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

Serum lipids, lipoproteins, and major apolipoproteins and their association with previous myocardial infarction were studied in patients with non-insulin-dependent diabetes mellitus (NIDDM) and nondiabetic subjects in East and West Finland in 1982-1984. NIDDM patients had higher age-adjusted serum triglyceride and apolipoprotein B levels and a higher apolipoprotein B/apolipoprotein A-I ratio, lower serum high density lipoprotein (HDL) cholesterol and apolipoprotein A-1 levels, and a lower HDL cholesterol/apolipoprotein A-1 ratio than nondiabetic subjects. With a few exceptions, these differences persisted after adjustment for body mass index, alcohol intake, physical activity, smoking, and hypertension, which suggests that the atherogenic serum lipoprotein pattern in NIDDM is an inherent feature of the disease. In general, the association of serum lipids, lipoproteins, and apolipoproteins with myocardial infarction was similar in nondiabetic subjects and NIDDM patients, although it was somewhat stronger in the diabetic subjects. A low serum HDL cholesterol/apolipoprotein A-1 ratio, which was closely linked to high serum triglyceride level, seemed to be more consistently related to myocardial infarction in NIDDM patients than in nondiabetic subjects. Serum lipids, lipoproteins, and apolipoproteins, either separately or in various combinations, could only to a small extent explain the higher prevalence of myocardial infarction in diabetic subjects compared with nondiabetic subjects when tested in multivariate analysis with other cardiovascular risk factors as background variables. The association between serum lipoproteins and myocardial infarction was largely similar in East and West Finland, two areas that differ markedly with respect to the occurrence of coronary heart disease.
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PMID:Serum lipids, lipoproteins, and apolipoproteins and the excessive occurrence of coronary heart disease in non-insulin-dependent diabetic patients. 277 12

Plasma lipid, lipoprotein, and apoprotein concentrations were measured in 169 patients with non-insulin-dependent diabetes mellitus (NIDDM), 78 with normal blood pressure, and 91 diagnosed and receiving drug treatment for hypertension. Plasma triglyceride, cholesterol, low-density lipoprotein-cholesterol, and apoprotein B concentrations were significantly higher (p = less than 0.05 to less than 0.001) in the hypertensive group. In addition, the ratios of high-density to low-density lipoprotein-cholesterol and of apoprotein A-1 to apoprotein B were significantly reduced (p less than 0.01) in patients with hypertension. The changes noted were independent of differences in sex distribution, degree of obesity, and level of glycemic control. These results indicate that substantial differences in plasma lipid, lipoprotein, and apoprotein concentrations are seen when normotensive patients with NIDDM are compared with patients who are also being treated for hypertension, and that all of the changes noted would increase the risk of coronary artery disease in the hypertensive group. Since all patients with hypertension were receiving anti-hypertensive medications, it is not clear if it is hypertension per se, or its treatment, that is responsible for the observed changes in lipid metabolism.
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PMID:Abnormal lipid metabolism in treated hypertensive patients with non-insulin-dependent diabetes mellitus. 336 49

Diuretic therapy is frequently accompanied by undesirable biochemical changes and side-effects. Two multicenter trials compared the effects of captopril combined with a diuretic to the administration of either agent alone in mild-to-moderate hypertensives. In addition to blood pressure, effects on serum potassium, uric acid, glucose, and cholesterol were examined. The first study (Study A) was conducted on 210 such patients randomly assigned to receive: 1) hydrochlorothiazide (H) 15 mg three times daily (t.i.d.); 2) captopril (C) 25 mg t.i.d.; or 3) C + H for 6 weeks. The second study (Study B) involved 415 patients randomly assigned to receive: 1) C 25 mg twice daily (b.i.d.) + H 25 mg b.i.d.; 2) C 50 mg b.i.d. + H 25 mg b.i.d.; 3) C 50 mg b.i.d. + placebo b.i.d.; 4) placebo b.i.d. + H 25 mg b.i.d.; or 5) placebo b.i.d. + placebo b.i.d. for 6 weeks. In both Studies A and B, all patients except those receiving placebo only (Study B-5) had significant (p less than 0.05) blood pressure reductions. In Study A, the combination of C + H (A-3) produced a significantly greater (p less than 0.001) reduction in blood pressure than either agent alone. In Study B, both C + H groups (B-1, B-2) had a significantly greater (p less than 0.01) blood pressure reduction than that seen with C alone (B-3). In Study A, those treated with H alone (A-1) had a significant (p less than 0.05) reduction in serum potassium and increases in uric acid, glucose, and cholesterol when compared to C alone (A-2) where no changes in these parameters were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Influence of an angiotensin converting-enzyme inhibitor on diuretic-induced metabolic effects in hypertension. 631 23

