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

The aim of the present study was to investigate the role of insulin on the renal mechanism of hyperuricemia in overweight patients with essential hypertension. Thirty-four essential hypertensives(EHT), receiving a regular diet containing 120mEq of sodium, 75mEq of potassium and 2000 kilocalories daily, were divided into two groups of non-obese(NHT) and obese(OHT) EHT. NHT as categorized as a body mass index (BMI) less than, and OHT as a BMI equal to or more than, 25 kg/m2 in male patients and 24 kg/m2 in female patients. In the early morning after overnight fast, renal uric acid and sodium clearance were examined while the patients remained in a supine position. During the two-hour clearance period, mean arterial pressure(MAP), heart rate(HR), endogenous creatinine clearance(Ccr), immunoreactive insulin(IRI), serum uric acid(SUA), fractional excretion of uric acid(FEUA) and sodium(FENa) were measured. Although there were no significant differences in age, MAP, HR, Ccr, nor SUA between the two groups, a higher ratio of female to male patients was found in OHT than in NHT. On the other hand, higher SUA and IRI and lower FEUA and FENa were observed in OHT than in sex-and Ccr-matched NHT. SUA was negatively correlated with FEUA in all patients (r = -0.392, p less than 0.05) and in NHT (r = -0.553, p less than 0.05), unlike in OHT. A significant negative correlation between BMI and FEUA was revealed in all EHT (r = -0.441, p less than 0.01) and in OHT (r = -0.597, p less than 0.01) but not in NHT. FEUA was positively correlated with FENa in all EHT (r = 0.554, p less than 0.001) as well as in NHT (r = 0.548, p less than 0.05) and OHT (r = 0.507, p less than 0.05). Moreover, there was a significant negative correlation between IRI and FENa in all EHT (r = -0.361, P less than 0.05) and in OHT (r = -0.470, p less than 0.05). However, no significant relation was demonstrated between IRI and SUA or FEUA in NHT or OHT. From these results, it is concluded that an attenuated renal excretion of uric acid related to natriuretic ability may play an important role in hyperuricemia in EHT. However, the role of hyperinsulinemia, which contributes to the blunting of natriuresis, might be relatively small in the renal mechanism of hyperuricemia in EHT, particularly in OHT.
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PMID:[The role of hyperinsulinemia on the renal mechanism of hyperuricemia in overweight patients with essential hypertension]. 181 26

Hyperinsulinemia has been implicated in the pathogenesis of the blood pressure elevation in patients with noninsulin-dependent diabetes mellitus, obesity, but also essential hypertension. In these conditions an increased cardiovascular reactivity to noradrenaline (NA) and angiotensin II (AII) can be observed. Using the euglycemic clamp technique, we determined the cardiovascular reactivity to graded infusions of NA and AII in nine healthy males before (Bas), and 1 and 6 h after infusion of insulin (50 mU/kg per h) was started. On separate days control experiments were carried out to control for any circadian variation. Insulin led to a decrease of the amount of circulating NA necessary to increase the diastolic blood pressure (DBP) 20 mmHg (actual experiment [mean +/- SEM]: Bas, 23.1 +/- 5.0; 1 h, 14.8 +/- 3.0; and 6 h, 12.3 +/- 3.1; and control experiment: Bas, 20.7 +/- 5.0; 1 h, 18.6 +/- 3.5; and 6 h, 17.3 +/- 3.3 nmol/liter; Bas vs. 1 and 6 h: P less than 0.05). Although the amount of NA infused to raise DBP 20 mmHg showed a similar decline after 1 h of insulin infusion, no such change from baseline could be observed at 6 h. This appeared to be due to an increase in NA clearance with more prolonged insulin infusion. Insulin exerted no effect on the amount of AII infused to increase DBP 20 mmHg (actual experiment: Bas, 27.6 +/- 6.4; 1 h, 28.8 +/- 10.0; and 6 h, 21.2 +/- 5.3; and control experiment: Bas, 33.6 +/- 5.7; 1 h, 34.2 +/- 6.1; and 6 h, 23.4 +/- 4.7 ng/kg/min; NS). We did observe a circadian variation in AII reactivity. Whether the increase in cardiovascular responsiveness to NA after administration of insulin contributes to the elevation in blood pressure frequently observed in patients with insulin resistance remains to be proven.
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PMID:Exogenous insulin augments in healthy volunteers the cardiovascular reactivity to noradrenaline but not to angiotensin II. 186 61

