PubMed Health⌕ Search

Biomedical subjects

F Broughton Pipkin

Publications and source records attributed to F Broughton Pipkin.

At least 73 records · Page 4Linked to original sources
PubMed1991

Platelet angiotensin II binding sites in normotensive and hypertensive women.

Specific binding of angiotensin II (AII) to platelets was measured in 89 women, 25 nulliparous non-pregnant women and 64 primigravida in the third trimester of pregnancy. There was significantly lower binding in the 25 pregnant women who were normotensive (2.3 fmol/10(9) cells) when compared with the non-pregnant women (9.0 fmol/10(9) cells P less than 0.001). Significantly higher platelet AII binding levels were found in the 39 women who had pregnancy induced hypertension (PIH) (5.5 fmol/10(9) cells) when compared with the 25 normotensive pregnant women (P less than 0.001). Of the 39 women with PIH, platelet AII binding was higher in the 23 women who had pre-eclampsia (7.0 fmol/10(9) cells), when compared with the 16 who had non-proteinuric PIH, (4.6 fmol/10(9) cells) although the difference was not statistically significant (P less than 0.04). The pressor response to AII is also diminished in pregnancy, yet less so if pregnancy induced hypertension develops. Platelets may provide a readily accessible tissue with which to study AII responsiveness in pregnancy.

Adult↗
PubMed1991

Platelet reactivity and serum thromboxane B2 production in whole blood in gestational hypertension and pre-eclampsia.

OBJECTIVE: To determine the nature and extent of changes in platelet reactivity in gestational hypertension and pre-eclampsia (using whole blood techniques which may be more physiological than those previously employed). DESIGN: Cross-sectional observational study. SUBJECTS: 8 normal primigravidae, 16 women with gestational hypertension and 12 women with pre-eclampsia, studied at around 36 weeks gestation. RESULTS: Platelet reactivity (aggregation and release reaction) induced by stimulation with adrenaline was decreased in the pre-eclamptic group. Serum thromboxane B2 production was unchanged in both hypertensive groups compared with the control group. CONCLUSIONS: In the context of evidence of platelet activation in pre-eclampsia, our findings are interpreted as reflecting platelet exhaustion.

Adult↗
PubMed1991

Factors influencing plasma renin and renin substrate in premature infants.

Concentrations of plasma renin (PRC) and plasma renin substrate (PRS) were measured during the first week of life in 52 infants born at less than 37 weeks' gestation (mean (SEM) gestation 30 (0.4) weeks, mean (SEM) birth weight 1.35 (0.08) kg). Both PRC (median 35, interquartiles 16.3, 94.5 ng/ml/hour) and PRS (median 2.3, interquartiles 1.3, 5.0 micrograms/ml) were raised compared with adults. The proportional rise in PRC was much greater than that in PRS, suggesting that PRS may be rate limiting in the generation of angiotensin I. Log10 PRC was inversely proportional to gestational age and a high urinary sodium loss was associated with a significantly raised log10 PRC. In hypoxaemic infants, there was a strong correlation between log10 PRS and haemoglobin concentration; this is a new observation in human infants but consistent with data available from other species.

Angiotensinogen↗
PubMed1990

A longitudinal study of respiratory changes in normal human pregnancy with cross-sectional data on subjects with pregnancy-induced hypertension.

Respiratory frequency, tidal volume, minute ventilation, oxygen consumption, carbon dioxide production, and end-tidal carbon dioxide tension were measured longitudinally during pregnancy and post partum in 20 normal subjects with a computer-assisted mass spectrometer. Resting tidal volume, minute ventilation, oxygen consumption, and carbon dioxide production increased during pregnancy. End-tidal carbon dioxide tension fell progressively during pregnancy. Respiratory exchange ratio was 0.9 at 36 to 39 weeks' gestation and 0.8 at 5-13 weeks post partum. Respiratory frequency did not change during pregnancy. The increase in minute ventilation is in excess of the increase of carbon dioxide production and the resultant fall in end-tidal carbon dioxide tension reflects a fall in systemic arterial blood carbon dioxide tension. The greater respiratory exchange ratio during late pregnancy as compared with post partum also reflects this hyperventilation during pregnancy. Fourteen subjects with pregnancy-induced hypertension studied cross-sectionally failed to show any difference in the respiratory variables measured when compared with normotensive subjects at a similar length of gestation.

Adult↗
PubMed1990

A cross-sectional study of basal platelet intracellular free calcium concentration in normotensive and hypertensive primigravid pregnancies.

