Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin resistance and hyperinsulinemia is now recognized in non-insulin-dependent diabetes, essential hypertension, obesity, atherosclerotic heart disease, dyslipidemia, heart failure, and in heavy smokers. Several mechanisms have been proposed to explain hyperinsulinemia, insulin resistance and its relationship to hypertension; reduced sodium excretion, activation of the sympathetic nervous system, increased activity of the sodium/hydrogen pump, and stimulation of cellular growth. Some of the nonpharmacological methods to control hyperinsulinemia are of benefit in the management of hypertension, most notably weight loss, exercise program, and reduced salt intake. High-fiber and reduced-protein diets also reduce hyperinsulinemia. Thiazide diuretics can result in insulin resistance, and insulin secretion may be inhibited, possibly associated with concomitant hypokalemia. beta-Blockers result in some reduction of glucose tolerance and mask some of the features of hypoglycemia. Angiotensin-converting enzyme (ACE) inhibitors and alpha-receptor blockers do not effect insulin resistance; probably the same is true for calcium antagonists. Although the effect on risk factors should not be discounted, it is the effect of treatment on hard end points, cerebrovascular accidents, myocardial infarction, or death that is most important. Evidence in hypertension is at present restricted to diuretics and beta-blocking drugs.
 ...
PMID:Hypertension and insulin resistance. 128 47

Insulin resistance is a frequently occurring abnormality. Although there can be insensitivity to any of insulin's actions, insulin resistance par excellence is a decreased insulin-mediated whole-body glucose disposal rate. A distinction is made between primary and secondary insulin resistance. Primary insulin resistance is of unknown origin, is only partially experimentally reproducible, and is essentially irreversible (spontaneously or by treatment). In addition, it is both pathway-specific (ie, glucose storage) and organ-specific (mostly skeletal muscle), and is compatible with a postreceptor defect in insulin action. Primary insulin resistance is found in a proportion (approximately 25%) of otherwise healthy people, in non-insulin-dependent diabetes mellitus, essential hypertension, and some forms of dyslipidemia. The idea of an insulin resistance syndrome derives from the striking pattern of overlap among these clinical conditions. Their tendency to cluster in the same individuals is evident from both cross-sectional and longitudinal observations. It is proposed that the insulin resistance syndrome is a large constellation of interrelated changes in metabolic, anthropometric, and hemodynamic variables centered around insulin resistance or hyperinsulinemia. There is a significant genetic component, a predisposing influence for non-insulin-dependent diabetes mellitus, hypertension, dyslipidemia, and possibly, a distinct atherogenic potential.
 ...
PMID:The insulin resistance syndrome. 134 29

Recent research has demonstrated that reduced insulin-stimulated glucose metabolism in skeletal muscle (insulin resistance) and hyperinsulinism are common features in widespread diseases such as essential hypertension, android obesity, non-insulin dependent diabetes mellitus, dyslipidemia (in the form of raised serum triglyceride and reduced serum high-density lipoprotein (HDL) cholesterol) and arteriosclerosis. Simultaneously, investigations in a comprehensive group of healthy middle-aged men have revealed insulin resistance in one fourth. On the basis of these observations, a working hypothesis is suggested which postulates that genetic abnormalities in one or more of the candidate genes in the modes of action of insulin occur in a great proportion of the population. These may result in insulin resistance (primary genetic insulin resistance). Primary insulin resistance may be potentiated by a series of circumstances such as ageing, high-fat diet, lack of physical activity, hormonal and metabolic abnormalities or drugs (secondary insulin resistance). As a consequence of the reduced effect of insulin on muscle tissue, compensatory hyperinsulinism develops. Depending on the remaining vulnerability of the individual the hyperinsulinism is presumed to result in development of one or more phenotypes. For example if the beta-cells of the pancreas are unable to secrete sufficient insulin to compensate the insulin resistance on account of genetic defects, glucose intolerance will develop. In a similar manner, hyperinsulinism in insulin-resistant individuals who are predisposed to essential hypertension is presumed to reveal genetic defects in the blood pressure regulating mechanisms and thus contribute to development of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Insulin resistance--a physiopathological condition with numerous sequelae: non-insulin-dependent diabetes mellitus (NIDDM), android obesity, essential hypertension, dyslipidemia and atherosclerosis]. 163 67

