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Biomedical subjects

M Bursztyn

Publications and source records attributed to M Bursztyn.

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

Dating people with anorexia nervosa and bulimia nervosa: attitudes and beliefs of university students.

Attitudes and beliefs about dating people with eating disorders were investigated in men and women using a questionnaire administered to 752 university students. Students believed that people with anorexia nervosa and bulimia nervosa had a difficult time dating, dates would involve conflict, and dating would be a negative experience. Students were more comfortable in casual interactions than more serious dating activities with people with anorexia nervosa and bulimia nervosa. Men were somewhat comfortable dating people with anorexia nervosa or bulimia nervosa, but less so for obesity. Most students believed dating people with anorexia nervosa and bulimia nervosa would not be a positive experience, and men stigmatized people with eating disorders differently than did women.

Adult↗
PubMed1998

Chronic exogenous hyperinsulinemia in pregnancy: a rat model of pregnancy-induced hypertension.

Insulin resistance and hyperinsulinemia are associated with essential hypertension. There is also evidence of hyperinsulinemia in women who developed hypertension in pregnancy (P). The present study examines whether chronic hyperinsulinemia in pregnant rats plays a role in the development of hypertension in pregnancy. A sustained-release insulin pellet was implanted subcutaneously in 15 Wistar rats (P-INS) 1 wk before and on day 7 of pregnancy; 14 control rats were sham-implanted (P-SHAM). Tail-cuff systolic BP (SBP), serum triglycerides, glucose, insulin, renal function, and urinary excretion of Na+ and of metabolites of nitric oxide were determined throughout pregnancy. Data were analyzed by ANOVA with basal body weight as covariate analysis of covariance. Results are expressed as the mean +/- SD. Body weight; water and food intake; urine volume; creatinine clearance; and level of proteinuria at the end of pregnancy were similar in both groups. The number of fetuses was 9 +/- 2.3 in P-INS versus 11 +/- 2.4 in pregnant control rats (P < 0.05). Before mating, SBP was similar, but at the end of pregnancy SBP was 110 +/- 18 mmHg in P-INS versus 85 +/- 12 mmHg in pregnant rats (P < 0.05). Serum triglycerides and Na+ were also higher in P-INS rats. The fractional excretion of Na+ was 3.1 +/- 1.0 versus 4.4 +/- 1.5, respectively (P < 0.01). The percent increase in nitric oxide metabolite excretion was 233 +/- 14 versus 370 +/- 17%, respectively (P < 0.01). Chronic hyperinsulinemia, without sugar supplementation, and hypertriglyceridemia may cause a decrease in the synthesis of nitric oxide in P-INS rats. The development of hypertension in these rats may be associated with an impaired vasodilatation, together with an increased renal sodium reabsorption.

Animals↗
PubMed1997

Antihypertensive effects of mibefradil in the treatment of mild-to-moderate systemic hypertension.

This report summarizes the results of 4 double-blind, placebo-controlled studies designed to determine the efficacy, tolerability, and dose-response characteristics of the novel T-channel-selective calcium antagonist, mibefradil, in the treatment of mild-to-moderate essential hypertension. Two of these studies were conducted in the general population of essential hypertensives, 1 in elderly patients, and 1 in patients on chronic hydrochlorothiazide treatment. A total of 1,116 patients were randomized to receive 1 of 7 doses of mibefradil (6.25-200 mg; n = 927), or placebo (n = 189). Each study demonstrated a significant linear dose response in the reduction of sitting diastolic (SDBP) and sitting systolic (SSBP) blood pressure. In all 4 trials, SDBP was significantly reduced with the recommended doses of 50 and 100 mg mibefradil (placebo-corrected treatment effects of -4.1 to -6.8 mm Hg and -8.8 to -11.1 mm Hg, respectively, for the 50- and 100-mg doses). A similar reduction in SSBP occurred in 3 of 4 studies at the 50-mg dose (-7.5 to -10.7 mm Hg) and in 4 of 4 studies at the 100-mg dose (-6.8 to -16.7 mm Hg). Lower doses did not reduce blood pressure significantly; doses > 100 mg had little additional effect and an increased incidence of adverse events. Overall, response and normalization rates were dose related and averaged 61% and 51%, respectively, for the 50-mg dose and 78% and 65%, respectively, for the 100-mg dose. The onset of the antihypertensive effect was gradual, with no first-dose effect; near maximal response was reached within 1-2 weeks. Trough/peak ratios ranged from 77-86% with the 50-mg dose and from 77-108% with the 100-mg dose, indicating a sustained effect over a 24-hour period. A slight decrease in heart rate was observed, ranging from -2.2 to -5.5 beats/min at the 50-mg dose and from -4.0 to -8.8 beats/min at the 100-mg dose. The efficacy and safety results were similar across all populations studied, including the elderly and hydrochlorothiazide-treated patients, indicating that no dose adjustment is needed for these populations. Thus, the results of these 4 placebo-controlled trials confirm that when taken at the recommended doses of 50 and 100 mg once daily, mibefradil is an effective, safe, and well-tolerated therapy for the treatment of mild-to-moderate hypertension.

