the important relationship between maternal plasma volume and fetal outcome. 5. The increased capillary permeability in women with pregnancy-induced hypertension was associated with a reduction in the plasma volume/interstitial fluid volume ratio but a normal extracellular fluid volume, suggesting that the reduced plasma volume did not result from sodium loss but rather from a redistribution of the total extracellular fluid volume. These changes did not differ significantly in subgroups with and without oedema.

Adult↗