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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Genetic predisposition to essential hypertension has been proposed as a risk factor for the development of diabetic nephropathy in type 1 (insulin-dependent) diabetes mellitus. An increased sodium-lithium countertransport activity (NaLiCT) has been suggested as a genetic marker for essential hypertension. We therefore evaluated NaLiCT in diabetic patients with (N = 39) or without (N = 23) diabetic nephropathy (DNP), patients with non-diabetic renal diseases (N = 42) and in healthy controls (N = 24). The NaLiCT was elevated in both diabetic patient groups compared to healthy controls (median 244; range 134 to 390 mumol.liter cells-1.hr-1), but was not different in patients with DNP (median 314; range 162 to 676), without DNP (median 325; range 189 to 627) and patients with non-diabetic renal disease (median 300; range 142 to 655). The genetic predisposition to DNP is illustrated by the fact that diabetic sibs of probands with DNP showed a higher occurrence of DNP than diabetic sibs of patients without DNP. We analyzed whether familial DNP clustered with an increased NaLiCT. The NaLiCT in sibs concordant for the presence of DNP (N = 10; median 307; range 217 to 428 mumol.liter cells-1.hr-1) was not significantly different from that in sibs concordant for absence of DNP (N = 15; median 279; range 189 to 442). We conclude that erythrocyte sodium-lithium countertransport activity cannot be used as a marker to identify patients at risk for the development of diabetic nephropathy.
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PMID:Is increased erythrocyte sodium-lithium countertransport a useful marker for diabetic nephropathy? 151 9

Recently, it was suggested that the role of hyperinsulinemia on the hypertensive mechanism of essential hypertension might be related to renal sodium handling and sympathetic nerve activity, especially in obese hypertensive patients. However, the interrelationship between insulin, obesity, renal sodium metabolism and sympathetic nerve activity in normotensive subjects (NT) still remains unclear. The present study, therefore, was undertaken to clarify the role of insulin on renal sodium handling and sympatho-adrenal function in overweight NT. The study consisted of 24NT, who were divided into two groups of twelve non-obese (NNT) and twelve obese (ONT) subjects. NNT was categorized as a body mass index (BMI) less than, and ONT as a BMI equal to or more than 25kg/m2. In the early morning, after overnight fasting, all subjects remained in a supine state and were examined for renal clearance test. During the two-hour clearance period, mean arterial pressure (MAP), heart rate (HR), endogenous creatinine clearance(CCr), urinary excretion of sodium (UNaV), fractional excretion of sodium (FENa), plasma immunoreactive insulin (IRI), plasma norepinephrine concentration (pNE), and plasma epinephrine concentration (pE) were determined. Although no significant difference was found in age, MAP, HR, pE, CCr or UNaV between the two groups, a significantly higher IRI (p less than 0.05) and lower FENa (p less than 0.05) were observed in ONT than in NNT. There was no significant correlation between IRI and UNaV, FENa or pE in ONT or in NNT. In addition, no significant correlation was shown between FENa and pNE or pE in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The role of insulin on renal sodium handling and sympathetic nerve activity in overweight normotensive subjects]. 151 24

Diabetes mellitus and essential hypertension are characterized by a continuous rise of prevalence with aging and this association may not be casual. Thirty nonobese nondiabetic elderly patients with primary hypertension and 28 healthy normotensives matched for age, sex, and body weight were evaluated for insulin secretion (oral glucose tolerance test, day-long glycemic and insulinemic profiles), action (euglycemic moderately hyperinsulinemic glucose clamp associated with 3H-3-glucose dilution technique), and clearance (120 min insulin/glucose infusion at two prefixed doses). Compared with normotensives, hypertensive elderly patients were characterized by the following: 1) plasma insulin and C-peptide were similar in basal conditions but significantly enhanced in response to both oral glucose and a mixed meal; 2) insulin-stimulated glucose uptake was significantly impaired with a similar rate of hepatic glucose production; 3) exogenous insulin metabolic clearance rate was significantly lower at both insulin infusion rates. The multiple alterations of insulin secretion, action and metabolism found in nonobese nondiabetic elderly hypertensives seem to support a role for this hormone in the regulation of arterial blood pressure.
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PMID:Impaired glucose metabolism and reduced insulin clearance in elderly hypertensives. 152 58

