PubMed Health⌕ Search

Biomedical subjects

E W Seely

Publications and source records attributed to E W Seely.

At least 37 records · Page 2Linked to original sources
PubMed1998

Regulation of the sodium pump in pregnancy-related tissues in preeclampsia.

OBJECTIVE: This study examined the expression of the three alpha-isoforms of the sodium pump in preeclampsia. Reductions in sodium pump number and activity in smooth muscle may underlie hypertension in preeclampsia. STUDY DESIGN: Northern and Western analyses were used to determine whether sodium pump alpha-isoform regulation in myometrium, placenta, and umbilical artery of women with preeclampsia differed from those with normotensive pregnancies. RESULTS: Levels of alpha1 and alpha3 messenger ribonucleic acid were reduced in myometrium of women with preeclampsia compared with normotensive pregnancies, as was alpha2 messenger ribonucleic acid in preeclamptic placenta. Protein expression of the alpha-isoforms was unaltered in placenta and umbilical artery from women with preeclampsia versus those with normotensive pregnancies, but myometrial alpha2 protein levels were reduced significantly in women with preeclampsia. Moreover, myometrial alpha1 protein expression was undetectable. CONCLUSIONS: Reduced smooth muscle sodium pump expression in preeclampsia may raise cell sodium, increase pressor sensitivity, or increase tone directly, which may contribute to hypertension in preeclampsia.

Adult↗
PubMed1998

Dissociation of vascular and adrenal responsiveness to angiotensin II following calcium channel blockade.

Calcium channel blockers as a class reduce both vascular resistance and systemic blood pressure. However, it is not known if different classes of calcium channel blockers have similar effects on the renin-angiotensin-aldosterone system. We investigated vascular and adrenal responses to endogenous and exogenous angiotensin II in normotensive subjects before and after receiving isradipine or diltiazem. Subjects achieved low salt balance before study and underwent an angiotensin II infusion and upright posture study. After re-achieving salt balance the subjects received either isradipine (n=10), or diltiazem (n=7) for three days before repeating the study. Both agents lowered blood pressure and significantly shifted the dose response relationship of angiotensin II and mean blood pressure (P<0.01). In contrast, aldosterone secretion in response to upright posture and angiotensin II infusion was significantly reduced (P<0.01) by isradipine but not by diltiazem. The in vitro effects of both agents on aldosterone secretion from bovine adrenal glomerulosa cells paralleled the in vivo observations showing that angiotensin II-stimulated aldosterone secretion was markedly blunted by isradipine and minimally by diltiazem. These results suggest a tissue specificity for the effects of different classes of calcium channel blockers. Dihydropyridine calcium channel blockers may exert their antihypertensive effect by blocking both vascular and adrenal responses to angiotensin II.

Adrenal Glands↗
PubMed1997

A prospective study of calciotropic hormones in pregnancy and post partum: reciprocal changes in serum intact parathyroid hormone and 1,25-dihydroxyvitamin D.

OBJECTIVE: The purpose of this study was to examine the hormones regulating calcium homeostasis longitudinally in pregnancy and post partum. STUDY DESIGN: Twenty-three women with normal pregnancies were studied in the second and third trimesters and post partum. At each time blood was analyzed for ionized calcium, vitamin D metabolites, and intact parathyroid hormone, and a 24-hour urine specimen was analyzed for creatinine, calcium, and sodium. RESULTS: Urinary calcium excretion was 250% to 300% higher during pregnancy than post partum (p < 0.00001). 1,25-Dihydroxyvitamin D levels were equivalent in the second and third trimesters but were twofold higher than postpartum values (p < 0.01). Ionized calcium was similar at all time points. Intact parathyroid hormone in the second and third trimesters was 50% of postpartum levels (p < 0.001). CONCLUSION: Pregnancy is associated with an increase in the levels of 1,25-dihydroxyvitamin D and a concomitant reciprocal fall in intact parathyroid hormone levels. The increase in serum 1,25-dihydroxyvitamin D values appears to be a key factor in providing for the increase in maternal calcium requirements during pregnancy.

Adult↗
PubMed1997

Age, gender, and non-modulation. A sexual dimorphism in essential hypertension.

