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Query: UMLS:C0020538 (
hypertension
)
170,190
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A recent study has shown that young, lean, hypertensive subjects are more insulin resistant than corresponding normotensive subjects. Whether this finding can also be demonstrated in the presence of non-insulin-dependent diabetes mellitus (NIDDM) is not known. Therefore, the degree of insulin resistance was studied in 26 middle-aged hypertensive patients with NIDDM (11 men, 15 women) and 14 normotensive patients with NIDDM (eight men, six women) matched for age, metabolic control and the duration of diabetes, utilizing the glucose clamp technique. Non-obese
NIDD
patients (body mass index less than 27.0 kg m-2) with
hypertension
(n = 11) had significantly lower glucose disposal rates (GDRs) during the last 60 min of euglycaemic (5.5 mmol l-1) and hyperinsulinaemic (approximately 600 pmol l-1) clamp studies than
NIDD
patients without
hypertension
(n = 6) (782 +/- 94 vs. 1418 +/- 97 mumol m-2 min-1, P less than 0.05). In contrast, GDRs were similar in obese
NIDD
patients with (n = 15) and without (n = 8)
hypertension
(802 +/- 90 vs. 849 +/- 90 mumol m-2/min-1, respectively, P = NS). Basal hepatic glucose output, suppression of hepatic glucose production during hyperinsulinaemia and insulin secretion capacity did not differ between hypertensive and normotensive subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Essential hypertension and insulin resistance in non-insulin-dependent diabetes. 251 72
Urinary albumin, measured by radioimmunoassay, was evaluated as a method to assess early renal impairment in 76 insulin (IDD) and 36 noninsulin (
NIDD
)-dependent diabetic patients. Mean albumin excretion in IDD and
NIDD
patients was significantly higher at 23 and 12 micrograms/100 ml glomerular filtrate (GF) respectively, compared to 4 micrograms/100 ml GF in normal subjects (P less than 0.001 and P less than 0.05). Abnormal albumin excretion from 20 to 200 micrograms/100 ml GF was observed in 30% of IDD patients (P less than 0.001) and 15% of
NIDD
patients (P less than 0.03). Albumin excretion was significantly increased in hypertensive IDD and
NIDD
patients. Significant correlations between albumin excretion and age, duration of diabetes and creatinine clearance were observed, but albumin excretion did not correlate with hemoglobin A1C. These data indicate that (1) 30% of IDD patients not clinically recognized as having renal impairment have abnormal albumin excretion, (2) albumin excretion may reflect renal impairment, since albumin excretion levels independently correlate with duration of diabetes and
hypertension
in both diabetic subgroups and to glomerular function in
NIDD
patients, and (3) measurement of urinary albumin by radioimmunoassay may be the most sensitive test to evaluate early renal disease in diabetes.
...
PMID:The interrelationships of radioimmunoassayable urinary albumin, renal function and diabetes. 372 Apr 98
49 diabetics (D) (26 IDD and 23
NIDD
) were compared to 32 controls (C). Absence of ischemic cardiopathy (IC) was confirmed by routine investigations and noninvasive cardiovascular techniques, including an exercise ECG using 12 leads and a thallium 201 scintigraphy. Our results show: a) a prolonged mean isovolumetric relaxation time (IVRT) as studied by the M mode echocardiography and phonomechanography: D = 0,10 sec +/- 0,04; C = 0,05 sec +/- 0,02; p less than 0,0001; b) a reduced mean EF slope: D = 97,48 +/- 37,08 mm / sec; C = 125,68 +/- 34,35; p less than 0,005; c) a high mean Weissler index (ratio of PEP to LVET): D = 40 +/- 0,08; C = 33 +/- 0,05; p less than 0,01. IVRT and EF slope abnormalities are related to increased myocardial stiffness and impaired LV compliance. In the absence of changes in preload and afterload, the high Weissler index reflects impaired contractility of the myocardium. These abnormalities are related neither to the duration of diabetes nor to the presence or severity of the complications. With the M mode echocardiography, mean diastolic and systolic thickness of the septum is greater in D with retinopathy than in C (p less than 0,005 and p less than 0,03 respectively); mean diastolic and systolic thickness of the posterior wall is greater in
NIDD
than in C (p less than 0,001 and p less than 0,025). We conclude that there is evidence of left ventricular functional abnormalities specific to diabetes and unrelated to IC and
hypertension
. Our findings support the hypothesis that they may be due to metabolic disorders and/or myocardial microangiopathy.
