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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The association of hypertension and obesity is poorly understood. Studies conducted in our laboratory over the last decade, in conjunction with recent clinical and epidemiological observations, suggest that hypertension in the obese is derived from a fundamental relationship between dietary intake and sympathetic nervous system (SNS) activity. The application of kinetic techniques to the measurement of norepinephrine (NE) turnover rate in sympathetically innervated tissues of laboratory rodents has defined a relationship between the SNS and dietary intake. Fasting or caloric restriction suppresses sympathetic activity in a variety of organs of the rat, including heart and interscapular brown adipose tissue. Overfeeding a mixed, palatable, "cafeteria" diet stimulates sympathetic activity in these same tissues. The stimulatory effect of mixed diets is due to the carbohydrate and fat content, because these two latter nutrients stimulate sympathetic activity even when total caloric intake is not increased. Insulin-mediated glucose metabolism within central neurons associated with the ventromedial hypothalamus (VMH) plays an important role in the relationship between dietary intake and SNS activity as indicated by the following observations: (1) Hypoglycemia (noninsulin-mediated) is associated with suppression of the SNS (despite concomitant adrenal medullary stimulation); (2) 2-deoxyglucose, an intracellular inhibitor of glucose metabolism, decreases sympathetic activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Obesity, metabolism, and the sympathetic nervous system. 264 3

The purpose of this study was to assess the effects of chronic insulin infusion on blood pressure and urinary sodium excretion in Wistar rats. Fifteen Male Wistar rats weighing about 220 g were used. The rats were housed in metabolic cage and measured urine volume. Osmotic minipumps filled with insulin (0.57 U/day, Insulin group, n = 9) or saline (0.014 cc/day, Control group, n = 6) were implanted subcutaneously under ether anaesthesia, and blood pressure, urine volume, urinary sodium excretion (UNaV), plasma renin activity (PRA), plasma norepinephrine concentration (PNE) were measured for 4 weeks. In insulin group, there were no significant changes on plasma glucose levels, but systolic blood pressure rose significantly from 119 mmHg to 140 mmHg after 4 weeks. In this group, urine volume, UNaV, and PRA were significantly lower than those of control group and PNE was tended higher but not significant (P less than 0.1). Exogenous NE was given intravenously to assess the endogenous NE activity. Blood pressure elevation caused by exogenous NE in insulin group was suppressed significantly than that of control group. On the basis of these findings, we conclude that insulin can cause high blood pressure due to sodium retention and activation of endogenous NE.
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PMID:[Insulin and hypertension--the mechanisms of high blood pressure during chronic insulin infusion]. 268 19

The prevalence of hypertension in patients with non-insulin-dependent diabetes mellitus (NIDDM) is considerably higher than in the non-diabetic population. Insulin resistance may contribute to this increased prevalence. Abnormal cellular calcium (Ca2+) homeostasis may link insulin resistance and high blood pressure in patients with NIDDM. Observations of abnormal cellular Ca2+ homeostasis in animal models of NIDDM and obesity as well as in diabetic patients are consistent with this hypothesis. Abnormalities in cellular Ca2+ homeostasis are also found in hypertensive animals and humans. Alterations in cell membrane phospholipid content and distribution may be the primary cause of abnormal plasma membrane Ca2+ fluxes in patients with NIDDM and hypertension.
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PMID:Role of cellular calcium metabolism in abnormal glucose metabolism and diabetic hypertension. 268 14

Hypertension may eventually develop in response to chronic slight retention of sodium and expansion of the extracellular fluid volume, either due to intrinsic pathology or to neurohormonal influences of the kidneys. As almost half of all juvenile diabetic patients sooner or later will develop diabetic nephropathy and hypertension, data are discussed which tend to indicate that renal sodium metabolism is altered already early during the course of diabetes. Compared to healthy subjects the absolute total tubular sodium reabsorption is increased by approximately 30-40 per cent, as is the filtered sodium load. Insulin may stimulate sodium reabsorption in man through an effect on the distal nephron segment. However, by means of combined lithium and 51Cr-labelled EDTA clearances it has been clearly demonstrated that the excess sodium reabsorption in ambulatory insulin-dependent diabetics exclusively takes place in the proximal tubules, while the distal tubular function appears normal. In these studied patients the extracellular fluid volume was also significantly increased. The increased fractional sodium reabsorption of the proximal tubules remains unaffected by increasing duration of diabetes and is also demonstrable in patients with overt diabetic nephropathy. Glucose is reabsorbed in the early portion of the proximal tubules coupled to Na+ transport, utilizing a common carrier protein. An increased load of glucose will therefore be expected to induce an increase in the proximal tubular reabsorption rate of sodium and water, at least as long as the proximal tubular reabsorption capacity for glucose is not exceeded to a degree inducing significant osmotic diuresis. This deviation from normal in proximal renal sodium and fluid handling may be relevant to the development of hypertension in long-term insulin-dependent diabetes.
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PMID:Renal sodium metabolism in relation to hypertension in diabetes. 269 46

The relationship between obesity and hypertension is complex and poorly understood. A developing body of information suggests that metabolic factors related to the obese state are importantly involved. The pertinent observations include: (1) Diet influences sympathetic nervous system activity. Fasting suppresses, while carbohydrate and fat feeding stimulate, sympathetic activity. (2) Dietary-induced changes in sympathetic activity contribute to the changes in metabolic rate that accompany changes in dietary intake. (3) Insulin-mediated glucose metabolism in the hypothalamus provides a link between dietary intake and sympathetic nervous system activity. And (4) hyperinsulinemia, a consequence of insulin resistance in the obese, is associated with hypertension. These observations have suggested the following hypothesis. Hyperinsulinemia results in sympathetic stimulation which drives thermogenic mechanisms, thereby increasing metabolic rate. The net result is a restoration of energy balance at the expense of hyperinsulinemia and increased sympathetic activity. Hypertension is thus the unfortunate consequence of hyperinsulinemia, which increases renal sodium reabsorption, and sympathetic stimulation of the heart, kidney, and vasculature. The data on which this hypothesis is constructed are reviewed and the implications discussed.
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PMID:Obesity, metabolism, and hypertension. 269 85