Glomeruli were isolated from rat kidneys using a passive sieving technique to study the mechanisms of basal and beta-adrenergic stimulated renin release. Glomeruli were enclosed within glass chambers and continuously superfused with Krebs media, or modified Krebs as described below, at a rate of 0.3 ml/min. The chamber effluent was collected in 10-minute fractions and measured for renin concentration (ng angiotensin I (A-1 generated) by radioimmunoassay. Basal renin was approximately 3 ng AI/ml/hr. Beta-adrenergic stimulation with isoproterenol (ISO), 178 micron M, increased renin concentration threefold (11 +/- 2 ng AI). The beta-blocker propranolol at 12 micron M halved ISO-stimulated renin, and at 120 micron M eliminated it. Doubling Krebs sodium concentration (280 mM) had no effect upon basal or ISO-stimulated renin release. Pretreating rast with DOCA and a high salt diet significantly reduced basal and abolished ISO-stimulated renin release. Increasing Krebs calcium (10 mM) did not affect basal but abolished ISO-stimulated renin release. Calcium-free Krebs had no significant effects. Increasing Krebs potassium (50 mM) increased basal renin fourfold (14 ng AI) while the absolute increase from basal due to ISO remained the same (23 ng AI). These results suggest that basal renin and ISO-stimulated renin are released via different mechanisms.
Hypertension
PMID:Control of renin release in isolated rat glomeruli. 702 20

Apolipoproteins A-1 and B concentration were measured in 201 Indian patients (32 females; 169 males) undergoing elective diagnostic coronary arteriography in order to assess the predictive power of apolipoproteins as a 'marker' of coronary artery disease (CAD). This association was also compared to that of other traditional risk factors: age, hypertension, diabetes, family history, smoking and plasma levels of total cholesterol, triglycerides, low and high density lipoproteins. The apolipoprotein (Apo) A-1 levels averaged 82.9 +/- 18.9 mg/dl in the normal coronary group (n = 43) and 76.0 +/- 18.1 mg/dl in the group with coronary artery disease (n = 158). The average Apo B levels in the normal coronary group and coronary artery disease group were 67.8 +/- 17.7 mg/dl and 78.9 +/- 19.5 mg/dl, respectively. Overall Apo B and triglyceride levels (of all lipid measures) showed larger univariate difference between the normal group (no coronary artery disease) and the group with coronary artery disease. The variable with strongest predictive power for coronary artery disease was the ratio of Apo A-1 to Apo B. These findings were confirmed using multiple logistic regression analysis adjusting for age and other traditional risk factors. Our results indicate that the measurement of apolipoproteins A-1 and B provide a better marker for predicting the presence of coronary artery disease as compared to traditional lipid measures. Overall the levels of these apolipoproteins seem to be lower in Indian population as compared to those reported from the West.
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PMID:Plasma levels of apolipoproteins A-1 and B in Indian patients with angiographically defined coronary artery disease. 781 63

The prevalence and clinical characteristics of hyperapobetalipoproteinemia (hyperapoB) and other phenotypes of dyslipoproteinemia were examined in 99 men (aged < or = 50 years) and 104 women (< or = 60 years) undergoing elective diagnostic coronary arteriography. HyperapoB was the most common phenotype (34%) associated with premature coronary artery disease (CAD). Only 20.2% of patients with CAD had a normal lipoprotein phenotype. The significant odds ratios for CAD were as follows: hypertriglyceridemic hyperapoB 17.45 (p < 0.0001), type IV 6.54 (p = 0.0001), type IIa 4.73 (p = 0.008), normotriglyceridemic hyperapoB 2.54 (p = 0.03) and type IIb 8.73 (p = 0.05). The strong association of hypertriglyceridemic hyperapoB with CAD reflected the multiplicative effect of increased low-density lipoprotein apolipoprotein B and endogenous hypertriglyceridemia, and was independent of the effects of age, sex, diabetes mellitus, systemic hypertension, body mass index and cigarette smoking. The ratio of apolipoprotein B to A-1 was better than those of low-density to high-density lipoprotein cholesterol and total to high-density lipoprotein cholesterol at discriminating dyslipidemic phenotypes from normal. Obesity was increased approximately 1.5 to two-fold in the hypertriglyceridemic phenotypes, diabetes was more prevalent in hypertriglyceridemic hyperapoB (6.8-fold; p < 0.001) and type IV (4.4-fold; p = 0.02), and hypertension was increased 1.5- to twofold in most dyslipidemic groups. The data indicate that hyperapoB and endogenous hypertriglyceridemia both contribute to the risk of premature CAD.
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PMID:Prevalence of hyperapobetalipoproteinemia and other lipoprotein phenotypes in men (aged < or = 50 years) and women (< or = 60 years) with coronary artery disease. 844 57