Adolescent↗
PubMed1997

Isradipine for the prevention of cyclosporine-induced hypertension in allogeneic bone marrow transplant recipients: a randomized, double-blind study.

BACKGROUND: Hypertension and nephrotoxicity frequently occur in patients who receive cyclosporine therapy after bone marrow transplantation (BMT). Isradipine, a calcium channel entry blocker, has been used successfully in cyclosporine-induced hypertension. METHODS: Thirty leukemic patients who received cyclosporine after BMT were randomized to receive isradipine (0.005 mg/kg) from 72 hr before commencement of cyclosporine therapy until day 100 after BMT or placebo. RESULTS: The placebo and isradipine groups were well matched. No differences were found between the isradipine and placebo groups in the level of blood pressure, renal function, marrow engraftment, or mortality. Hypertension incidence was surprisingly low (30% a week after hospital discharge and 10% by day 100 after BMT), and did not differ between the groups. CONCLUSIONS: Isradipine does not harm immunohematopoietic reconstitution after BMT; therefore, it may be used in this setting, although the previously reported incidence of hypertension has been exaggerated.

Adult↗
PubMed1997

Mibefradil, a novel calcium antagonist, in elderly patients with hypertension: favorable hemodynamics and pharmacokinetics.

A multicenter, double-blind, placebo-controlled study of 310 elderly patients with mild-to-moderate essential hypertension was conducted in 20 sites throughout Europe, Brazil, and Israel to assess the antihypertensive efficacy, tolerability, safety, and dose-response characteristics of the novel calcium antagonist mibefradil in the elderly. Patients were randomly assigned to receive once-daily doses of 6.25, 12.5, 25, 50, or 100 mg of mibefradil or placebo for 4 weeks. Statistically significant and clinically relevant reductions in sitting diastolic blood pressure (SDBP) and sitting systolic blood pressure (SSBP) were observed with the 50 and 100 mg doses. Therapeutic responses reached 88.5% for SDBP and 76.5% for SSBP in the 100 mg group. Trough/peak ratios were > 75% in SDBP and SSBP with the 50 mg and 100 mg doses. At doses of 50 to 100 mg once daily, mibefradil was well tolerated and effective with a high antihypertensive response rate and consistent 24-hour blood pressure control in elderly patients.

Aged↗
PubMed1997

New developments in drug therapy of hypertension.

The explosion of new knowledge about the complex mechanisms mediating high blood pressure is providing new targets for drug therapy of hypertension and other cardiovascular disorders. This article reviews the current status of several new approaches in the management of hypertension, including vasopressin antagonists, natriuretic peptide clearance inhibitors, endothelin antagonists, renin inhibitors, angiotensin receptor antagonists, and selective T-type calcium ion channel antagonists.

Animals↗
PubMed1997

Effect of acute N-nitro-L-arginine methyl ester (L-NAME) hypertension on glucose tolerance, insulin levels, and [3H]-deoxyglucose muscle uptake.

