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Parathyroid hormone and insulin-resistance in essential hypertension
96A
ASH XV ABSTRACTS
not efficient in subgroup A. The diabetes mellitus, in our study, shows a clear significant negative effect on the systolic function of the left ventricle in the hypertensive patients. In hypertensive patients with heart failure the endothelial dysfunction and/or the insufficient treatment of diabetes may contribute to appearance of systolic dysfunction of the left ventricle. The coexistence also of diabetes and hyperlipidaemia could indicate underlying coronary arterial disease which may predispose to failure. Key Words: Hypertension; systolic dysfunction; diabetes mellitus E043 PARATHYROID HORMONE AND INSULINRESISTANCE IN ESSENTIAL HYPERTENSION G. Andronico, M.T. Mangano, R. Ferraro-Mortellaro, G. Mule, G. Cerasola. Internal Medicine and Hypertension Centre, University of Palermo, Italy. Some studies have suggested a role of parathyroid hormone (PTH) in hypertension; moreover, insulin-resistance has been found in patients with primary hyperparathyroidism even in absence of hypertension. To observe the relationships between PTH and insulin-resistance in hypertension, we studied 61 patients with mild to moderate essential hypertension without diabetes mellitus, renal failure or hyperparathyroidism and 14 healthy subjects as controls. After at least 2 weeks of pharmacological washout, fasting blood glucose, insulin and intact PTH were measured. PTH levels were higher in hypertensive than in normotensive subjects (29.6⫾1.2 vs 22.6⫾1.1 ng/mL⫺p:0.006). In Hypertensive patients, however, we found no relationship between 24h systolic or diastolic pressure and PTH values. When hypertensives were divided in thirds on the basis of their PTH, in the higher third compared with the lower third we found higher blood glucose levels (90.1⫾2.6 vs 83.1⫾1.9 mg/dL⫺p:0.04) but lower insulin levels (15.7⫾1.2 vs 25.1⫾4.9 mU/L p⬍0.05) and lower insulin/glucose ratio (as insulin-resistance index) (0.17⫾0.01 vs 0.32⫾0.07⫺p:0.02). An inverse relationship, moreover, was found in hypertensives between insulin-resistance index and PTH values (r: ⫺0.29⫺p:0.03). Our results show that hypertensive subjects are characterized by higher PTH levels than healthy people. Insulinresistance appears to be lower in the group with higher PTH values. We need other studies to clarify these aspects of arterial hypertension. Key Words: Insulin-resistance; insulin; parathyroid hormone E044 ACE-INHIBITOR TREATMENT CORRECTS THE DEFECT IN VASCULAR INSULIN RESISTANCE IN HYPERTENSION N.D. Feldman*, N.D. Schmidt. Robarts Research Institute and University of Western Ontario, London, Canada Insulin resistance is a risk factor for hypertension, although the causality of the relationship has not been proved. Systemic insulin resistance parallels resistance to the vasodilat-
AJH–APRIL 2000 –VOL. 13, NO. 4, PART 2
ing effect of insulin. Systemic insulin resistance has been shown to be improved by both lifestyle modification as well as some specific antihypertensive therapies—including ACE-inhibition. Whether vascular insulin resistance can be improved by antihypertensive therapy was unknown. Therefore, we determined the effect of therapy with the ACE-inhibitor, quinapril, on vascular sensitivity to insulin (assessed by the dorsal hand vein linear variable differential transformer—LVDT technique) in 12 hypertensive subjects using a randomized double-blinded, crossover design. At the baseline LVDT assessment, vascular sensitivity to insulin was found to be significantly inversely correlated with BMI and significantly positively correlated with urinary sodium excretion. Three months of therapy with quinapril was associated with a significant improvement in vascular sensitivity to insulin, as determined by a decrease in the ED50 for insulin (Placebo⫽501⫾189 U/min; Quinapril⫽276⫾100 U/min, p⬍0.05). Also, maximal isoproterenol-mediated relaxation was