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

Hyperinsulinemia and insulin resistance have been proposed to play a role in human and experimental hypertension. To characterize this relation further, we examined the pressor responses to periarterial nerve stimulation (PNS) and norepinephrine infusion in the isolated mesenteric vasculature of the normal rat before and after insulin (10, 100, and 1,000 microunits/ml) infusion. The pressor responses to PNS were similar before and after insulin, except at the highest dose of insulin (1,000 microunits/ml) and the highest frequency of PNS (10 Hz). However, insulin significantly increased the pressor responses to norepinephrine. This increase in responsiveness was evident at all doses of insulin studied. In contrast, insulin did not affect the pressor responses to either angiotension II or serotonin administration. The mechanism or mechanisms for the augmented pressor response to norepinephrine after insulin infusion remain to be determined. However, the selectivity of the response for norepinephrine and the absence of a marked pressor increase after PNS indicate that the mechanism probably involves either the alpha-receptor itself or an amplification of the postreceptor signal transduction. The role of chronic hyperinsulinemia and insulin resistance in the pathogenesis of essential hypertension requires further study.
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PMID:Insulin enhances pressor responses to norepinephrine in rat mesenteric vasculature. 173 63

The insulin sensitivity of five essential hypertensive patients was compared to five patients with renovascular hypertension, five patients with primary hyperaldosteronism, and five normotensive subjects, using the euglycemic hyperinsulinemic clamp technique. Essential hypertensive patients had significantly lower insulin sensitivity than patients with hyperaldosteronism and renovascular hypertensive patients (P = .0066, P = .004, respectively). Hyperaldosteronism patients also had less insulin sensitivity than renovascular hypertensive patients (P = .016). A significant negative correlation was found between body mass index and insulin sensitivity index for essential hypertension patients only (r = -0.87, P less than .003). No such correlation was found in the secondary hypertension patients. The findings suggest a causal relationship between insulin resistance and the development of essential hypertension. Secondary hypertension, on the other hand, is not such an insulin resistant state.
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PMID:Insulin resistance in secondary hypertension. 173 30

Kidney disease is a primary cause of morbidity and mortality in diabetic patients. Factors that predetermine development of nephropathy remain unknown. Poor glycemic control, insulin requirement, duration of diabetes and family history of hypertension appear to be associated with an increased risk. Arterial hypertension, which is twice as common in diabetic patients as in the normal population, accelerates the progression of diabetic nephropathy. The pathophysiologic mechanisms responsible for hypertension appear to be different in IDDM and NIDDM. In IDDM, hypertension occurs usually as a consequence of diabetic renal disease. Conversely, the pathogenesis in NIDDM appears to be multifactorial. In either condition, aggressive blood pressure control is the single most important intervention proven to retard the progression of nephropathy. A stepped-care approach similar to that for essential hypertension with slight modifications is indicated in the treatment of the hypertensive diabetic patient with nephropathy. Nonpharmacological therapy, including dietary protein restriction, should be used as first step. Selection of the ideal antihypertensive must be based not only on efficacy but also on its side effect profile. Angiotensin converting enzyme inhibitors and calcium antagonists have a low incidence of side effects and do not induce metabolic disturbances. Therefore, they are the agents of choice for patients who do not respond to nonpharmacological therapy alone. Thiazide diuretics and beta-blockers should be used as first line therapy only for specific indications. Antihypertensive therapy combined with good glycemic control and dietary protein restriction constitute the standard of care for diabetic patients with hypertension and renal disease.
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PMID:Hypertension and kidney disease of diabetes mellitus. 176 55