This study was conducted to test the hypothesis that acute, widespread N-nitro-L-arginine methyl ester (L-NAME) induced vasoconstriction and hypertension may affect glucose tolerance and insulin sensitivity in normal rats. Comparisons were made of blood pressure, intravenous glucose tolerance, and insulin response and [3H]-deoxyglucose tissue uptake between L-NAME and control treated rats. Chronically instrumented, awake rats were administered L-NAME (30 mg/kg) (n = 8) or saline (0.3 mL) (n = 8) intravenously. After blood pressure stabilized, a bolus injection containing glucose (300 mg/kg) and trace [3H]-deoxyglucose was administered. Arterial blood was sampled for evaluation of glucose tolerance, insulin response, and [3H]-deoxyglucose muscle uptake. L-NAME treated rats had a persistent 54 +/- 4 mm Hg blood pressure rise while fasting, and postload plasma glucose and insulin responses did not differ, nor did heart and striated muscle [3H]-deoxyglucose uptake differ. In conclusion, acute L-NAME induced hypertension does not result in glucose intolerance, hyperinsulinemia, or decreased [3H]-deoxyglucose muscle uptake.

Animals↗
PubMed1997

Role of vasopressin in essential hypertension: racial differences.

BACKGROUND: Arginine vasopressin (AVP), in addition to being an antidiuretic hormone, might also have pressor effects relevant to the maintenance of hypertension. Results from several experimental and clinical studies suggested that the pressor function of AVP is more important in low-renin hypertension and in the salt-loaded state and that it might be further maximized under sympathetic suppression. OBJECTIVE: To assess whether selective vasopressin receptor inhibition lowers the blood pressure in a racially diverse group of low-renin hypertensive subjects. METHODS: Thirty-nine hypertensive subjects (16 Caucasian, 23 African-American) eating a 200 mmol/day sodium diet were administered a single intravenous dose of a selective vasopressin receptor antagonist and their blood pressure was monitored constantly for the ensuing 3 h. The protocol was repeated 3 days later after treatment with a single oral dose of 0.4 mg clonidine. RESULTS: Of these patients, 54% had their blood sampled for determination of hormone profiles. African-Americans with hypertension had higher baseline plasma AVP levels than did Caucasians (1.13 +/- 0.05 versus 0.37 +/- 0.06 pg/ml, respectively, P < 0.05), and lower plasma renin activity (0.34 +/- 0.07 versus 1.03 +/- 0.08 ng/ml per h, respectively, P < 0.05). Selective vasopressin receptor inhibition lowered the mean arterial pressure in African-Americans but not that in Caucasians (lowering by 28 +/- 4 mmHg in African-Americans versus lowering by 5 +/- 3 mmHg in Caucasians, P < 0.05). Moreover, vasopressin receptor blockade further reduced the arterial pressure in African-Americans but not that in Caucasians after pretreatment with clonidine. CONCLUSION: AVP seems to play a more important role as a pressor hormone in maintaining the elevation of arterial pressure in African-American hypertensives than it does in Caucasian hypertensives.

Antidiuretic Hormone Receptor Antagonists↗
PubMed1996

Hypertension in the Jerusalem 70 year olds study population: prevalence, awareness, treatment and control.

As part of the Jerusalem 70 year olds study, we evaluated the prevalence, awareness, treatment and control of hypertension (blood pressure > or = 160 mm Hg systolic and/or > or = 95 mm Hg diastolic, or current treatment with prescribed antihypertensive medications). The study cohort consisted of 448 participants, 224 of whom had hypertension. Relative to other populations, awareness was high (87%). Although the treatment rate was also relatively high (86%), the control rate was only 43%. Untreated isolated systolic hypertension was uncommon (5%), as was orthostatic hypotension (6.9%). Thus, despite a remarkable degree of awareness and treatment rate of hypertension, control levels were disappointingly low. This finding, if confirmed, requires further elucidation.

Aged↗
PubMed1996

The siesta and ambulatory blood pressure: is waking up the same in the morning and afternoon?