Hypertension and obesity are closely related. Obese patients tend to have increased intravascular volume and cardiac output and decreased total peripheral vascular resistance and plasma renin activity. Lean patients with essential hypertension usually have increased total peripheral resistance. Left ventricular adaptation in obesity consists of eccentric left ventricular hypertrophy (LVH), regardless of the level of arterial pressure. Obesity and hypertension occurring together place a dual burden on the left ventricle and are associated with systolic and diastolic dysfunction, lipid abnormalities, insulin resistance, and a propensity for frequent, complex ventricular arrhythmias. Congestive heart failure and sudden death are common sequelae of obesity-hypertension and LVH. Treatment should include vigorous efforts at weight reduction and sodium restriction. Diuretics are ideal agents from a hemodynamic standpoint but often do not improve the total risk profile, with the possible exception of indapamide (Lozol). Calcium blockers may be ideal agents because of their favorable effects on both hemodynamics and total cardiovascular risk profile.
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PMID:Left ventricular hypertrophy. Its relationship to obesity and hypertension. 153 69

Insulin resistance has been described in nonobese subjects with essential hypertension. At present it is unknown whether hypertension per se may lead to the onset of insulin resistance. To examine this question we studied in vivo insulin action in two rat models of genetic hypertension. Four groups of conscious rats were studied: Milan hypertensive (MHS), Milan normotensive (MNS), spontaneously hypertensive (SHR), and Wistar-Kyoto (WKY). Mean arterial pressure was increased in SHR vs. WKY in both the fed (184 +/- 5 vs. 126 +/- 6 mmHg; P less than 0.001) and fasting (160 +/- 5 vs. 129 +/- 5; P less than 0.001) states. During high-dose insulin clamps, total body glucose uptake (mg.kg-1.min-1) was similar in MNS (28.7 +/- 1.4) vs. MHS (33.6 +/- 3.0) and in WKY (34.6 +/- 1.8) vs. SHR (35.7 +/- 2.4). During low-dose insulin clamps, suppression of hepatic glucose production (3.5 +/- 0.6 vs. 3.0 +/- 0.5 mg.kg-1.min-1) and stimulation of glycolysis (12.9 +/- 0.8 vs. 14.4 +/- 1.5 mg.kg-1.min-1) were similar in WKY vs. SHR, whereas glucose uptake (24.6 +/- 1.9 vs. 18.3 +/- 1.2 mg.kg-1.min-1; P less than 0.01) and muscle glycogenic rate (10.2 +/- 1.1 vs. 6.5 +/- 1.1 mg.kg-1.min-1; P less than 0.05) were increased in SHR vs. WKY. In conclusion, 1) feeding markedly augments blood pressure in hypertensive but not in normotensive rats, and 2) hepatic and muscle insulin sensitivity are normal or increased in two different rat models of genetic hypertension. These results provide evidence that high blood pressure per se does not invariably lead to the development of insulin resistance.
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PMID:In vivo insulin action in genetic models of hypertension. 153 44

The association between hypertension and hyperinsulinemia/insulin resistance is well established but presently unexplained. Among several possible explanations, a connection between the two abnormalities can be envisioned at the level of the microvasculature in skeletal muscle. In fact, the insulin resistance of essential hypertension has been localized in skeletal muscle; in this tissue, on the other hand, rarefaction of the smaller arterioles can generate a rise in blood pressure. Thus, it is theoretically possible that structural changes in small vessels (caused by hypertension) may limit the diffusion of insulin and substrates from the intravascular space to the target cell surface. Alternatively, chronic hyperinsulinemia (caused by primary insulin resistance) could induce changes in small vessel walls (or their reactivity to pressor stimuli) capable of raising blood pressure. The details of these potential mechanisms are laid out within the framework of the hemodynamic phase of in vivo insulin action, and the available evidence bearing on them is discussed.
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PMID:Insulin and blood pressure: possible role of hemodynamics. 154 Oct 41

Peripheral insulin resistance is a feature of essential hypertension, but there is little information about hepatic insulin sensitivity. To investigate peripheral and hepatic insulin sensitivity and activity of the hepatic glucose/glucose 6-phosphate (G/G6P) substrate cycle in essential hypertension, euglycemic glucose clamps were performed in eight untreated patients and eight matched controls at insulin infusion rates of 0.2 and 1.0 mU.kg-1.min-1. A simultaneous infusion of (2(3)H)- and (6(3)H)glucose, combined with a selective detritiation procedure, was used to determine glucose turnover, the difference being G/G6P cycle activity. Endogenous hepatic glucose production (EGP) determined with (6(3)H)glucose was similar in hypertensive and control groups in the postabsorptive state (11.0 +/- 0.3 v 10.9 +/- 0.3 mumol.kg-1.min-1) and with the 0.2 mU insulin infusion (4.9 +/- 0.5 v 4.0 +/- 0.8 mumol.kg-1.min-1). With the 1.0 mU insulin infusion, glucose disappearance determined with (6(3)H)glucose was lower in the hypertensive group (21.8 +/- 2.4 v 29.9 +/- 2.4 mumol.kg-1.min-1, P less than .001). G/G6P cycle activity was similar both in the postabsorptive state (2.2 +/- 0.4 v 2.7 +/- 0.4 mumol.kg-1.min-1) and during insulin infusion (0.2 mU, 2.5 +/- 0.3 v 2.9 +/- 0.4; 1.0 mU, 4.7 +/- 0.3 v 5.3 +/- 1.1 mumol.kg-1.min-1 for hypertensive and control groups, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin action and hepatic glucose cycling in essential hypertension. 154 71