The nature of the association between essential hypertension and insulin resistance remains unknown. We measured plasma glucose and insulin levels after an oral glucose tolerance test (OGTT), as well as insulin sensitivity (using a euglycemic hyperinsulinemic clamp), glucose turnover (Rd; using [6,6-2H2]- and [3-3H]glucose isotopic dilution), and forearm net balance of glucose (using arterial-venous difference) in 22 hypertensive patients with high (H2) red blood cell (RBC) sodium-lithium countertransport (Na(+)-Li+ CT; greater than 0.41 mmol.l RBC-1.h-1), 21 hypertensive patients with normal (H1) Na(+)-Li+ CT, and 22 normotensive controls (C). After OGTT, H2 patients had higher plasma glucose and insulin levels than H1 and C. During euglycemic hyperinsulinemia (approximately 100 microU/ml) Rd was lower in H2 [21.7 +/- 1.4 (SE) mumol.kg-1.min-1] than in H1 (44.3 +/- 2.9; P less than 0.01) and C (48.1 +/- 3.0; P less than 0.01), and an inverse correlation was found between rates of Na(+)-Li+ CT and Rd in H1 and H2 (rs = -0.76; P less than 0.01). Forearm glucose uptake was 40-50% lower in H2 compared with H1 and C (P less than 0.01). Lactate concentration increased more in C (from 511 +/- 24 to 1,207 +/- 69 microM) and in H1 (from 564 +/- 40 to 1,122 +/- 99) than in H2 (from 581 +/- 42 to 950 +/- 102, P less than 0.05 vs. both). Forearm blood flow increased more in C (31%, P less than 0.05) and H1 (22%, P less than 0.05) than in H2 (12%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin resistance is associated with high sodium-lithium countertransport in essential hypertension. 176 28

Late diabetic effects are the sequelae of for a long time super elevated blood sugar levels. The diabetic nephropathy is the cause of the secondary arterial hypertension. The investigation seeks for the connections between the diabetes mellitus and the essential, that is primary hypertension. The two diseases frequently appear and clearly increase in the second half of life. Moreover, they are above average frequently associated with each other. Among brothers and sisters of diabetic hypertensives in comparison to normal cohorts clearly increased high blood pressure prevalences were found. The insulin resistance which could be proved in a great number of hypertensive and which has been known since more than two decades might be the connecting link between hypertension and diabetes mellitus. Like the obesity the essential hypertension can be associated with all degrees of an insulin hyposensitiveness. The sodium-retaining effect of the insulin might explain the increased sodium content of the body in hypertensives. The differential diagnostics of the essential hypertension should therefore seek for conditions of an insulin resistance. The type II diabetic lacks a release of bradykinin during muscle work. Thus the glucose uptake into the cell is unfavourable influenced and demands an increased insulin excretion. This genetically (?) fixed defect is found also in essential hypertensives. It could be the connecting link between the two diseases. ACE-inhibitors have via a kininase II inhibition an effect also on the bradykinin decomposition and can favourable influence the glucose uptake into the muscle. An improved insulin effect among the ACE-inhibitors was described. Therefore, they should be preferred in the treatment of hypertensive diabetics.
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PMID:[Diabetes mellitus and arterial hypertension. In search of the connecting link]. 177 26

Insulin resistance is the cornerstone for the development of non-insulin-dependent diabetes mellitus (NIDDM). Free fatty acids (FFAs) cause insulin resistance in muscle and liver and increase hepatic gluconeogenesis and lipoprotein production and perhaps decrease hepatic clearance of insulin. It is suggested that the depressing effect of insulin on circulating FFA concentration is dependent on the fraction derived from visceral adipocytes, which have a low responsiveness to the antilipolytic effect of insulin. Elevated secretion of cortisol and/or testosterone induces insulin resistance in muscle. This also seems to be the case for low testosterone concentrations in men. In addition, cortisol increases hepatic gluconeogenesis. Cortisol and testosterone have "permissive" effect on adipose lipolysis and therefore amplify lipolytic stimulation; FFA, cortisol, and testosterone thus have powerful combined effects, resulting in insulin resistance and increased hepatic gluconeogenesis. All these factors promoting insulin resistance are active in abdominal visceral obesity, which is closely associated with insulin resistance, NIDDM, and the "metabolic syndrome." In addition, the endocrine aberrations may provide a cause for visceral fat accumulation, probably due to regional differences in steroid-hormone-receptor density. In addition to the increased activity along the adrenocorticosteroid axis, there also seem to be signs of increased activity from the central sympathetic nervous system. These are the established endocrine consequences of hypothalamic arousal in the defeat and defense reactions. There is some evidence that suggests an increased prevalence of psychosocial stress factors is associated with visceral distribution of body fat. Therefore, it is hypothesized that such factors might provide a background not only to a defense reaction and primary hypertension, suggested previously, but also to a defeat reaction, which contributes to an endocrine aberration leading to metabolic aberrations and visceral fat accumulation, which in turn leads to disease.
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PMID:Metabolic implications of body fat distribution. 177