Epidemiologic studies have shown that insulin is a risk factor for coronary heart disease (CHD). Clinical studies have also demonstrated positive correlations between insulin and blood pressure, triglycerides, total cholesterol, fibrinogen, and plasminogen activator inhibitor. Moreover, there is an inverse correlation between insulin and high-density lipoprotein (HDL). These studies have provided evidence in support of the biologic plausibility of epidemiologic observations, but they have not clearly established insulin's role in the pathogenesis of human cardiovascular diseases (CVD) such as hypertension. In fact, there is considerable evidence that insulin resistance (abnormal nonoxidative glucose disposal), not hyperinsulinemia, is the primary insulin-related abnormality in human hypertension, and that hyperinsulinemia occurs as a response to insulin resistance. Skeletal muscle appears to be the primary site of insulin resistance in essential hypertension, although other organs, such as the kidneys and liver--key sites for cell and water homeostasis and lipoprotein regulation, respectively--may respond normally to insulin. Adipocytes also appear to be a site of insulin resistance. Thus, the putative interrelationship between hyperinsulinemia and insulin resistance, on the one hand, and with blood pressure and lipoproteins, on the other, is a complex one and may involve organ-specific insulin resistance. Altered cation transport is one of several mechanisms by which insulin resistance might raise blood pressure. The Na+, K(+)-ATPase and Ca(2+)-ATPase pumps are insulin sensitive. Thus, when insulin resistance is present, the activity of these pumps in the smooth muscle of the arterial wall might be reduced. This would lead to an intracellular accumulation of sodium and calcium, thereby sensitizing the vascular wall to pressor substances. Moreover, secondary hyperinsulinemia will occur, and insulin has been shown to stimulate sympathetic nervous system activity and to increase renal tubular absorption of sodium. Insulin is also a growth factor and therefore might have a trophic effect on the vessel wall, one that could initiate and/or sustain hypertension as well as atherosclerosis. Abnormal lipoprotein metabolism is yet another possible explanation for the accelerated atherosclerosis that has been observed in persons with abnormal carbohydrate tolerance and insulin resistance. Hyperinsulinemia and insulin resistance both play a role in the expression of elevated very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) levels as well as in the depression of HDL levels. Coronary risk reduction has been disappointing when blood pressure has been lowered with treatment regimens based on thiazide diuretics and/or beta blockers. Thiazides and some beta blockers may further impair tissue insulin sensitivity and often cause blood lipoprotein abnormalities.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Epidemiologic and clinical aspects of insulin resistance and hyperinsulinemia. 186 24

In this review, the relationship between hypertension and abnormal carbohydrate metabolism is explored. A review of the current literature reveals that people with hypertension are also likely to suffer from insulin resistance, glucose intolerance, and hyperinsulinemia. Likewise, hypertension is prevalent in obese and diabetic patients. Deficiency of insulin at the cellular level may be a common mechanism in the development of hypertension in patients with type I or type II diabetes mellitus. Essential hypertension appears to be an insulin-resistant state. Insulin resistance may engender hypertension by increasing peripheral vascular resistance as well as by increasing salt retention at the level of the kidney. Therefore effective antihypertensive therapy should include agents that do not adversely affect carbohydrate metabolic abnormalities. Commonly used antihypertensive agents, such as thiazide, thiazide-like diuretics, and beta-blockers, are associated with glucose intolerance and increased insulin resistance. In contrast, angiotensin-converting enzyme inhibitors, calcium antagonists, and peripheral alpha-blockers (such as prazosin and terazosin) do not adversely affect glucose tolerance or insulin sensitivity. In addition, alpha-blockers have a positive effect on the serum lipid profile. The entire multifactorial cardiac risk profile must be considered when choosing therapeutic agents for conditions that have an impact on cardiovascular disease.
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PMID:Is hypertension an insulin-resistant state? Metabolic changes associated with hypertension and antihypertensive therapy. 187 73

In 40 patients (pts) with essential hypertension (EH) the plasma levels of insulin, glucagon, gastrin and prolactin during 2 week therapy with nifedipine were evaluated. In pts with EH there were higher levels of hormones than in control subjects. During nifedipine therapy there was no elevation of the plasma hormone levels although the blood pressure was lowered. This study shows that there are other than hypertension factors in the pathogenesis of elevated hormone levels in EH.
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PMID:[Essential hypertension. Treatment with nifedipine and levels of insulin, glucagon, gastrin and prolactin]. 194 46

Hypertension and diabetes mellitus are both common conditions which frequently co-exist. The calcium channel blockers are potentially diabetogenic since insulin secretion may be impaired by their use. The aim of this study was to determine whether nitrendipine, a second generation dihydropyridine derivative calcium antagonist, is capable of interfering with carbohydrate metabolism and insulin secretion in hypertensive diabetics at the doses commonly used in therapy. In a 12-week double blind placebo-controlled randomized clinical trial, the effects of nitrendipine (20 mg/day) on arterial blood pressure, glycaemic homeostasis and other metabolic parameters were evaluated in 30 patients with mild to moderate essential hypertension and type II diabetes mellitus. The results showed nitrendipine to be an effective antihypertensive agent which neither impaired the overall glucose homeostasis nor caused any other potentially harmful metabolic side effect. In conclusion, these data suggest that the calcium channel antagonist nitrendipine is a metabolically safe drug to use in the treatment of hypertension, especially in patients with diabetes mellitus.
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PMID:[Antihypertensive efficacy of nitrendipine and its effects on carbohydrate metabolism. A controlled clinical study versus placebo]. 194 44