...
PMID:[Existence of asymptomatic changes in left ventricular function in the diabetic. Noninvasive study]. 400 44
In Seattle, Washington, the prevalence of diabetes was 20% in second-generation (Nisei) Japanese-American men and 16% in Nisei women 45-74 years old, while the prevalence of impaired glucose tolerance (IGT) was 36% in Nisei men and 40% in Nisei women. Hyperglycemia was less and duration of diabetes shorter in women. Related to diabetes and IGT in Nisei were higher fasting plasma insulin levels and central (visceral) adiposity. Prevalence of diabetes was low among the younger (34-53 years old) third-generation (Sansei) men and women. Among self-reported non-diabetic Sansei, however, prevalence of IGT was 19% in men and 29% in women, and IGT was associated with both increased fasting plasma insulin levels and more visceral fat, suggesting that many Sansei are at risk of future diabetes. An important lifestyle factor in the development of
NIDD
in Japanese Americans appeared to be dietary saturated (animal) fat. Another factor may be physical inactivity. In Japanese-American women, menopause also appeared to be an important risk factor. These risk factors may be related to fostering the accumulation of visceral fat and the development of insulin resistance. Five-year follow-up examinations performed in non-diabetic Nisei men and women have yielded additional information concerning the prognosis of IGT. Of those women who were IGT at baseline, 34% were diabetic at follow-up while 17% returned to normal. In men who had been IGT at baseline, 18% were diabetic at follow-up while 36% returned to normal. Over the 5-yr follow-up interval, proportionally more women progressed from normal to IGT (54%) then went from IGT to normal (17%). For men, roughly equal proportions went from normal to IGT (37%) as from IGT to normal (36%). It would therefore appear that greater proportions of Nisei women are progressing to IGT and to
NIDD
than are Nisei men. This observation may be related to the increased risk of developing central obesity and insulin resistance following menopause. Prevalence of cardiovascular disease (
hypertension
, peripheral vascular disease, and/or coronary heart disease) was increased in Japanese Americans with IGT and
NIDD
. Neuropathy and retinopathy were associated only with
NIDD
.
...
PMID:Diabetes and diabetes risk factors in second- and third-generation Japanese Americans in Seattle, Washington. 785 32
The objective of this study was to determine the prevalence of
hypertension
in diabetic patients in an urban Sudanese population compared with a non-diabetic group. It was found that there was a higher prevalence of diastolic hypertension (44%) in the non-insulin-dependent (NIDM) patients. The blood pressures did not correlate with age, duration of diabetes or nephropathy (9% of cases), but obesity which was detected in 34% of the
NIDD
group may possibly explain the high prevalence of
hypertension
.
...