Epidemiological evidence supports a link between hyperinsulinemia and blood pressure. In nondiabetic, normotensive individuals, the male sex, age, obesity, and body fat distribution all are associated with higher systolic and diastolic blood pressure and with higher plasma insulin concentrations. Nevertheless, when accounting for the above physiological variables, blood pressure still is independently related to plasma insulin. In the general population, hypertensive individuals have multiple metabolic abnormalities (glucose intolerance, hyperinsulinemia, and dyslipidemia). A striking pattern of overlap exists among obesity, diabetes, and hypertension. Physiological studies (euglycemic insulin clamp) have shown that essential hypertension per se is a state of insulin resistance: lean, nondiabetic subjects with untreated hypertension have a mean 40% reduction in the ability of physiological hyperinsulinemia to stimulate whole-body glucose uptake. Other insulin actions (suppression of hepatic glucose output, lipolysis, lipid oxidation, and promotion of K+ uptake) are conspicuously preserved. In perfused forearm studies, local (intra-arterial) hyperinsulinemia induces subnormal rates of glucose uptake and glycogen synthesis in the skeletal muscle of individuals with essential hypertension. In the San Antonio Heart Study, parental history of non-insulin-dependent diabetes mellitus (NIDDM) is associated with hyperinsulinemia and higher blood pressure and serum lipid levels in nondiabetic probands. In this biethnic population, however, hyperinsulinemia and NIDDM are more prevalent (approximately threefold) among Mexican-Americans than non-Hispanic whites, but hypertension is more prevalent among the latter.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Essential hypertension: an insulin-resistant state. 169 27

Overall 183 children with arterial hypertension (AH) were examined. Of these, 122 suffered from primary arterial hypertension (PAH). The lipid spectrum was defined in blood plasma of 95 children with PAH and in 30 normals. The same investigation was carried out in 109 parents of the children suffering from PAH. The lipid spectrum was established to be heterogeneous. 77.9% of the patients had dyslipidemia. A significant relationship was established between the stage of PAH and the nature of lipidemia as was a close interrelation between alterations in the lipid spectrum of blood plasma and hereditary load as regards essential hypertension.
 ...
PMID:[The characteristics of lipid metabolism in children with primary arterial hypertension]. 176 67

Essential hypertension is frequently associated with several metabolic abnormalities, of which obesity, glucose intolerance, and dyslipidemia are the most common. This report discusses the epidemiologic evidence for the coexistence of these risk factors and questions why hyperinsulinemia and essential hypertension cosegregate. The euglycemic insulin clamp and the insulin suppression test are documented with respect to the physiologic functions of insulin, and the mechanisms of insulin resistance in essential hypertension are discussed. Evidence to suggest that insulin resistance is a marker for an "atherogenic syndrome" is reviewed. It is concluded that all the hemodynamic and metabolic disorders of essential hypertension and insulin resistance are closely related. The clinical approach to the patient with any of the abnormalities in question should take into consideration the whole cluster, with therapy aimed at ameliorating the entire hemodynamic-metabolic profile.
 ...
PMID:Essential hypertension, metabolic disorders, and insulin resistance. 200 56

Hypertension that occurs before the age of 60 years is strongly aggregated in families, mostly due to genetic factors with weaker contributions from a shared family environment. Hypertension is probably a heterogeneous collection of overlapping subsets of pathophysiological mechanisms, such as dyslipidemia, obesity, hyperinsulinemia and cation metabolism. Highly heritable traits such as sodium-lithium countertransport, urinary kallikrein excretion and a body fat pattern index show evidence of major gene segregation in families with hypertension. They are thought to be intermediate phenotypes in the chain of pathophysiological events leading from specific genes to the distant phenotype of hypertension. They provide evidence of measurable contributions from single gene traits to the susceptibility to hypertension. Genetic linkage studies have suggested that other specific loci (e.g. histocompatibility leukocyte antigen, blood group MN and the haptoglobin protein) contribute to the susceptibility to hypertension. DNA sequencing has shown a point mutation for lipoprotein lipase that conveys susceptibility to lipid abnormalities, and possibly also hypertension, as seen in families with dyslipidemic hypertension. Further application of these approaches, especially in families that include multiple siblings with hypertension, shows promise of a true understanding of how the combined effects of a few specific genes, the polygenic background and selected environmental factors can lead to essential hypertension. This understanding should foster better tailored and more effective approaches to the prevention, diagnosis and treatment of hypertension.
 ...
PMID:Multigenic human hypertension: evidence for subtypes and hope for haplotypes. 209 95