The angiotensinogen gene is one of the very few related by linkage analysis to human hypertension, but the linkage has been consistently shown only among males. Moreover, polymorphisms in this gene predict an abnormal renal responsiveness to angiotensin II, a feature of non-modulation, but again, only among males. To pursue these related bridges between genetics and physiology, we evaluated the effects of sex on a second feature of non-modulation, the aldosterone response to infused angiotensin II during low sodium balance. We tested the resultant hypothesis-that non-modulation would be less frequent in women-by conducting identical protocols on 225 hypertensive inpatients (70 women, 155 men). Non-modulation was strikingly less frequent among women (26%; 95% confidence interval, 16% to 37%) than men (49%; 95% confidence interval, 40% to 57% (P = .001). We tested the hypothesis that sex steroids play a role by comparing young, premenopausal women (< 35 years) with women who were perimenopausal (45 to 55 years) and postmenopausal (> 55 years). Among the youngest women, the frequency of non-modulation was only 7%, significantly less than in young men (41%, P = .02). A steady increase in non-modulation frequency accompanied advancing age in women, reaching 47% in those older than 55 years, equal to the fraction of men affected. Age influenced non-modulation frequency in men far less. We conclude that a striking sex difference underlies the non-modulation phenotype and that female sex hormones may confer protection against a genotypic predisposition in women. This "override" of genotype, manifest by a very low frequency of non-modulation in young women, may participate in their known protection against cardiovascular disease.

Adolescent↗
PubMed1996

Primary hyperaldosteronism in pregnancy. A case report.

BACKGROUND: Primary hyperaldosteronism is an uncommon disorder, and there are few reports of its occurrence and management in pregnancy. CASE: Primary hyperaldosteronism was suspected before pregnancy in a 31-year-old women with refractory hypertension and hypokalemia. Pregnancy evaluation revealed suppressed renin levels and high aldosterone levels; computed tomography revealed a 1-cm mass in the left adrenal gland. The patient became pregnant before completion of evaluation and treatment. On high doses of nifedipine and nadolol, the first-trimester blood pressure was 130/98 mm Hg and remained high in the early second trimester. In view of the risks of poorly controlled hypertension, adrenalectomy was performed at 15 weeks' gestation, with rapid improvement in blood pressure and elimination of the patient's requirement for large doses of potassium daily. Antihypertensive medication was withdrawn, with maintenance of normal blood pressure until 36 weeks' gestation. At that time the blood pressure rose slightly but responded to bed rest. A healthy female infant was delivered at term by cesarean section. CONCLUSION: Previous reports of emergency preterm delivery and a case of neonatal mortality in the setting of hyperaldosteronism in pregnancy confirm the significant risks associated with this condition. In our patient, adrenalectomy in the early second trimester resulted in a rapid and sustained improvement in hypertension, reversal of hypokalemia and a good pregnancy outcome.

Adrenal Glands↗
PubMed1995

Digitalis-like factor and digoxin-like immunoreactive factor in diabetic women with preeclampsia, transient hypertension of pregnancy, and normotensive pregnancy.

An endogenous sodium pump inhibitor, or digitalis-like factor (DLF), has been postulated to mediate essential hypertension. It may also play a role in preeclampsia. However, studies of this factor in hypertensive pregnancy have not provided consistent findings. Part of this may be due to the absence of subclassification of pregnant women with pregnancy-induced hypertension (PIH) when assessing these parameters. In this study we explored serum DLF and digoxin-like immunoreactive factor (DLIF) in insulin-dependent diabetic (IDDM) women with normotensive pregnancies or PIH, comparing them to each other and to nondiabetic pregnant women. Our results demonstrated that nondiabetic women with preeclampsia (PE, PIH with proteinuria) had significantly increased serum DLF and DLIF compared to normotensive pregnant women (NL BP). Women with transient hypertension of pregnancy (THP, PIH without proteinuria) had intermediate values (DLF. NL BP: 3.3 +/- 0.6, THP: 4.8 +/- 1.1, PE: 7.6 +/- 1.3% inhibition [Na,K]-ATPase, P < .05 ANOVA; DLIF. NL BP: 0.22 +/- 0.02, THP: 0.28 +/- 0.03, PE: 0.35 +/- 0.02 ng digoxin equivalents/mL, P < .05 ANOVA). Pregnant normotensive IDDM women had significantly higher serum DLF and DLIF activity than their nondiabetic counterparts (DLF. non-IDDM NL BP: 3.3 +/- 0.6 v IDDM NL BP: 8.8 +/- 1.2% inhibition [Na,K]-ATPase, P = .0008; DLIF. non-IDDM NL BP: 0.22 +/- 0.02 v IDDM NL BP: 0.31 +/- 0.02 ng digoxin equivalents/mL, P = .005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Diagnosis of Candida thyroiditis by fine needle aspiration.