Blood pressure is generally normal in insulin-dependent diabetic patients in the absence of nephropathy. Despite this, exchangeable sodium is increased. Blood pressure rises with the development of incipient nephropathy, and hypertension is common in patients with overt nephropathy. Exchangeable sodium is then markedly increased, but plasma renin is not suppressed. Raised BP in diabetic nephropathy is probably sustained, in part at least, by sodium retention and inappropriate activity of the renin-angiotensin system. There is an increased prevalence of hypertension among patients with non-insulin-dependent diabetes (NIDDM). In normotensive patients, exchangeable sodium is elevated and plasma renin is suppressed. In hypertensive patients, exchangeable sodium is less markedly increased, while plasma renin is again suppressed. These findings are in contrast with those in diabetic nephropathy, and are in keeping with the hypothesis that hypertension in NIDDM is usually due to coexisting essential hypertension. Also in keeping with this suggestion is an increased prevalence of raised BP among the siblings of NIDDM patients. Prolonged hyperinsulinaemia precedes the diagnosis of NIDDM, and hypertension is often present at the time of diagnosis. Insulin resistance and compensatory hyperinsulinaemia might lead to an increase in BP by a number of putative mechanisms, such as enhancing renal sodium retention, by an effect on cell membrane ion exchange mechanisms or by enhancing activity of the sympathetic nervous system. This seems a fertile area for further research, although a causal link between insulin resistance and hyperinsulinaemia on the one hand, and raised BP on the other, remains to be proved.
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PMID:The causes of raised blood pressure in insulin-dependent and non-insulin-dependent diabetes. 195 22

A wide range of non-pharmacological manoeuvres have been tried for the control of BP but the majority of studies have not examined diabetic patients. Alteration of individual dietary components is difficult to achieve and results difficult to interpret. A high fibre, low fat, moderate salt restricted diet is as efficacious as drug therapy in some hypertensive diabetic patients. Similar diets have been recommended for all diabetic patients by the British Diabetic Association and the European Association for the Study of Diabetes. This diet has the added advantage of improving glycaemic control and plasma lipid profiles. The benefits of behavioral modifications are variable, with some being better than placebo. Although there is no evidence for a hypertensive effect of smoking, it should be strongly discouraged in diabetic patients because of the added cardiovascular risk it places upon them. Studies of dietary control of BP indicate that a response should be observed after three months of treatment. If blood pressure remains elevated after this time the patient should be treated with pharmacological agents. Hyperinsulinaemia may be important in the pathogenesis of Type II diabetes, coronary artery disease and essential hypertension. Dietary manoeuvres which reduce plasma insulin levels may prove to be of benefit in all of these conditions, but as yet data are not available to support this hypothesis.
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PMID:The non-drug treatment of hypertension in the diabetic patient. 195 27

To determine the contribution of skeletal muscle to the insulin resistance of essential hypertension, insulin-stimulated forearm glucose uptake was quantitated in 12 control (age, 32 +/- 3 years) and 12 hypertensive subjects (age, 36 +/- 2 years) using the forearm perfusion technique. Peripheral insulin levels were raised acutely (approximately 60 microU/mL), while blood glucose concentration was clamped at its basal value (90 mg/dL) by a variable glucose infusion. During insulin stimulation, whole body glucose uptake was lower in hypertensive (4.5 +/- .3 mg.kg-1.min-1) than in normal subjects (5.8 +/- .4 mg.kg-1.min-1, P less than .05). Similarly, the amount of glucose taken up by the forearm was markedly reduced in the hypertensive (5.3 +/- .91 mg.L-1.min-1) compared with the control group (8.7 +/- 1.1 mg.L-1.min-1). No appreciable difference was observed as to forearm blood flow (39 +/- 4 mL.L-1.min-1 and 37 +/- 5 mL.L-1.min-1) in hypertensive patients. These results indicate that skeletal muscle is a major site of insulin resistance in essential hypertension and that this defect is independent of muscle perfusion.
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PMID:Skeletal muscle is a primary site of insulin resistance in essential hypertension. 196 Nov 28

Non-selective and to a lesser extent selective beta-blockers are known to slightly deteriorate glucose metabolism. This may be of clinical relevance, since patients with essential hypertension suffer from reduced insulin-sensitivity and some studies showed an increased incidence of diabetes type II with beta-blocker-treated hypertensive patients. However, it is not clear whether this effect is due to hypertension per se or in addition by antihypertensive treatment. The possible mechanisms by which beta-blockers influence carbohydrate metabolism are discussed. Insulin secretion is inhibited by beta-blockers in vitro. However, no effect is seen in vivo in man. Hepatic glucose production in theory may be influenced, but no effect is demonstrable. Muscular glucose uptake could be reduced; some data exist showing reduced peripheral insulin sensitivity, although there are controversial results. In conclusion, a deterioration of carbohydrate metabolism by beta-blockers is established, the mechanism whereby remains obscure.
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PMID:Effects of beta-blocking agents on insulin secretion and glucose disposal. 197 44


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