1. The intracellular free calcium concentration ([Ca2+]i) in washed human platelets was measured using the fluorescent indicator, fura-2, in a cross-sectional study of 36 normotensive, primigravid volunteers, 12 in each trimester of pregnancy and a further 12 at 6 weeks post partum. The results were compared with those obtained from 30 normal female volunteers not using oral contraception. 2. The mean basal [Ca2+]i in the platelets of the pregnant women in the first two trimesters (115.6 +/- 6.7 and 120.1 +/- 5.7 nmol/l, respectively) was not shown to differ significantly from that of normal non-pregnant volunteers (112.3 +/- 2.9 nmol/l). However, during the third trimester a significant increase in [Ca2+]i was noted (134.0 +/- 4.9 nmol/l; P less than 0.05), with a return to normal values in the post-partum period (108.2 +/- 6.1 nmol/l). 3. [Ca2+]i was also measured in the platelets of a group of 12 primigravid pregnant women in the third trimester whose pregnancies were complicated by gestational hypertension (pregnancy-induced hypertension and pre-eclampsia). A significant rise in basal [Ca2+]i was noted in the platelets of primigravidae whose pregnancies were complicated by pre-eclampsia (163.6 +/- 8.8 nmol/l) as compared with normotensive, third-trimester primigravidae (P less than 0.02). However, no correlation could be demonstrated between [Ca2+]i and systemic blood pressure.

Adult↗
PubMed1990

Influence of raising maternal blood pressure with angiotensin II on utero-placental and feto-placental blood velocity indices in the human.

1. The effect of doubling doses of angiotensin II on maternal systemic blood pressure and arcuate and fetal umbilical artery Doppler velocity profiles has been investigated in 10 women in first- and 10 in second-trimester pregnancy. Ten non-pregnant women were also studied. 2. A progressive decrease in the pressor response to angiotensin II in early pregnancy as previously described was confirmed. 3. Angiotensin II induced a significant dose-dependent increase in the pulsatility index (a measure of downstream resistance) in the umbilical artery in both first- and second-trimester patients. There was an apparent increase in the threshold response of the pulsatility index to angiotensin II in the umbilical artery as pregnancy progressed. There was also a significant correlation between changes in maternal systolic or diastolic pressure and change in umbilical artery pulsatility index, but this did not differ between the two trimesters. This suggests that the increase in pulsatility index is related to blood pressure rather than angiotensin II. This is consistent with reports that angiotensin II does not cross the haemomonochorial placenta. 4. Basal pulsatility index in the arcuate artery fell with increasing gestation. There was a significant inverse association between the evoked change in maternal systemic blood pressure and the change in arcuate artery pulsatility index, suggesting local vasodilatation. 5. We conclude that acutely increasing maternal blood pressure leads to increased vascular resistance on the fetal side of the circulation.

Adult↗
PubMed1990

Platelet angiotensin II binding and plasma renin concentration, plasma renin substrate and plasma angiotensin II in human pregnancy.

1. The results are presented of a cross-sectional study of 25 non-pregnant and 125 pregnant/postnatal women in whom platelet angiotensin II binding and plasma angiotensin II, plasma renin concentration and plasma renin substrate were measured. 2. Platelet angiotensin II binding was significantly lower in the first-trimester patients as compared with the non-pregnant women (P less than 0.001). Specific binding remained low in the second and third trimesters, and in those patients studied 24 h after delivery. However, higher values, approximating to the non-pregnant level, were found 6 weeks postnatally (n = 25 for each group). 3. Plasma angiotensin II, plasma renin concentration and plasma renin substrate increased in pregnancy, with the increase becoming statistically significant as compared with the non-pregnant women in the second trimester. Maximal median values of plasma angiotensin II and plasma renin substrate were found in the third trimester, but maximal median values of plasma renin concentration were found in the second trimester. The concentrations of all three hormones fell after delivery. 4. There was an inverse correlation between platelet angiotensin II binding and simultaneously measured endogenous levels of plasma angiotensin II (P less than 0.02) and plasma renin substrate (P less than 0.05) in the 25 non-pregnant subjects. These findings support the concept of the angiotensin II receptor concentration being regulated by the plasma angiotensin II level. There was no correlation between platelet angiotensin II binding and plasma renin concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1990

A longitudinal study of platelet behaviour and thromboxane production in whole blood in normal pregnancy and the puerperium.

A longitudinal study of platelet behaviour (platelet aggregation and release reaction) in whole blood and of serum thromboxane B2 production was performed before, during and after normal pregnancy. The response of platelets to arachidonic acid and to adrenaline was significantly increased in the third trimester. Six weeks after delivery, values were still modestly increased but return to non-pregnant values was complete by 12 weeks. Serum thromboxane B2 production was unchanged throughout pregnancy and the puerperium.

Arachidonic Acid↗
PubMed1990

Determinants of fetal and maternal atrial natriuretic peptide concentrations at delivery in man.

