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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes mellitus is commonly associated with systolic and diastolic hypertension, and a wealth of epidemiological data suggest that this association is independent of age and obesity. Much evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive patients, whether obese or of normal body weight, are compared with age- and weight-matched normotensive controls, a heightened plasma insulin response to a glucose challenge is found consistently. A state of cellular resistance to insulin action subtends the observed hyperinsulinism. Using the insulin/glucose clamp technique in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms: sodium retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and proliferation of vascular smooth-muscle cells. Physiological maneuvers, such as caloric restriction (in the overweight patient) and regular physical exercise, can improve tissue sensitivity to insulin; good evidence indicates that these maneuvers also can lower blood pressure in both normotensive and hypertensive individuals. Insulin resistance and hyperinsulinemia also are associated with an atherogenic plasma lipid profile. Elevated plasma insulin concentrations enhance very-low-density lipoprotein (VLDL) synthesis, leading to hypertriglyceridemia. Progressive elimination of lipid and apolipoproteins from the VLDL particle leads to an increased formation of intermediate density and low-density lipoproteins, both of which are atherogenic. Last, insulin per se, independent of its effects on blood pressure and plasma lipids, is known to be atherogenic. The hormone enhances cholesterol transport into arteriolar smooth-muscle cells and increases endogenous lipid synthesis by these cells. Insulin also stimulates the proliferation of arteriolar smooth-muscle cells, augments collagen synthesis in the vascular wall, increases the formation of and decreases the regression of lipid plaques, and stimulates the production of a variety of growth factors. In summary, insulin resistance appears to be a syndrome that is associated with a clustering of metabolic disorders, including type II diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic cardiovascular disease.
J Cardiovasc Pharmacol 1992
PMID:Insulin resistance, hyperinsulinemia, and coronary artery disease: a complex metabolic web. 128 37

A double-blind, placebo-controlled study was carried out over 120 days to assess the metabolic tolerance and patient acceptability of nicardipine in 20 patients with Type 2 diabetes mellitus and slight hypertension. Following a 21-day washout period during which all patients received placebo, 13 men and 7 women (mean age 45 years, systolic blood pressure 150-165 mm Hg or diastolic blood pressure 85-100 mm Hg) were randomly assigned to treatment with oral nicardipine 60-90 mg/day (n = 9) or placebo (n = 11). No significant differences were observed between the nicardipine- and placebo-treated groups in terms of fasting and postprandial blood glucose concentrations, fasting plasma insulin levels, or glycosylated hemoglobin A1c after 60 and 120 days' treatment. There was also no change in the plasma levels of total cholesterol, HDL-cholesterol, triglycerides, and apolipoproteins. Side effects were minor and did not differ significantly between groups. All patients who had received nicardipine for 120 days wished to pursue treatment. Nicardipine, which was well tolerated, appears to be an interesting alternative for the treatment of mild essential hypertension in Type 2 diabetic patients, although further studies are required to establish its effects on renal function in this population.
J Cardiovasc Pharmacol 1990
PMID:The influence of nicardipine in type 2 diabetic patients with slight hypertension. 136 5

Calcium antagonists have become widely used as antihypertensive treatment in diabetic patients, although data concerning a possible influence on glucose tolerance, insulin secretion, and platelet aggregation during long-term, placebo-controlled studies are lacking. Therefore, the effects of isradipine, a new calcium antagonist, on glucose tolerance and insulin secretion during a 75-g oral glucose tolerance test (OGTT) and on ADP- and collagen-induced maximum first-wave platelet aggregation (Tmax%) were studied in 11 type II diabetic patients with borderline hypertension. After a 2-week washout period, patients were treated with placebo or isradipine for 8 weeks in a double-blind, crossover study. Systolic blood pressure was lowered significantly after isradipine therapy compared to placebo (127 +/- 3 vs. 139 +/- 6 mm Hg; p less than 0.05). Fasting blood glucose (153 +/- 14 vs. 157 +/- 16 mg/dl; NS), glucose levels, and basal (17 +/- 4 vs. 17 +/- 2 mU/ml; NS) and stimulated insulin during the OGTT remained unchanged after either treatment. Platelet aggregation after stimulation with different concentrations of ADP and collagen showed no significant differences. These data indicate that calcium antagonists have no adverse effects on glucose tolerance, insulin secretion, and platelet aggregation in type II diabetes mellitus, and are therefore useful in the treatment of hypertension in diabetic patients.
J Cardiovasc Pharmacol 1990
PMID:Platelet aggregation and metabolic control are not affected by calcium antagonist treatment in type II diabetes mellitus. 169 14