PMID:Pattern of blood pressure in African diabetics: report from Sudan. 858 69
In the present study we investigated the effect of a selective alpha 1-adrenergic blocker (doxazosin), an angiotensin-converting enzyme (ACE) inhibitor (captopril), and a calcium channel antagonist (nifedipine) on renal function in hypertensive non-insulin-dependent diabetic patients. 30
NIDD
hypertensive patients (age = 50 +/- 3 years; BMI = 30 +/- 1 kg/m2) (mean +/- SEM) were studied before and after a 12-week period of antihypertensive treatment. Ten patients were treated with doxazosin (Cardura) (2-8 mg once daily or 8 mg b.i.d.), 9 with captopril (Capoten) (25-50 mg b.i.d.), and 11 with nifedipine (Procardia-XL) (30-60 mg once daily). Blood pressure, creatinine clearance, 24-hour urinary protein excretion, fasting plasma glucose concentration and glycosylated hemoglobin were measured before and after drug treatment. Fasting plasma glucose and glycosylated hemoglobin (HbA1c) were similar in all three groups prior to the start of antihypertensive therapy and did not change significantly from baseline in any treatment groups. In the doxazosin group creatinine clearance rose from 99 +/- 8 to 122 +/- 8 ml/1.73 m2.min (p < 0.01), while 24-hour urinary protein excretion declined from 2.66 +/- 0.05 to 1.76 +/- 0.02 mg/day/ml/1.73 m2.min (p < 0.01). In diabetics treated with captopril creatinine clearance rose from 93 +/- 6 to 109 +/- 9 ml/1.73 m2.min (p < 0.05), while the 24-hour urinary protein excretion fell from 2.70 +/- 0.05 to 2.03 +/- 0.04 mg/day/ml/1.73 m2.min (p < 0.05). In patients treated with nifedipine creatinine clearance did not change (97 +/- 6 vs. 94 +/- 7 ml/1.73 m2.min), while 24-hour urinary protein excretion decreased from 2.84 +/- 0.04 to 1.95 +/- 0.03 mg/day/ml/1.73 m2.min. Systolic and diastolic blood pressure were similar in doxazosin (150 +/- 3/95 +/- 2 mm Hg), captopril (153 +/- 3/93 +/- 1), and nifedipine (155 +/- 4/93 +/- 1) groups prior to the start of antihypertensive therapy and declined to 143 +/- 3/84 +/- 3 (doxazosin), 139 +/- 3/82 +/- 3 (captopril), and 141 +/- 3/84 +/- 1 (nifedipine) mm Hg (all p < 0.01 vs. pretreatment). In summary, both doxazosin and captopril treatment were associated with significant rises in GFR, while all three antihypertensive agents caused a significant decline in proteinuria. These results indicate that alpha-adrenergic blockers, ACE inhibitors, and calcium channel antagonists can safely and effectively be used in the clinical management of non-insulin-dependent diabetic patients with
hypertension
.
...
PMID:Effect of alpha-adrenergic blockers, ACE inhibitors, and calcium channel antagonists on renal function in hypertensive non-insulin-dependent diabetic patients. 885 95
Insulin resistance appears to be a causative mechanism for the development of essential hypertension. Insulin resistance syndrome consists of a cluster of abnormalities that aggravate preexisting tendencies to develop
hypertension
, resulting in a cascade of physiologic alterations and ultimately leading to increased rates of heart attack, stroke, and peripheral vascular disease. Like
hypertension
,
NIDD
is mediated by insulin resistance and is expressed in individuals with limited beta-cell reserve. Episodes of increased insulin resistance, such as aging, weight gain, and pregnancy, cannot be compensated for in these states, and glucose intolerance results. In the case of pregnancy, the temporary state of insulin resistance unmasks individuals with an early beta-cell defect and allows for identification of high-risk groups at a time when therapeutic interventions could result in primary prevention of disease. Evidence is beginning to accumulate that preeclampsia is at least partially mediated by insulin resistance as well, and that individuals with preeclampsia may have clinically silent but persistent alterations in insulin resistance. If this condition proves a corollary to gestational diabetes, there may be an opportunity to intervene for primary prevention of some forms of essential hypertension as well. The availability of new pharmacologic agents to enhance insulin sensitivity represents a true opportunity effectively to prevent the long-term complications associated with insulin resistance and hyperinsulinemia. To achieve this goal, early and accurate identification of populations at risk is essential. A complete understanding of the role of insulin resistance in the generation of preeclampsia will aid significantly in the discovery of the genetic polymorphisms and intracellular pathways by which insulin resistance is translated into cardiovascular disease, stroke, and nephropathy.
...
PMID:Insulin resistance and preeclampsia. 989 20