Tyrosine kinases have been implicated in vascular smooth muscle cell proliferation and contraction. Underlying mechanisms may involve C(a2+) -dependent pathways. This study assesses relationships between angiotensin II (Ang II)-stimulated phospholipase C-mediated Ca2+ transients and tyrosine kinase-dependent pathways in vascular smooth muscle cells. Intracellular free Ca2+ concentration ([Ca2+]i) was measured in primary cultured unpassaged vascular smooth muscle cells derived from mesenteric resistance vessels of Wistar-Kyoto rats with the use of fura 2 methodology. [Ca2+]i effects of Ang II (1 nmol/L) were determined in vascular smooth muscle cells in which tyrosine kinase pathways were stimulated by insulin (70 muU/mL; 0.5 nmol/L), insulin-like growth factor-I (1 ng/mL; 0.13 nmol/L), or platelet-derived growth factor-BB (1 ng/mL; 0.04 nmol/L) and in cells in which tyrosine kinase was inhibited by specific inhibitors (1 mumol/L tyrphostin A-23 and genistein). Ang II elicited a rapid and transient [Ca2+]i response (from 94 +/- 8 to 239 +/- 5.8 nmol/L). Activation of the receptor tyrosine kinase by insulin, platelet-derived growth factor, and insulin-like growth factor-I significantly reduced (P < .01) Ang II-induced [Ca2+]i to 161 +/- 7, 189 +/- 3.7, and 183 +/- 5 nmol/L, respectively. In the presence of tyrphostin A-23 and genistein, Ang II-stimulated [Ca2+]i remained persistently elevated and failed to return to basal levels. Tyrphostin A-1, the inactive tyrphostin analogue, had not significant effect on Ang II-induced [Ca2+]i. This study demonstrates that activation of tyrosine kinase pathways reduces Ang II-elicited [Ca2+]i responses, whereas tyrosine kinase inhibition prevents [Ca2+]i recovery after agonist stimulation. Interaction between tyrosine kinase- and phospholipase C-dependent signaling pathways modulates vascular smooth muscle cell [Ca2+]i responses to Ang II.
Hypertension 1996 May
PMID:Tyrosine kinase signaling pathways modulate angiotensin II-induced calcium ([Ca2+]i) transients in vascular smooth muscle cells. 862 Dec 2

We examined whether the levels of fibrinogen are elevated in the offspring of middle-aged coronary patients. One hundred and seventy-six young subjects were divided into two groups. Group A consisted of 100 children and youngsters (mean age 17 +/- 6 years) whose fathers had sustained a myocardial infarction under the age 55 years without associated history of diabetes mellitus or hypertension. Seventy-six healthy young subjects (mean age 18 +/- 5 years) matched for gender, dietary and smoking habits without familial history of coronary artery disease, diabetes mellitus or hypertension served as the control group (group B). Fibrinogen, total cholesterol, triglycerides, high and low density lipoprotein cholesterol, apolipoprotein A-1, apolipoprotein B and lipoprotein (a) were measured. Sons and daughters with a history of premature paternal myocardial infarction had higher levels of fibrinogen compared with control subjects (304.1 +/- 60 vs 274 +/- 53 mg. dl-1, P < 0.001). This difference was maintained when the above groups were divided into single sex groups. Total cholesterol, low density lipoprotein cholesterol, apolipoprotein B and lipoprotein (a) were also significantly higher in group A. Children of affected individuals who had a good lipid profile also had significantly higher fibrinogen levels compared to control group. The results support the hypothesis that the higher plasma levels of fibrinogen in the offspring of middle-aged coronary men could partially explain their predisposition for coronary artery disease. Since the levels of fibrinogen have a major genetic component, they could be a useful marker in identifying children at high risk for coronary artery disease, especially among those with no lipid abnormalities.
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PMID:Fibrinogen in the offspring of men with premature coronary artery disease. 868 12