Many lipoprotein abnormalities are seen in the untreated, hyperglycemic diabetic patient. The non-insulin-dependent diabetic (NIDDM) patient with mild fasting hyperglycemia commonly has mild hypertriglyceridemia due to overproduction of TG-rich lipoproteins in the liver, associated with decreased high-density lipoprotein (HDL) cholesterol levels. The more hyperglycemic untreated NIDDM and insulin-dependent diabetic (IDDM) patient have mild to moderate hypertriglyceridemia due to decreased adipose tissue and muscle lipoprotein lipase, (LPL) activity. These patients also have decreased HDL cholesterol levels associated with defective LPL catabolism of TG-rich lipoproteins. Treatment of diabetes with oral sulfonylureas or insulin corrects most of the hypertriglyceridemia and some of the decrease in HDL cholesterol. The abnormality in adipose tissue LPL activity corrects slowly over several months of therapy. The treated IDDM patient often has normal lipoprotein levels. The treated NIDDM patient may continue to have mild hypertriglyceridemia, increased intermediate-density lipoprotein levels, small dense low-density lipoproteins (LDL) with increased apoprotein B, and decreased HDL cholesterol levels. The central, abdominal distribution of adipose tissue in IDDM is associated with insulin resistance, hypertension, and the above lipoprotein abnormalities. Improvement in glucose control, in the absence of weight gain, leads to lower triglyceride and higher HDL cholesterol levels. In addition, the diabetic patient is prone to develop other defects that, in themselves, lead to hyperlipidemia, such as proteinuria, hypothyroidism, and hypertension, treated with thiazide diuretics and beta-adrenergic-blocking agents. When a diabetic patient independently inherits a common familial form of hypertriglyceridemia, he might develop the severe hypertriglyceridemia of the chylomicronemia syndrome.
J Cardiovasc Pharmacol 1990
PMID:Pathophysiology of hyperlipidemia in diabetes mellitus. 171 Jul 39

Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by hyperglycemia secondary to increased hepatic glucose output and impaired extrahepatic insulin sensitivity. Many NIDDM patients also have raised serum triglyceride and low-density lipoprotein (LDL) cholesterol levels, which may require drug therapy, as well as increased plasma nonesterified fatty acid concentrations. Some hypolipidemic agents such as bezafibrate lower fatty acid levels as well as LDL cholesterol and triglycerides. It has been suggested that raised fatty acid levels may be responsible in part for the increased hepatic glucose output and insulin insensitivity of NIDDM. Several groups have therefore sought to examine the effects of fibrates on glycemic control in NIDDM. In our own studies, we used bezafibrate (200 mg t.i.d.) in a double-blind, placebo-controlled design for 3 months. Fasting blood glucose, serum insulin, C-peptide, plasma nonesterified fatty acids, blood lactate and alanine, serum triglycerides, and LDL cholesterol were all lowered. HbA1 showed no significant change. Meal hormone and metabolite profiles were all improved although this reflected mainly the lower premeal values. The results of our and other studies are sufficiently encouraging to suggest that bezafibrate could provide alternative first-line drug therapy in hyperlipidemic NIDDM patients when diet alone has failed.
J Cardiovasc Pharmacol 1990
PMID:Effect of bezafibrate on metabolic profiles in non-insulin-dependent diabetes mellitus. 171 Jul 41