enhanced (Placebo⫽92⫾15% of baseline distension; Quinapril⫽151⫾31% p⬍0.05). There was no effect of ACE-inhibition on nitroglycerin-mediated relaxation. Phenylephrine-mediated vasoconstriction was not altered. ACE-inhibitors have been shown, in both hypertensive patients, and those at high risk of atherosclerotic disease, to delay the appearance of diabetes as well as its complications. The current study suggests the hypothesis that this beneficial effect of ACE-inhibitors may be related to their beneficial effects on vascular function in general, and on insulinmediated vascular responses, in particular. Key Words: Insulin; vascular reactivity; ACE-inhibitors E045 MICROALBUMINURIA AND SYSTOLIC BLOOD PRESSURE IN OBESITY L.X. Cubeddu* and I.S. Hoffmann. Center for the Detection and Treatment of Silent Cardiovascular Risk Factors (SIL-DETECT); Central University of Venezuela, Caracas, Venezuela, Nova Southeastern Univ, School of Pharmacy, Ft. Lauderdale, Florida, USA The presence of microalbuminuria has become an important tool for therapeutic intervention. In this study we investigated whether the dysmetabolic syndrome of obesity was associated with or could occur in the absence of microalbuminuria. The study was conducted in 71 clinically healthy, glucose tolerant Hispanics (age:43⫾1.4 yr, SBP:117⫾2 mmHg, DBP:77⫾1.3 mmHg, urinary albumin excretion (UAE):10.2⫾0.6 mg/24 hr). Subjects were classified as lean (BMI⬍25), overweight (BMI⬎25⬍30) and obese (BMI⬎30 kg/m2). Greater BMI was associated with higher bwt, waist to hip ratio (WHR), BP, fasting insulin, triglyceride, post glucose-load insulin and glucose, and lower HDL levels. No differences in the UAE (mg/24 hr) were found between lean (9.0⫾0.9; median:9.1), overweight (11.3⫾1.2; median:10.5) and obese (11.1⫾1.2; median:9.7) subjects. No microalbuminuria (UAE⬎30 mg/24 hr) was not found in any of the subjects. For all subjects combined, as well as for each of the groups separately, the UAE was unrelated to the BMI, WHR, body weight, triglyceride, cholesterol (total, LDL or HDL),
ASH XV ABSTRACTS
not efficient in subgroup A. The diabetes mellitus, in our study, shows a clear significant negative effect on the systolic function of the left ventricle in the hypertensive patients. In hypertensive patients with heart failure the endothelial dysfunction and/or the insufficient treatment of diabetes may contribute to appearance of systolic dysfunction of the left ventricle. The coexistence also of diabetes and hyperlipidaemia could indicate underlying coronary arterial disease which may predispose to failure. Key Words: Hypertension; systolic dysfunction; diabetes mellitus E043 PARATHYROID HORMONE AND INSULINRESISTANCE IN ESSENTIAL HYPERTENSION G. Andronico, M.T. Mangano, R. Ferraro-Mortellaro, G. Mule, G. Cerasola. Internal Medicine and Hypertension Centre, University of Palermo, Italy. Some studies have suggested a role of parathyroid hormone (PTH) in hypertension; moreover, insulin-resistance has been found in patients with primary hyperparathyroidism even in absence of hypertension. To observe the relationships between PTH and insulin-resistance in hypertension, we studied 61 patients with mild to moderate essential hypertension without diabetes mellitus, renal failure or hyperparathyroidism and 14 healthy subjects as controls. After at least 2 weeks of pharmacological washout, fasting blood glucose, insulin and intact PTH were measured. PTH levels were higher in hypertensive than in normotensive subjects (29.6⫾1.2 vs 22.6⫾1.1 ng/mL⫺p:0.006). In Hypertensive patients, however, we found no relationship between 24h systolic or diastolic pressure and PTH values. When hypertensives were divided in thirds on the basis of their PTH, in the higher third compared with the lower third we found higher blood glucose levels (90.1⫾2.6 vs 83.1⫾1.9 mg/dL⫺p:0.04) but lower insulin levels (15.7⫾1.2 vs 25.1⫾4.9 mU/L p⬍0.05) and lower insulin/glucose ratio (as insulin-resistance index) (0.17⫾0.01 vs 