The paper is devoted to a study of the time course of lipid metabolism, analysis of glucose tolerance, change in indices of immunoreactive insulin, glucagon and C-peptide before the start of verapamil therapy and 6 mos. after it during monotherapy with this drug. These parameters were investigated in the blood serum using biochemical methods and radioimmunoassays. A marked antihypertensive effect was achieved in patients suffering from noninsulin dependent diabetes mellitus with concomitant essential hypertension of the 2nd degree. No negative effect on the pancreatic hormone secretion was noted. Lipid transport indices were improved.
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PMID:[Use of finoptin in patients with non-insulin-dependent diabetes mellitus with concomitant essential hypertension]. 178 2

Obesity, essential hypertension, and diabetes mellitus share certain metabolic disturbances. The predictive value of disordered glucose metabolism and insulin action for hypertension are discussed. Several studies have examined the relationship between hypertension and glucose metabolism in diverse populations, and tend to indicate a predictive role for insulin and glucose metabolism disturbances in the development of hypertension.
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PMID:Glucose, insulin, and insulin resistance as biochemical predictors of hypertension. 178 48

A possible link between hyperinsulinemia and blood pressure was studied in non-obese subjects with normal glucose tolerance. First, the responses in plasma glucose and serum insulin to an oral glucose load (75-g oral glucose tolerance test) were compared between 42 patients with essential hypertension and 93 normotensive control subjects. Second, of the 93 normotensive subjects, the relations of serum insulin levels to blood pressure, serum cholesterol, and triglycerides concentrations were assessed in 8 hyperinsulinemic (serum insulin level [during fasting, or after glucose loading, or both] greater than 2 S.D. higher than the mean) and 8 pair-matched normoinsulinemic subjects (serum insulin level within 1 S.D. of the mean), individually matched for age, sex, and body mass index. Plasma glucose and serum insulin responses to the glucose load in hypertensive subjects were identical to the respective responses in normotensive subjects, while the mean total serum cholesterol level was slightly higher (p less than 0.05) in hypertensive subjects. The respective values for systolic and diastolic blood pressures, and total serum cholesterol and triglycerides concentrations were comparable in hyperinsulinemic and normoinsulinemic subjects. These results did not suggest a close association between hyperinsulinemia and elevated blood pressure in non-obese middle-aged Japanese subjects with normal glucose tolerance.
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PMID:Hyperinsulinemia and blood pressure in non-obese middle-aged subjects with normal glucose tolerance. 180 10

A hypotensive effect of active vitamin D treatment (alphacalcidol 1 mg daily) has previously been reported in three double-blind, placebo-controlled studies over 4-6 months in subjects with mild primary hyperparathyroidism (HPT), intermittent hypercalcemia and essential hypertension. The commonly used antihypertensive drugs, thiazides and betablockers, both induce impairments in both glucose and lipid metabolism and the thiazides are known to cause an elevation of serum urate. The effects of vitamin D treatment on these metabolic variables were recorded in these studies. Alphacalcidol did not induce any changes in fasting glucose HbA1c or insulin, serum triglycerides, cholesterol or serum urate in any of the treated groups. Neither was HDL cholesterol affected, except for a rise seen in the HPT subjects. It is therefore concluded that no major metabolic alterations in glucose or lipid metabolism or serum urate accompany the hypotensive effect of vitamin D.
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PMID:No major metabolic alterations accompany the hypotensive effect of active vitamin D. 181 79


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