Twenty patients with essential hypertension, 5 with dyslipidemia type IIa and 15 with that of type IIb, were treated with bezafibrate, 200 mg/day. As control group, 20 normo or dislipemic patients with essential hypertension receiving no hypolipidemic drugs, and chosen at random, showed no significant changes of the mean values of serum total cholesterol and triglycerides at three evaluations made in a period of about six months. Six patients were males (60 +/- 4 years) and 14 females (57 +/- 2 years). The levels of cholesterolemia and triglyceridemia were evaluated before the administration of the drug and on the 28th and 56th day of its use. The mean initial value of total cholesterol (n = 20) was 334 +/- 10 mg/dl, lowering significantly (P less than 0.01) to 274 +/- 7 mg/dl and 279 +/- 11 mg/dl. Initial triglyceridemia level (n = 15) was 544 +/- 85 mg/dl, decreasing significantly (P less than 0.01) to 234 +/- 36 and 245 +/- 36. Percentual mean decrease of cholesterolemia was respectively 16 +/- 4% and 14 +/- 5% and that of triglyceridemia was 46 +/- 8% for both evaluations. Side effects of the drug were not seen with the indicated dose. The therapy was useful to lower the dislipemic values of the essential hypertensive patients, in spite of no consistent changes in their diet and physical activity and of its use for a short period.
 ...
PMID:[Treatment of essential hypertension and hypercholesterolemia with or without hypertriglyceridemia, with low dose of bezafibrate (200 mg/day)]. 213 71

Lowering blood pressure is not totally effective in preventing the atherosclerotic complications of systemic hypertension. In hypertensive patients both platelet hyperaggregation and dyslipidemia have been suggested as important risk factors. The effect of 8 weeks' treatment with ketanserin on blood pressure, serum lipid parameters (cholesterol, triglycerides, LDL, HDL-C, apolipoprotein A1 and B) and platelet aggregation, induced by collagen, ADP, arachidonic acid, was evaluated in 10 patients with essential hypertension. Ketanserin was effective in lowering blood pressure in all patients, 6 of whom became normotensive. Both CHOL and TG levels and APO B were significantly reduced, whereas HDL-C and APO A1 were significantly increased after treatment. These results might be attributed to the antagonistic activity of ketanserin on alpha-1 adrenoceptors with a consequent inhibition of phosphodiesterase. Platelet aggregation, after stimulation with collagen and arachidonic acid, was significantly reduced secondary to the inhibition of intraplatelet serotonin synthesis and release. These results suggest that keranserin is effective in reducing blood pressure and in achieving normal serum lipid pattern and platelet aggregation. Therefore, this drug might be helpful in controlling the main risk factors for cardiovascular damage.
 ...
PMID:Effects of ketanserin administration on lipid metabolism and platelet aggregation in hypertensive patients. 227 4

Essential hypertension is a heterogeneous group of disorders with different causes. This report reviews approaches taken and results found in current studies of the genetic and environmental determinants of essential hypertension. Recent observations from the University of Utah Cardiovascular Genetics Research Clinic and published data from other studies are cited. Several biochemical tests show strong associations with hypertension and substantial major gene and/or polygenic determination including: urinary kallikrein excretion, intracellular sodium concentration, sodium-lithium countertransport, plasma haptoglobin phenotypes, MN blood groups, and familial dyslipidemia.
 ...
PMID:Definition of genetic factors in hypertension: a search for major genes, polygenes, and homogeneous subtypes. 246 8


1 2 3 4 5 6 7 8 9 10 Next >>