A follow-up study of 1939 diabetic patients with a mean observation period of 9.4 years was carried out in Osaka, Japan. The mortality rates per 1000 person-years were 31.35 for males and 21.99 for females, and the ratios of observed to expected number of deaths were 1.69 for males and 1.74 for females, indicating an excess mortality for diabetic patients of both sexes and higher mortality in males than in females in Japan. Factors related to the prognosis of the patients were age, elevated fasting glucose level, lower obesity index, hypertension, diabetic retinopathy, and albuminuria at entry to the study. Insulin treatment was also associated with poor prognosis. Cerebro-cardiovascular and renal disease were the major causes of death in diabetic patients; heart disease killed 19.5%, cerebrovascular disease 16.7% and renal disease 13.1%. The relatively high frequency of renal disease as a cause of death in type 2 diabetes, especially in patients with a lower age of onset, was noteworthy, suggesting some difference in the clinical manifestations of diabetes between Japan and Western countries. Malignant neoplasms accounted for 25% of deaths, and cirrhosis of the liver for 6.4%.
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PMID:Mortality and causes of death in type 2 diabetic patients. A long-term follow-up study in Osaka District, Japan. 275 88

Diabetes and hypertension are independent risk factors of coronary heart disease as well as of other cardiovascular diseases, and their combination substantially enhances the risk. Hypertension is twice to four times as frequent in diabetics than in the non-diabetic population. The most frequent form is essential hypertension which affects the relatively most numerous group of the II diabetics but may occur also in type I diabetics. Insulin dependent diabetics suffer more frequently from "renal diabetic hypertension" and tend to develop hyporeninaemic hypoaldosteronism. Other types of hypertension found in diabetics are systolic hypertension and hypertension with orthostatic hypotension. In an effort to improve the adverse prognosis of diabetics with hypertension it is essential to pay systematic attention to early detection of high blood pressure, its differential diagnosis and treatment, and to detect, and if possible eliminate, other risk factors of cardiovascular diseases.
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PMID:[Special problems in diabetics with hypertension]. 280 Mar 85

Diabetes mellitus is associated with an increased incidence of hypertension and renal failure. Alterations in the renin-angiotensin system may contribute to the development of cardiovascular disorders in diabetics. This study examined diabetic associated changes in angiotensin converting enzyme (ACE). ACE activity was measured in serum, lung and kidney tissue derived from normoglycemic or 3-48 day streptozotocin (STZ)-induced diabetic rats. Serum and tissue ACE activity were not altered 3 days post STZ treatment. Serum ACE activity significantly increased in the diabetic group relative to controls, beginning 12 days post STZ treatment. Insulin treatment for 10 days partially normalized serum ACE activity. Therefore, STZ-induced diabetes produced significant changes in ACE activity that are partially corrected by insulin treatment.
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PMID:The effect of streptozotocin-induced diabetes and insulin treatment on angiotensin converting enzyme activity. 282 28

The aim of this study was to determine whether chronic hyperinsulinemia, comparable to that found in obesity-associated hypertension, causes sustained increases in mean arterial pressure (MAP) or potentiates the hypertensive effects of angiotensin II (ANG II). Insulin infusion (0.5 or 1.0 mU/kg/min, IV), with plasma glucose held constant by IV glucose infusion, for seven to 28 days raised plasma insulin by five- to ten-fold, but did not significantly change MAP in dogs with reduced kidney mass that were maintained on high sodium intake. In dogs infused with ANG II to cause mild hypertension, insulin for 28 days did not potentiate the hypertension. Insulin infusion did, however, cause modest sodium retention during the first few days of infusion. These findings suggest that additional factors besides hyperinsulinemia per se are responsible for obesity-associated hypertension.
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PMID:Does chronic hyperinsulinemia cause hypertension? 292 97

A noninvasive single injection technique for the measurement of glomerular filtration rate (GFR) using technetium99m diethylene triamine pentaacetic acid (DTPA) was developed for use in the rat. GFR measurements obtained by the technique correlated well with those obtained by Cr51 EDTA infusion (R = 0.95, n = 7). The coefficient of variation was 8.4%. GFR was measured over 4 weeks in diabetic and control rats. GFR increased with time in both groups, with no difference between the groups; however, when corrected for body weight, diabetes was associated with an increased GFR (diabetic 13.6 +/- 1.7 vs. control 10.4 +/- 0.1 ml/min/kg p less than 0.001). Insulin treated rats had higher GFRs than untreated diabetics (p less than 0.05), but GFR/kg was reduced to that of nondiabetic controls. High protein intake in diabetic rats caused an increase in GFR after 1 week of diabetes, but this was not sustained by the fourth week. Genetic hypertension and angiotensin converting enzyme (ACE) inhibition with ramipril had no effect on GFR in diabetic rats. We conclude that serial measurement of GFR in the diabetic rat is accurate and reproducible. Genetic hypertension, high protein intake, and ACE inhibition have little effect on GFR in experimental diabetes.
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PMID:Glomerular filtration rate in early experimental diabetes. 296 59


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