0.32⫾0.07⫺p:0.02). An inverse relationship, moreover, was found in hypertensives between insulin-resistance index and PTH values (r: ⫺0.29⫺p:0.03). Our results show that hypertensive subjects are characterized by higher PTH levels than healthy people. Insulinresistance appears to be lower in the group with higher PTH values. We need other studies to clarify these aspects of arterial hypertension. Key Words: Insulin-resistance; insulin; parathyroid hormone E044 ACE-INHIBITOR TREATMENT CORRECTS THE DEFECT IN VASCULAR INSULIN RESISTANCE IN HYPERTENSION N.D. Feldman*, N.D. Schmidt. Robarts Research Institute and University of Western Ontario, London, Canada Insulin resistance is a risk factor for hypertension, although the causality of the relationship has not been proved. Systemic insulin resistance parallels resistance to the vasodilat-
AJH–APRIL 2000 –VOL. 13, NO. 4, PART 2
ing effect of insulin. Systemic insulin resistance has been shown to be improved by both lifestyle modification as well as some specific antihypertensive therapies—including ACE-inhibition. Whether vascular insulin resistance can be improved by antihypertensive therapy was unknown. Therefore, we determined the effect of therapy with the ACE-inhibitor, quinapril, on vascular sensitivity to insulin (assessed by the dorsal hand vein linear variable differential transformer—LVDT technique) in 12 hypertensive subjects using a randomized double-blinded, crossover design. At the baseline LVDT assessment, vascular sensitivity to insulin was found to be significantly inversely correlated with BMI and significantly positively correlated with urinary sodium excretion. Three months of therapy with quinapril was associated with a significant improvement in vascular sensitivity to insulin, as determined by a decrease in the ED50 for insulin (Placebo⫽501⫾189 U/min; Quinapril⫽276⫾100 U/min, p⬍0.05). Also, maximal isoproterenol-mediated relaxation was enhanced (Placebo⫽92⫾15% of baseline distension; Quinapril⫽151⫾31% p⬍0.05). There was no effect of ACE-inhibition on nitroglycerin-mediated relaxation. Phenylephrine-mediated vasoconstriction was not altered. ACE-inhibitors have been shown, in both hypertensive patients, and those at high risk of atherosclerotic disease, to delay the appearance of diabetes as well as its complications. The current study suggests the hypothesis that this beneficial effect of ACE-inhibitors may be related to their beneficial effects on vascular function in general, and on insulinmediated vascular responses, in particular. Key Words: Insulin; vascular reactivity; ACE-inhibitors E045 MICROALBUMINURIA AND SYSTOLIC BLOOD PRESSURE IN OBESITY L.X. Cubeddu* and I.S. Hoffmann. Center for the Detection and Treatment of Silent Cardiovascular Risk Factors (SIL-DETECT); Central University of Venezuela, Caracas, Venezuela, Nova Southeastern Univ, School of Pharmacy, Ft. Lauderdale, Florida, USA The presence of microalbuminuria has become an important tool for therapeutic intervention. In this study we investigated whether the dysmetabolic syndrome of obesity was associated with or could occur in the absence of microalbuminuria. The study was conducted in 71 clinically healthy, glucose tolerant Hispanics (age:43⫾1.4 yr, SBP:117⫾2 mmHg, DBP:77⫾1.3 mmHg, urinary albumin excretion (UAE):10.2⫾0.6 mg/24 hr). Subjects were classified as lean (BMI⬍25), overweight (BMI⬎25⬍30) and obese (BMI⬎30 kg/m2). Greater BMI was associated with higher bwt, waist to hip ratio (WHR), BP, fasting insulin, triglyceride, post glucose-load insulin and glucose, and lower HDL levels. No differences in the UAE (mg/24 hr) were found between lean (9.0⫾0.9; median:9.1), overweight (11.3⫾1.2; median:10.5) and obese (11.1⫾1.2; median:9.7) subjects. No microalbuminuria (UAE⬎30 mg/24 hr) was not found in any of the subjects. For all subjects combined, as well as for each of the groups separately, the UAE was unrelated to the BMI, WHR, body weight, triglyceride, cholesterol (total, LDL or HDL),