Matched maternal venous (MV), umbilical artery (UA) and umbilical vein (UV) concentrations of atrial natriuretic peptide [ANP] were measured in 36 normotensive women at term delivery (23 vaginal, 13 caesarean) and 17 non-pregnant women in the first half of the menstrual cycle. MV [ANP] at caesarean section was similar to that in non-pregnant women, but UA and UV [ANP] were higher (P less than 0.01 for both). UA, but not UV, [ANP] was markedly raised after vaginal delivery. Plasma concentrations of aldosterone [ALD] were measured in 16 of the matched sets of samples. No statistically significant association was found between [ANP] and [ALD] in either maternal or fetal samples. Neither maternal nor fetal [ANP] correlated with serum Na+ or osmolality, haematocrit, blood pressure or heart rate.

Adult↗
PubMed1990

Studies on the human ovarian renin-angiotensin system: optimization of assay methodology and effects of follicular stimulants.

The renal and genital tracts share a common embryological origin; it is thus not surprising that tissues from both can synthesize renin. Preliminary studies showed extremely high concentrations of renin in follicular fluid (FRC) following ovarian stimulation for in-vitro fertilization. This necessitated complete revalidation of the renin assays and showed that data obtained using commercial kits were invalid. An assay protocol was developed using a 1:2 dilution of follicular fluid taken into EDTA (0.3 mol/l) and o-phenanthroline (0.05 mol/l). The assay was performed at pH 7.5 in the presence of excess exogenous (sheep) renin substrate, with incubation periods of 5, 10 and 15 min at 37 degrees C. This protocol resulted in the linear generation of angiotensin I (AI). Activation of inactive renin was performed using eightfold more trypsin than was required for plasma samples. Follicular renin substrate concentrations (FRS) were measured using the same assay methodology as used for measurement of plasma renin substrate concentrations (PRS). Storage of samples at -18 degrees C for up to 2 months was found not to affect the FRC, although repeated freeze-thaw cycles did. FRC and plasma renin concentrations (PRC) were very similar in 25 unstimulated control women, studied in the follicular phase of the menstrual cycle. Trypsin activation increased follicular total renin concentration (FTRC) more than plasma total renin concentration (PTRC) (P less than 0.0001). FRS was slightly higher than PRS (P less than 0.02). Ovarian stimulation with clomiphene citrate (CC; six women) was without effect on these parameters.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗
PubMed1989

Human alpha- and beta-calcitonin gene-related peptides are vasodilators in human chorionic plate vasculature.

Calcitonin gene-related peptide receptors are known to be present in the placenta. We studied the effect of alpha- or beta-calcitonin gene-related peptide or carrier on human chorionic plate arteries preconstricted with angiotensin II. Both forms of calcitonin gene-related peptides evoked dose-dependent relaxation, the magnitude of which was proportional to the initial response to angiotensin II.

Calcitonin Gene-Related Peptide↗
PubMed1989

Prostacyclin attenuates both the pressor and adrenocortical response to angiotensin II in human pregnancy.

1. The effects of angiotensin II (ANG II) infusion without and with simultaneous infusion of prostacyclin (PGI2; 1.4 pmol min-1 kg-1; 5 ng min-1 kg-1) have been studied in 16 women in second-trimester pregnancy. Ten received one infusion of ANG II alone, followed by its infusion together with PGI2; the remainder received two identical infusions of ANG II alone as controls. 2. PGI2 administration was associated with a small fall in diastolic pressure (P less than 0.01) and a proportionally greater rise in heart rate (P less than 0.001). Small rises in basal plasma renin and ANG II concentrations and a fall in aldosterone concentration were not statistically significant. 3. The diastolic pressor response to ANG II was blunted during PGI2 infusion by comparison with controls (P less than 0.025); this diminution in response was greatest in patients who had initially been most sensitive to ANG II (P less than 0.02). 4. The evoked increment in plasma aldosterone during ANG II infusion was considerably reduced (P less than 0.005) in the presence of PGI2. 5. These data further support the hypothesis of a role for PGI2 in relation to the blunted pressor response to ANG II of normal pregnancy. The apparent inhibitory effects of PGI2 on aldosterone secretion may partly explain the previously described dissociation between the renin-angiotensin system and aldosterone in pregnancy.

Adrenal Cortex↗
PubMed1989

The fetal outcome in a randomized double-blind controlled trial of labetalol versus placebo in pregnancy-induced hypertension.

The effects of labetalol were compared with those of placebo in a multicentre randomized double-blind and prospective study of 152 patients with mild to moderate, non-proteinuric pregnancy-induced hypertension. Labetalol in a dose of 100 mg three times daily, increasing to 200 mg three times daily where required, significantly reduced maternal mean arterial pressure. There was some reduction in preterm delivery, neonatal respiratory distress syndrome and jaundice in the labetalol-treated group. Intrauterine growth retardation and neonatal hypoglycaemia occurred with the same frequency in both groups. There were no perinatal deaths. Labetalol appears to be an effective agent in the management of mild to moderate pregnancy-induced hypertension. The data from this study suggest possible advantages and no apparent disadvantages for the fetus during its use.

Adult↗