To assess the effects of genetic predisposition of essential hypertension on early renal function in recent insulin-dependent diabetics, we studied inulin, para-aminohippuric, sodium, and lithium clearances in 69 unselected diabetics with (n = 20) and without (n = 49) a family history of essential hypertension. Despite similar metabolic control, glomerular filtration rate and mean arterial pressure were significantly higher in diabetics with than in those without a family history of hypertension. However, no difference was found between the two groups regarding renal vascular resistance, sodium excretion, or fractional proximal and distal sodium reabsorption. Renal responses to acute captopril (75 mg) administration were evaluated in 27 patients (six with family history of hypertension). Captopril decreased filtration fraction and mean arterial pressure similarly in both groups, whereas glomerular filtration rate and renal vascular resistance decreased more dramatically in diabetics with family history of hypertension. These findings indirectly suggest an abnormal response to angiotensin of vascular tone in recent diabetics with familial predisposition to hypertension. Renal response to acute nicardipine (2.5 mg i.v.) administration was analyzed in 24 patients (five with family history of hypertension). In both groups, nicardipine similarly decreased mean arterial pressure and renal vascular resistance and induced a marked natriuretic effect due to a predominant reduction in proximal reabsorption of sodium. However, the increase in sodium excretion was twofold to threefold more pronounced in diabetics with a family history of hypertension. Whether these early renal abnormalities may contribute to the risk of diabetic nephropathy, as suggested by retrospective studies, remains to be determined.
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PMID:Renal abnormalities in normotensive insulin-dependent diabetic offspring of hypertensive parents. 155 69

Type 2 diabetes mellitus is characterized by impaired insulin release and sensitivity, elevated blood sugar and unfavourable changes in blood lipids. Insulin resistance and adverse blood lipids are also seen in the state of essential hypertension (the metabolic syndrome). Patients should learn to measure their own blood sugar. Treatment usually begins with regulation of the diet for 3-6 months. If this treatment fails, the next step is to give oral antidiabetic agents. Insulin treatment is required 1) when blood sugar is excessively high; 2) when oral agents fail; and 3) in case of increased need of insulin due to intercurrent disease. Antihypertensive treatment should not have adverse metabolic effects in patients with type 2 diabetes.
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PMID:[Treatment of non-insulin dependent diabetes (type 2 diabetes mellitus)]. 155 62

Individual dietary regulation is still an important part of all forms of treatment of diabetes. In insulin dependent diabetes (IDDM) it is rational to advise the patient 1) to arrange his diet so that this results in a low glycaemic response, which implies a relatively high intake of dietary fibre and polysaccharides, 2) to distribute the food into 5-6 daily meals and 3) to consume a low-fat diet. This prevents too pronounced postprandial hyperglycaemia and hypoglycaemia between meals. Simultaneously, insulin sensitivity is increased and not only the insulin requirement but also peripheral hyperinsulinism tend to be reduced. Dietary regulation in IDDM is thus a compensation for the defective synchronization of variations in the plasma levels of glucose and insulin in the present day forms of insulin therapy. Nine out of ten diabetic patients are non-insulin dependent (NIDDM). The great majority are obese, 50% have essential hypertension and just as many have dyslipidaemia (raised serum triglyceride and reduced serum high density lipoprotein (HDL)-cholesterol). The condition is characterized pathophysiologically by insulin resistance in muscle, fat and liver tissue and delayed and frequently reduced glucose-stimulated secretion of insulin. The most important element in dietary regulation in NIDDM is, therefore, reduction of the energy content of the food with the object of achieving and maintaining reduction in weight. Even moderate reduction, in the majority of NIDDM patients, will have the effect that metabolism of carbohydrates and lipids becomes approximately normal on account of considerable increase in insulin sensitivity and to a lesser degree increased secretion of insulin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Dietary treatment of diabetes mellitus. Background and rationale for recommendations in the 1990's]. 141 88


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