The antihypertensive effect of nitrendipine, 20 mg once daily was studied in 30 patients with mild or moderate hypertension and type II diabetes mellitus under metabolic control. Blood pressure was measured at the end of a 15-day washout period from previous antihypertensive treatment and on the 15th, 30th, 60th, and 90th day of treatment. Systolic blood pressure and diastolic blood pressure were significantly reduced by nitrendipine. The reduction involved lying and orthostatic blood pressure and was maintained throughout the treatment period. Heart rate, fasting and postprandial glycemia, and lipid profile were not significantly affected by nitrendipine. It is concluded that this drug effectively lowers blood pressure in diabetic hypertensive subjects with no alteration of lipid and glucose metabolism.
J Cardiovasc Pharmacol 1991
PMID:Effect of nitrendipine in mild or moderate essential hypertensive subjects with type II diabetes. 172 69

Three hundred and thirty one carotid endarterectomies were performed on 279 patients during a period of twenty years from 1965 to 1984. The indication for surgery was transient ischemic attack in 67.4%, stroke in 22.7% and asymptomatic carotid stenosis in 10.0% of the operations. The overall major cerebral complication rate attending the operation was 9.6%. During the last four years' period from 1981 to 1984 the procedure morbidity was 3.6% and there was no mortality. Postoperative complications comprised 31 ipsilateral strokes and one contralateral stroke; the complications occurred during the first 24 hours in 28 cases and on the fourth or fifth day in four cases. Of these patients 11 succumbed to internal carotid thrombosis, one to cerebral infarction without thrombosis and one to intracerebral hemorrhage. The associated factors for major complications were analyzed retrospectively in the light of 32 parameters. Patients of advanced age, patients with type II diabetes mellitus, elevated serum triglycerides, high-grade stenosis or occlusion of the contralateral carotid artery, negative smoking history and those undergoing a second operation proved to be at high risk of early postoperative cerebral complications. These complications can be reduced by intraoperative use of heparin, preoperative ASA treatment and a short clamping time. Also peroperative use of shunt is obviously of benefit.
J Cardiovasc Surg (Torino)
PMID:Early cerebral complications in carotid endarterectomy: risk factors. 234 71

So-called insulin resistance is a frequent phenomenon and a marker of increased risk for both type II diabetes mellitus and atherosclerosis. Today, insulin resistance is widely understood as a tissue- and pathway-specific defect of insulin-stimulated glucose uptake into skeletal muscle that is compensated for by hyperinsulinemia, leading to a cluster of undesirable hypertensiogenic, diabetogenic, and atherogenic processes. Additional defects of insulin-stimulated muscle blood flow and cellular kation balance are presently attracting increasing awareness. Clinical and experimental evidence suggests that angiotensin-converting enzyme (ACE) inhibition ameliorates both insulin-stimulated skeletal-muscle glucose uptake and blood flow in insulin-resistant states by a direct stimulation of cellular glucose uptake, which appears to be kinin-mediated. This improvement of insulin sensitivity could mean not only improvement of glucose metabolism, but also reduction of chronically elevated serum insulin and the ensuing atherogenic consequences (hyper- and dyslipidemia, sympathetic overactivity, growth of vascular smooth-muscle cells, hypertension, etc.). Ca(2+)-channel blockers that do not increase heart rate appear to exert direct antiatherogenic effects while being metabolically neutral. Thus, the combination of Ca(2+)-channel blockade by sustained release verapamil and ACE inhibition by trandolapril in insulin-resistant type II diabetic patients with essential hypertension appears to be promising in terms of possible synergistic effects.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1994
PMID:Possible synergistic effect of ACE inhibition and calcium-channel blockade on insulin sensitivity in insulin-resistant type II diabetic hypertensive patients. 751 94