We have shown previously that blood pressure (BP) reduction after the siesta is similar to that after night sleep. As cardiovascular events cluster around morning waking hours, when there is a sharp rise of BP and heart rate (HR), the double-product of which is a major determinant of cardiac oxygen consumption, we also investigated changes after the siesta. Twenty-four-hour ambulatory BP monitorings of 156 consecutive patients referred for evaluation of hypertension who reported the siesta (afternoon nap) were analysed. The mean daytime awake BP and HR were 145 +/- 18/80 +/- 10 mm Hg and 71 +/- 11 beats per minute (bpm). During night sleep and the siesta BP decreased significantly (P < 0.00001) to 126 +/- 20/67 +/- 10 and 125 +/- 17/65 +/- 10 mm Hg, respectively. HR decreased during the siesta (69 +/- 11 bpm; P < 0.00001) but even more so (P < 0.00001) during the night (62 +/- 8 bpm; P < 0.00001). When normotensive subjects (n = 38), untreated (n = 33) and treated hypertensives (n = 85) were evaluated separately, they all had similar trends. However, when percentage rise over the sleeping baseline was considered, there were no significant differences in the rise of BP after the siesta and night sleep. The rise in HR for the normotensives and treated hypertensives was 16% and 8%, respectively, higher in the morning than after the siesta (P < 0.0004 and P < 0.001, respectively). The double-product increased significantly more in the morning than after the siesta (both P < 0.0001) in the normotensives (by 20%) and treated hypertensives (by 10%). In untreated hypertensives the rise in HR and double-product was no different between the time periods. In conclusion, there is a higher rise of HR and double-product in the morning. The relatively lower rise after the siesta may indicate a lesser increase in cardiac oxygen consumption and, therefore, lesser potential for acute ischemia.

Adult↗
PubMed1996

Does insulin have a role in hypertension?

There is a growing body of evidence linking insulin resistance and hyperinsulinaemia with hypertension. Vascular delivery of insulin and glucose to the striated muscle may be rate-limiting for them to exercise their effects. We therefore studied the effects of experimentally induced hypertension (renovascular and DOCA-salt) on muscle uptake of [(3)H]-deoxyglucose ([(3)H]-DOG)(non-metabolized glucose analog). In both models of induced hypertension uptake of [(3)H]-DOG was compared with the corresponding normotensive controls. Spontaneously hypertensive rats (SHR), however, had a reduced [(3)H]-DOG muscle uptake relative to normotensive WKY rats. To clarify a pro-hypertensive role on insulin it was administered by means of a sustained release subcutaneous implant to normotensive rats for 2 months and we could not detect hypertension in the resting state, though a transient hypertensive response to acute saline loading was present. On the other hand, young SHR made hyperinsulinaemic by the same method had an accelerated development of hypertension relative to control SHR. Thus it is not hypertension as such but the genetic susceptibility that is associated with insulin effects on blood pressure. In human hypertension we evaluated exercise (a maneuver known to improve insulin-sensitivity and reduce blood pressure) in non-obese essential hypertensive subjects. Three months of exercise training was associated with improved glucose tolerance and insulin clearance rate, but had no effect on 24-h ambulatory blood pressure. Thus, in essential hypertension insulin does not contribute significantly to the maintenance of hypertension. Taken together, our data indicate that hypertension does not cause insulin resistance and that exogenous hyperinsulinaemia does not produce hypertension in normotensive rats. However, in genetically determined hypertension insulin may play a role in its development.

Animals↗
PubMed1995

Insulin-like growth factor-I (IGF-I) and IGF-I receptor gene expression in the kidney of the chronically hypoinsulinemic rat and hyperinsulinemic rat.