Infective thyroiditis is an uncommon condition, and fungal infection of the thyroid gland is rare. We present a case of Candida thyroiditis in a patient with leukaemia and review the three previous reports of this entity in the world's literature. We conclude that Candida thyroiditis should be considered in immunosuppressed patients with known infection who develop fever and neck pain, that gallium scanning may help localise the infection to the thyroid gland; that fine needle aspiration is a useful diagnostic test, and that thyroid dysfunction is common with Candida thyroiditis.

Adult↗
PubMed1994

Case report: postpartum hypopituitarism in a patient with sickle cell trait.

The authors report a case of hypopituitarism in a 28-year-old woman who appeared to develop this in conjunction with a pregnancy 4 years previously. The patient had clear-cut evidence of secondary hypoadrenalism and secondary hypothyroidism. A magnetic resonance imaging scan revealed a partially empty sella of normal size. The patient had no prior evidence of peripartum hypotension or other obstetrical catastrophe. Her only recognizable risk factor was the presence of sickle cell trait. The authors speculate that her sickle trait predisposed her to develop pituitary infarction during her first pregnancy. The authors also review three previous cases linking sickle cell syndromes with hypopituitarism and suggest that this case further supports the concept that sickle cell syndromes can predispose affected individuals to pituitary infarction and ultimately to subsequent hypopituitarism.

Adult↗
PubMed1994

Corticotrophin releasing hormone levels in human plasma and amniotic fluid during gestation.

OBJECTIVE: Corticotrophin releasing hormone, a hypothalamic neuropeptide also made in placenta, may regulate fetal maturation in a stress-responsive manner. The objectives of this study were: (1) to determine if levels of corticotrophin releasing hormone in the amniotic fluid correlate with fetal lung maturation; (2) to confirm that third trimester plasma levels of corticotrophin releasing hormone are increased in patients with pregnancy-induced hypertension compared to normotensives, and (3) to increase the recovery of extracted corticotrophin releasing hormone from plasma and amniotic fluid. DESIGN: (1) Levels of corticotrophin releasing hormone in amniotic fluid during the third trimester were compared with those of saturated phosphatidyl choline. (2) Corticotrophin releasing hormone levels were measured in a group of normotensive pregnant women during the entire gestation period. Corticotrophin releasing hormone levels during the third trimester were compared in normotensives and patients with pregnancy-induced hypertension. PATIENTS: Twenty-one non-pregnant normal volunteers and 63 pregnant women. MEASUREMENTS: Blood pressure, corticotrophin releasing hormone in plasma and amniotic fluid, and saturated phosphatidyl choline in amniotic fluid. RESULTS: Corticotrophin releasing hormone levels in amniotic fluid samples during the third trimester ranged from 12 to 98 pmol/l and positively correlated with the saturated phosphatidyl choline levels, but not with gestational age. A significant difference existed in plasma corticotrophin releasing hormone concentration between gestational age-matched third trimester normotensive and hypertensive gravids: corticotrophin releasing hormone levels were significantly lower in normotensives (223 +/- 65 pmol/l) than in patients with pregnancy-induced hypertension (544 +/- 106 pmol/l, P = 0.001). Plasma corticotrophin releasing hormone increased with gestational age from 51 pmol/l (range 8.4-85) at 25-32 weeks to 375 pmol/l (range 35-1386) at 33-40 weeks. During the third trimester the rise in plasma corticotrophin releasing hormone conformed to an exponential mathematical model of a positive feedback loop between placental corticotrophin releasing hormone and fetal adrenal cortisol. CONCLUSIONS: During the third trimester of pregnancy there is a positive correlation between the level of amniotic fluid corticotrophin releasing hormone and that of saturated phosphatidyl choline. The positive correlation between amniotic fluid corticotrophin releasing hormone and saturated phosphatidyl choline, but not between amniotic fluid corticotrophin releasing hormone and gestational age, suggests that a factor(s), such as stress, may affect both amniotic fluid corticotrophin releasing hormone and saturated phosphatidyl choline in parallel. Furthermore, our data are consistent with the hypothesis that the rise in placental corticotrophin releasing hormone is coupled to an increase in fetal glucocorticoid and lung maturation, and that stresses such as pregnancy-induced hypertension may accelerate this process.