Cardiovascular risk factors such as hypertension, diabetes, and dyslipemia are associated with an impaired endothelium-dependent vasodilation. In patients with type 2 diabetes mellitus, these risk factors are frequently clustered. We investigated whether long-term treatment with the angiotensin-converting enzyme (ACE) inhibitor perindopril can improve endothelium-dependent vasodilation in this particular group of patients. We selected 10 patients with type 2 diabetes and hypertension (age 59.4 +/- 3.2 years, body mass-index 29.7 +/- 1.5 kg.m-2, blood pressure 169 +/- 6/92 +/- 1 mm Hg, total cholesterol 6.6 +/- 0.3 mM). Using venous occlusion plethysmography, we recorded the increases in forearm blood flow (FBF) in response to three vasodilator stimuli: (a) 5 min of forearm ischemia, (b) infusion of the endothelium-dependent vasodilator methacholine (Mch) into the brachial artery (0.03, 0.3, and 1.0 micrograms/min/100 ml), and (c) intraarterial infusion of the endothelium-independent vasodilator sodium nitroprusside (SNP 0.06, 0.2, 0.6 microgram/min/100 ml). This procedure was repeated after 6 months of treatment with perindopril 4-8 mg/day. Forearm vascular resistance (FVR) was calculated by the quotient of the mean arterial pressure (MAP) and the FBF. Perindopril reduced blood pressure (BP) by 19/10 mm Hg (p < 0.05) and increased baseline FVR, but improved neither the maximal percentage decrease in vascular resistance induced by Mch (from -80 +/- 2 to -82 +/- 2%) nor that induced by SNP (from -73 +/- 3 to -72 +/- 3%). Perindopril decreased the FVR reached after the ischemic stimulus from 6.5 +/- 1.2 to 4.8 +/- 0.6 U (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1995 Apr
PMID:Effect of long-term angiotensin-converting enzyme inhibition on endothelial function in patients with the insulin-resistance syndrome. 759 36

Obesity is the most common reason for insulin resistance with consequent hyperinsulinemia. Other reasons for hyperinsulinemia are type II diabetes mellitus and a genetic predisposition with a family history of hypertension. Hyperinsulinemia is considered to cause blood pressure elevation and is generally accepted as an independent risk factor for atherosclerosis. However, insulin per se does not elevate blood pressure, but rather reduces total peripheral vascular resistance in experimental studies. Blood pressure might be elevated by other mechanisms secondary to hyperinsulinemia, however, such as enhanced renal sodium retention, elevated intracellular free calcium, and increased activity of the sympathetic nervous system. Indeed, subjects whose blood pressure is salt-sensitive exhibit hyperinsulinemia after glucose loading, and normotensive subjects with glucose-induced hyperinsulinemia will develop hypertension within 5 years more often than normoinsulinemic subjects. In primary hypertension, the incidence of insulin resistance and hyperinsulinemia is much higher than in normotensive controls. However, not all reported studies show a relationship between hyperinsulinemia and blood pressure elevation, and in some experimental studies no blood pressure elevation could be induced by prolonged hyperinsulinemia. Therefore, it is still unclear whether hyperinsulinemia induces hypertension or is only casually associated with it. Nevertheless, treatment of hyperinsulinemia is recommended to avoid secondary complications. Treatment should begin with weight reduction and physical exercise, which will improve insulin resistance. Hypertension benefits more from weight reduction than from exercise. If drug therapy of hypertension is required, angiotensin-converting enzyme (ACE) inhibitors and calcium-channel blockers are the drugs of first choice. In addition, beta-blockers and centrally acting drugs appear to be of certain benefit. However, diuretics must be used carefully, because they ameliorate insulin resistance, induce dyslipoproteinemia, and stimulate the sympathetic nervous system.
J Cardiovasc Pharmacol 1994
PMID:Hyperinsulinemia, insulin resistance, and hypertension. 789 93


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