Acute streptozotocin (STZ)-induced diabetes in rats causes a transient increase in insulin-like growth factor-I (IGF-I) in the kidney, followed by a rapid renal hypertrophy and constant renal hyperperfusion. However, renal IGF-I levels return to normal within 4 days. Thus, hyperperfusion, which is independent of renal hypertrophy of the chronically diabetic kidney, is not explained by increased renal IGF-I. We studied IGF-I and IGF-I receptor gene expression in the kidney of rats with long-standing STZ-induced diabetes. IGF-I mRNA level in the chronically diabetic kidney was approximately 50% of that in control rats, whereas IGF-I receptor mRNA was increased approximately threefold. Ten days' treatment with insulin 65 days after induction of diabetes resulted in a glucose-dependent decrease in IGF-I receptor mRNA. Chronic hyperinsulinemia with near normoglycemia did not change gene expression of either IGF-I or IGF-I receptor. The studies suggest that glucose levels per se, independent of insulin levels, play an important role in the regulation of IGF-I receptor gene expression in the chronically diabetic kidney. Furthermore, kidney hyperperfusion in chronic diabetes is coupled with the increase in IGF-I receptor mRNA, despite normal kidney IGF-I levels.

Animals↗
PubMed1995

Chronic exogenous hyperinsulinaemia accelerates the development of hypertension in spontaneously hypertensive rats.

1. An association between hyperinsulinaemia, insulin resistance and hypertension was previously described in spontaneously hypertensive rats (SHR). We therefore tested whether chronic exogenous hyperinsulinaemia, which did not affect blood pressure of normotensive rats, may aggravate hypertension in young SHR. 2. Insulin was administered for 4 weeks by a graded increase of a sustained release insulin implant, without carbohydrate supplementation. 3. Initial bodyweight of seven SHR and five sham-implanted control SHR, aged 6-8 weeks, was not different between the groups or by week 4. 4. Glucose levels decreased in the treated rats [2-way ANOVA F(1:10) = 18.7. P < 0.005] and were 7.3 +/- 0.1 mmol/L in the controls and 4.4 +/- 0.7 mmol/L in the treated SHR, respectively. Insulin levels were comparable at baseline and increased to 1002 +/- 978 pmol/L in treated rats at week 4 while remaining 270 +/- 78 pmol/L in the controls [F(1:10) = 6.1, P < 0.05]. The systolic blood pressure (tail-cuff) was significantly increased in insulin treated SHR in weeks 1-3[F(1:10) = 5.1, P < 0.05] though it was comparable at baseline and week 4. 5. In the presence of a hypertensive predisposition, chronic exogenous hyperinsulinaemia accelerates the time course of the development of hypertension without affecting its severity.

Animals↗
PubMed1995

Insulin-induced renal dysfunction in regular Sabra rats.

1. We tested the effects of chronic hyperinsulinaemia on renal function. Hyperinsulinaemia, in the range of 1.5-4 times the control levels, was achieved using a sustained-release insulin implant. Sham-treated rats served as controls. 2. Experiment 1. Acute saline loading: seven sham and seven hyperinsulinaemic rats received an acute saline load (4 mL/100 g). Two h post-load urea and creatinine excretion rats were (mu mol/min) 15 +/- 5 and 9 +/- 4, and 0.17 +/- 0.05 and 0.10 +/- 0.04, respectively; P < 0.05 for both. 3. Experiment 2. Chronic saline loading: 12 sham- and 24 insulin-treated rats drank saline for 8 weeks plus 4% NaCl in the food for 2 more weeks. By week 10 plasma creatinine (mu mol/L) was 62 +/- 12 and 78 +/- 13, and creatinine clearance (mL/min) was 1.9 +/- 0.5 and 1.5 +/- 0.4, respectively; P < 0.05 for both. 4. Experiment 3. Regular diet: 10 sham- and 14 insulin-treated rats had, by week 8, plasma creatinine (mu mol/L) of 75 +/- 34 and 96 +/- 37 and creatinine clearance (mL/min) of 1.260 +/- 0.025 and 0.97 +/- 0.22, respectively; P < 0.02 for both. Bodyweight, resting blood pressure and urinary Na+ and K+ excretion were comparable in sham- and insulin-treated rats. 5. In three experimental settings long-term hyperinsulinaemia was associated with a subtle but significant renal dysfunction. This finding may be related to the aetiology of renal complications of hypertension and diabetes mellitus, both of which are insulin-resistant and hyperinsulinaemic states.

Animals↗