Amniotic Fluid↗
PubMed1994

[Ca2+]i signaling in pregnant human myometrium.

The purpose of the present study was to determine the changes in intracellular ionized calcium concentration ([Ca2+]i) or [Ca2+]i sensitivity accompanying spontaneous and agonist-induced contraction of human myometrium at term pregnancy, as well as to quantify the response to three prototypical agonists: 1) oxytocin, 2) vasopressin, and 3) phenylephrine. Uterine biopsies were obtained at the time of cesarean section from patients who delivered at or near full-term gestation. These preparations were used to measure isometric force development and [Ca2+]i levels with the luminescent calcium indicator aequorin. Concentration-response relationships were determined with respect to isometric force development in the presence of the agonist. [Ca2+]i-force relationships were determined with respect to spontaneous phasic contractions, as well as agonist-induced phasic and tonic contractions. The results provide evidence that the phasic nature of term human myometrium is due to 1) the resting [Ca2+]i level being less than the calcium threshold for contractions and 2) the inability of the tissue to maintain high [Ca2+]i levels for prolonged periods of time. In addition, calcium-independent mechanisms of regulation were suggested by the relatively minor calcium sensitizing action of oxytocin and the observation that relaxation of tonic contractions preceded the fall in [Ca2+]i levels.

Calcium↗
PubMed1994

Glucose intolerance as a predictor of hypertension in pregnancy.

Insulin resistance is associated with and may be causal in essential hypertension, but the relation between insulin resistance and hypertension arising de novo in pregnancy is unclear. Transient hypertension of pregnancy (new-onset nonproteinuric hypertension of late pregnancy) is associated with a high risk of later essential hypertension and thus may have similar pathophysiology. To assess the association between glucose intolerance and subsequent development of proteinuric and nonproteinuric hypertension in pregnancy in women without underlying essential hypertension or overt glucose intolerance, we performed a retrospective case-control study comparing glucose levels on routine screening for gestational diabetes mellitus among women subsequently developing hypertension. Women who developed hypertension in pregnancy (n = 97) had significantly higher glucose levels on 50-g oral glucose loading test (P < .01) and a significantly higher frequency of abnormal glucose loading tests (> or = 7.8 mmol/L) (P < .01) than women who remained normotensive (n = 77). Relative glucose intolerance was particularly common in women who developed nonproteinuric hypertension. Women who developed hypertension also had greater prepregnancy body mass index (P < or = .0001) and baseline systolic and diastolic blood pressures (P < or = .0001 for both), although all subjects were normotensive at baseline by study design. However, after adjustment for these and other potential confounders, an abnormal glucose loading test remained a significant predictor of development of hypertension (P < .05) and, specifically, nonproteinuric hypertension in pregnancy (P < .01). Among a subgroup of women in whom insulin levels were also measured (n = 80), there was a nonsignificant trend toward higher insulin levels in women developing hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1994

Relation of pressor responsiveness to angiotensin II and insulin resistance in hypertension.