The purpose of the study was to examine the contribution of alterations in lipoprotein metabolism to the progression of very-low-level albuminuria in insulin-dependent diabetes mellitus (IDDM). We measured serum concentrations of lipids, lipoproteins, and apolipoproteins in 53 normoalbuminuric diabetic patients without overt hypertension, whom we restudied after 10 years. Albuminuria was measured as the urinary albumin to creatinine ratio (UA/UC) in repeated early-morning samples. Over 10 years, UA/UC increased significantly (P < .001), and five patients (9.4%) progressed to microalbuminuria. The increase in albuminuria was significantly and positively related to the baseline serum concentrations of total cholesterol (P < .05), low-density lipoprotein (LDL) cholesterol (P = .05), non-high-density lipoprotein (HDL) cholesterol (P < .05), and apolipoprotein (apo) B (P < .001), but no significant associations were found with triglycerides, HDL cholesterol, apo A-1, or lipoprotein(a) [Lp(a)]. The relative risk of developing microalbuminuria for a serum apo B concentration more than 1.1 g/L was 3.8 (95% confidence interval [CI], 1.9 to 7.7). In multiple linear regression analysis, serum apo B (P < .05) and glycated hemoglobin ([HbA] P < .05) at baseline were significant independent predictors of the increase in albuminuria, with no significant associations found for sex, smoking, duration of diabetes, mean arterial blood pressure (BP), or family history of cardiovascular disease and hypertension; the regression model predicted 42% of the variation in UA/UC at 10 years. The findings suggest that an abnormality in the metabolism of apo B may be independently associated with progression of very-low-level albuminuria and possibly with the development of early nephropathy in IDDM patients.
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PMID:Apolipoprotein B independently predicts progression of very-low-level albuminuria in insulin-dependent diabetes mellitus. 878 Dec 97

Angiotensin II (Ang II), a potent vasoactive peptide with mitogenic potential, influences vascular smooth muscle cell contraction and growth through receptor-linked pathways that increase intracellular free Ca2+ concentration ([Ca2+]i) and pH (pHi). Activation of these second messengers by Ang II may involve tyrosine kinase-dependent signaling pathways. This study determined the role of tyrosine kinases in Ang II-stimulated pHi, and in simultaneously measured contractile and [Ca2+]i responses, as well as growth in cultured vascular smooth muscle cells from mesenteric arteries of Wistar-Kyoto rats. pHi was determined by fluorescent digital imaging using 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl ester (BCECF-AM). Vascular smooth muscle cell [Ca2+]i and contractile responses were assessed simultaneously by fura 2 methodology and by photomicroscopy in cells grown on rat tail collagen gels. Cell growth was determined by DNA and protein synthesis as measured by [3H]thymidine and [3H]leucine incorporation, respectively. The Ang II receptor subtypes (AT1 or AT2) through which Ang II mediates effects were assessed with [Sar1,Ile8]Ang II (a nonselective subtype antagonist), losartan (a selective AT1 antagonist), and PD 123319 (a selective AT2 antagonist). To determine whether tyrosine kinases influence Ang II-stimulated responses, cells were pretreated with 10(-5) mol/L tyrphostin A-23 (a specific tyrosine kinase inhibitor). Ang II increased pHi in a dose-dependent manner (pD2, 9.2+/-0.2) and significantly increased vascular smooth muscle cell contraction (30%) and [Ca2+]i (pD2, 7.4+/-0.1). Ang II (10(-7) mol/L) increased DNA ([3H]thymidine incorporation) and protein synthesis ([3H]leucine incorporation). [Sar1,Ile8]Ang II and losartan but not PD 123319 abolished Ang II-elicited responses. Tyrphostin A-23 significantly attenuated Ang II-stimulated pHi responses; it also inhibited [Ca2+]i and contractile responses and cell growth. The inactive analogue tyrphostin A-1 did not alter Ang II-stimulated actions. These results provide novel evidence for a role of tyrosine kinases in Ang II-mediated pHi responses in vascular smooth muscle cells and indicate that tyrosine kinases participate in the regulation of signal transduction associated with AT1 receptor subtype-mediated contraction and growth.
Hypertension 1997 Aug
PMID:Angiotensin II regulates vascular smooth muscle cell pH, contraction, and growth via tyrosine kinase-dependent signaling pathways. 926 Sep 84


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