To test the hypothesis that the hypertension associated with insulin resistance is secondary to an altered responsiveness of the vasculature to pressor agents, we evaluated the relationship between insulin resistance and pressor responses to angiotensin II (AII) in 21 hypertensive (HT) and 8 normotensive (NT) subjects on both a high (200 meq) and a low (10 meq) sodium diet. When sodium balance was achieved, each supine fasting subject underwent an AII infusion at a rate of 3 ng/kg per min for 60 min, with blood pressure monitored every 2 min. On the next day under similar conditions, a euglycemic hyperinsulinemic clamp was performed, with plasma glucose clamped at 90 mg/dl for 120 min. There was no significant relationship between the glucose disposal rate (M) or the insulin sensitivity index (M divided by the mean insulin level [M/I]) and blood pressure response to AII in the NTs, but a highly significant (P < 0.019) negative correlation (r = -0.55) in the HTs. Furthermore, in eight lean HTs whose body mass index was identical to that observed in the NTs, the relationship was even more striking (P < 0.008; r = -0.85). The results on high and low salt diets were similar; however, the M and M/I were significantly increased (P < 0.05) in the NTs but not HTs with sodium restriction. In conclusion, HTs but not NTs display a striking correlation between pressor response to AII and insulin resistance. This relationship is independent of the level of sodium intake. Furthermore, sodium intake modifies insulin sensitivity in NTs but not HTs. These results strongly suggest that a primary change in pressor response to vasoactive agents in insulin-resistant subjects can contribute to their elevated blood pressure.

Adult↗
PubMed1993

Impact of diabetes on sodium-lithium countertransport in pregnancy-induced hypertension.

The purpose of this study was to assess the impact of type I diabetes on sodium-lithium countertransport (CTT) in normotensive third trimester women and those with pregnancy-induced hypertension (PIH). CTT was measured in the following groups: nonpregnant diabetic and nondiabetic women, pregnant nondiabetics with and without PIH, and pregnant diabetics with and without PIH. CTT was determined as external sodium-stimulated lithium efflux from lithium loaded red cells [mmoles/liter of cells x hours = units (U)]. In the nonpregnant state, nondiabetics and diabetics demonstrated similar CTT activity (0.20 +/- 0.02 U, n = 22, v 0.26 +/- 0.03 U, n = 18). In pregnancy, normotensive nondiabetics and diabetics had CTT activity similar to each other, the values of both being significantly higher than those in nonpregnant women (0.39 +/- 0.03 U, n = 26, v 0.46 +/- 0.05 U, n = 17). Nondiabetics with PIH demonstrated higher CTT (0.53 +/- 0.03 U, n = 30) than normotensive pregnant nondiabetics (P = .002). However, diabetics with PIH and CTT activity (0.48 +/- 0.04 U) indistinguishable from normotensive pregnant diabetics (0.46 +/- 0.05 U). There were no differences in gestational age, renal function, or glycohemoglobin that could explain these observations. Therefore, we conclude that PIH in type I diabetic women, in contrast to PIH in nondiabetic pregnant women, is not associated with a further elevation in CTT.

Adult↗
PubMed1993

Circadian sleep regulation in the absence of light perception: chronic non-24-hour circadian rhythm sleep disorder in a blind man with a regular 24-hour sleep-wake schedule.

Sleep disturbances and the failure to entrain circadian rhythms to the 24-hour day have been reported in the majority of totally blind subjects. The present case study of a totally blind man with a well-documented recurring sleep disturbance was designed to investigate the mutual relationship between sleep and the circadian timing system. The 63-year-old subject, a high school teacher with a regular work schedule, had suffered from cyclically recurring insomnia for the past 28 years. Analysis of a sleep log that he had kept for the past 15 years suggested that his circadian rhythms were not entrained to the 24-hour day. During a 3-month inpatient study, the period of the endogenous circadian pacemaker was assessed by analysis of ambulatory core body temperature, urinary excretion and a series of estimates of the phase of core body temperature cycles and plasma cortisol levels during constant routines. All circadian markers revealed periods in the range of 24.22-24.27 hours, with no evidence for a modulation of the observed periods by the sleep-wake cycle. During this 3-month inpatient study, a complete cycle of the subject's sleep disturbance and remission was polysomnographically documented while the subject lived on a regular 24-hour schedule. Because the subject's circadian rhythms were free-running and his sleep times were fixed, sleep occurred at virtually all circadian phases. Analysis of sleep latency, REM sleep latency, sleep duration, wake in sleep episode and REM sleep during sleep episode revealed a strong modulation by circadian phase. These findings in this blind man suggest that: 1) the period of his cyclically recurring sleep disturbance is directly related to the nonentrained period of an endogenous circadian pacemaker that drives circadian variation in core body temperature, urinary excretion, plasma cortisol and sleep propensity; 2) both his sleep structure and the severity of his daily sleep disruption are directly related to circadian phase and 3) his circadian pacemaker, which has an endogenous period that deviates only 0.2-0.3 hours from 24 hours, cannot be entrained by periodic daily exposure to nonphotic time cues, including a very regular 24-hour sleep-wake schedule.

Blindness↗
PubMed1993

Effect of sodium intake on insulin sensitivity.

To examine the effects of sodium intake on insulin sensitivity, we performed euglycemic insulin clamp studies (40 mU.m-2.min-1) in eight healthy normotensive nondiabetic white males (age = 36 +/- 5 yr; wt = 66 +/- 3 kg) after 5 days on high (200 meq/day)- and low (10 meq/day)-sodium diets administered in random order. High sodium intake was associated with significantly greater urinary sodium excretion (160 +/- 7 vs. 8 +/- 2 meq/day; P < 0.0001), suppression of plasma aldosterone (7 +/- 3 vs. 38 +/- 6 ng/dl; P < 0.001) and renin (1.5 +/- 0.2 vs. 6.0 +/- 0.9 ng.ml-1.h-1; P < 0.005) levels, but no change in blood pressure (116 +/- 3/63 +/- 2 vs. 114 +/- 3/64 +/- 2 mmHg; P = not significant). The rate of glucose infusion during the clamp was significantly reduced during the high- vs. low-sodium diet (279 +/- 19 vs. 334 +/- 24 mg.m-2.min-1; P < 0.01). This impairment in insulin sensitivity was not related to changes in serum potassium, epinephrine, norepinephrine, cortisol, or growth hormone but was highly correlated with an increment in circulating free fatty acid levels during high sodium intake (r = 0.82, P < 0.05). These data suggest that 1) high sodium intake may exacerbate insulin resistance by increasing circulating free fatty acids, and 2) differences in sodium intake may influence measures of insulin sensitivity in other disease states.

Adult↗
PubMed1993

Stimulation of plasminogen activator inhibitor in vivo by infusion of angiotensin II. Evidence of a potential interaction between the renin-angiotensin system and fibrinolytic function.

BACKGROUND: Recent clinical trial data indicate that the use of angiotensin converting enzyme (ACE) inhibitors among patients with left ventricular dysfunction results in reduced rates of coronary thrombosis, a provocative finding that suggests a potential interaction between the renin-angiotensin system and fibrinolytic function. METHODS AND RESULTS: In four normotensive subjects and six hypertensive patients, we investigated whether infusion of angiotensin II (Ang II) affected circulating levels of plasminogen activator inhibitor-1 (PAI-1), the most important physiological inhibitor of tissue-type plasminogen activator (t-PA). Overall, mean levels of PAI-1 antigen increased significantly from 20.1 ng/mL before Ang II infusion to 36.0 ng/mL at the end of Ang II infusion (p = 0.008), whereas no change in PAI-1 was observed for control subjects infused with 5% dextrose (p = 0.46). Among the normotensive subjects for whom graded doses of Ang II were infused at 0, 1, 3, and 10 ng.kg-1.min-1, mean PAI-1 levels increased sequentially from 14.7 ng/mL to 23.0, 26.8, and 33.5 ng/mL, a dose-response relation that, compared with controls, was highly significant (p < 0.001). Among the hypertensive patients for whom a single 45-minute infusion of Ang II was given at a dose of 3 ng.kg-1.min-1, PAI-1 levels increased from 23.7 to 37.7 ng/mL, whereas PAI-1 levels among control subjects infused with 5% dextrose decreased from 16.9 to 10.8 ng/mL (p = 0.04). Finally, when compared with infusion of 5% dextrose solution, infusion of Ang II appeared to have little effect on circulating levels of t-PA antigen. CONCLUSIONS: These in vivo data suggest that infusion of Ang II results in a rapid increase in circulating levels of PAI-1, a finding that may help to explain clinical observations linking the renin-angiotensin system and thrombotic risk.

Angiotensin II↗