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

Patients with essential hypertension have been reported to have higher levels of urinary calcium excretion (UCaV) than normotensive persons. We tested the hypothesis that the calciuria of hypertension is due to dietary factors and evaluated several alternate mechanisms. UCaV was studied in 15 patients with essential hypertension compared with 16 age- and gender-matched normotensive control subjects. For subjects taking self-selected, free-living diets, the difference in UCaV between normotensive (130 +/- 14 mg/day) and hypertensive subjects (201 +/- 37 mg/day) was not significant (p = 0.1). However, in a controlled diet with moderately restricted sodium intake (88 mEq), urinary calcium excretion was significantly higher (p = 0.02) in the hypertensive than in the normotensive group receiving 400 mg calcium (204 +/- 25 vs 132 +/- 13 mg/day) and 1400 mg calcium (272 +/- 31 vs 187 +/- 25 mg/day). Twenty-four-hour UCaV was directly and significantly correlated with blood pressure (r = 0.63 for standing systolic blood pressure; p < 0.001). A 1000 mg oral calcium load caused similar changes in UCaV (0.12 +/- 0.11 vs 0.12 +/- 0.07 mg per 100 ml glomerular filtration) and serum ionized calcium level (0.06 +/- 0.08 vs 0.06 +/- 0.02 mmol/L) in normotensive and hypertensive subjects, respectively, suggesting that there was no difference in intestinal calcium absorption between the groups. Fasting UCaV did not differ between the hypertensive (8.9 +/- 4.5 mg per 2 hours) and normotensive groups (10.9 +/- 11.5 mg per 2 hours).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary calcium excretion in essential hypertension. 140 38

Changes in both calcium and insulin metabolism have been described in essential hypertension. Low levels of plasma ionized calcium (Ca2+) and high levels of insulin have previously been associated with vascular complications and coronary heart disease. In the present study, indices of calcium metabolism and fasting serum insulin were related to electrocardiographic (ECG) variables in 58 patients with untreated hypertension. Fasting insulin was found to be related to heart rate (r = 0.47, P < 0.001), diastolic interval (r = -0.39, P < 0.004) and electrical axis (r = -0.29, P < 0.03) while Ca2+ was found to be correlated with the QRS amplitude (r = -0.32, P < 0.03) and diastolic interval (r = 0.37, P < 0.02). Furthermore, non-ionized serum calcium was correlated with the QRS duration (r = 0.36, P < 0.02), ST-segment interval (r = -0.49, P < 0.002) and QT interval (QoT, r = -0.42, P < 0.008). These correlations were still significant when the influences of age, sex, obesity, blood pressure and heart rate were taken into account in the multiple regression analysis. In conclusion, the present study demonstrates that calcium and insulin metabolism are related to several basic characteristic functions of the heart, such as the systolic and diastolic function, as well as to signs of left ventricular hypertrophy.
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PMID:Fasting insulin, calcium metabolism and the electrocardiogram in hypertensive subjects. 850 22

The authors examined the activity of the antioxidative enzymes superoxide dismutase (SOD) and glutathione peroxidase (GP) in the blood of patients with permanent essential hypertension and hypertensive crises and changes in the activity of these enzymes when monotherapy with the calcium antagonist corinfar was used. A total of 62 patients (age 52.7 +/- 0.7 years) with hypertension and 25 apparently healthy volunteers (age 43.9 +/- 0.7 years) were examined. The activity of SOD and GP was found to be decreased by 33 and 22%, respectively, in patients with permanent hypertension and by 40 and 32%, respectively, during hypertensive crises. When hypertension was treated with corinfar, the activity of COD and GP was increased by 10 and 18%, respectively. Concurrently, these patients had subjective and clinical improvement. The findings suggest that impaired lipid peroxidation makes a great contribution to the pathogenesis of essential hypertension. It can be assumed that the use of antihypertensive agents producing effects on the level of lipid peroxidation products and the enhancements of the activity of antioxidative enzymes.
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PMID:[Changes in the activity of antioxidant enzymes in patients with hypertension]. 140 12

Angiotensin-converting enzyme (ACE) inhibitors and calcium antagonists have, by reason of their potentially favourable pharmacological profile, become increasingly established in the treatment of hypertension in recent years. In a double-blind randomized study with an initial placebo phase, carried out by practising physicians and thus aimed at the "usual" practice patients with essential hypertension, we assessed (1) the antihypertensive effect and tolerability of an ACE inhibitor (ramipril, 5 mg/d) or a calcium antagonist (nitrendipine, 20 mg/d) given in a single daily dose, and (2) a possible age-dependent blood pressure (BP) effect of these therapies. In the 4 weeks' placebo phase, the two treatment groups were comparable as regards average age (49.6 and 49.4 years), age-range (27-67 and 25-64 years) and BP. Fifty-two patients completed the following 6 weeks' phase with active drug therapy. On ramipril (n = 26), the BP measured 24-25 hours after the last drug administration was reduced in the supine position from an average of 155/102 to 142/91 mmHg (mean reduction -10.1%) and in the upright position from 156/106 to 141/96 mmHg (-9.3%). Nitrendipine (n = 26) reduced the average BP from 155/102 to 147/94 mmHg (-6.8%) and from 155/106 to 146/99 mmHg (-6.6%) respectively. BP-lowering effects of both treatments were largely independent of age. Including the patients who discontinued the study prematurely because of side effects (1 on ramipril, 4 on nitrendipine), the "intention to treat analysis" shows BP normalization rates (diastolic < or = 90 mm Hg) of 55% (ramipril) and 30% (nitrendipine) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Monotherapy with the ACE-inhibitor ramipril or the calcium antagonist nitrendipine in essential hypertension]. 141 8

Calcium entry blockers have been shown to exert hemodynamic and diuretic effects in the kidney. The diuretic effects can be demonstrated most clearly in the isolated perfused kidney, not influenced by compensatory mechanisms such as a lower blood pressure or changes of hormones. However, they can also be shown in vivo in humans. We studied the renal effects of calcium entry blockade after the first dosage and after continued oral dosages of 20 mg nicardipine tid in patients with essential hypertension and in normotensive controls. Renal function was determined during maximal free water clearance, allowing estimation of changes in "proximal" and "distal" tubular sodium reabsorption. Results showed a natriuretic effect. In the control subjects, clearance results were compatible with a decrease of proximal and distal tubular reabsorption, but in the hypertensive group natriuresis was mainly achieved by an increase of the glomerular filtration rate and a decrease of fractional distal reabsorption. In both groups the natriuresis occurred concomitantly with a lower blood pressure. The ratio plasma renin activity/plasma aldosterone concentration increased, although nicardipine did not inhibit the increase of plasma aldosterone during angiotensin II infusion. Pre-treatment with the calcium entry blocker nitrendipine enhanced the natriuretic effect of atrial natriuretic factor (ANF) in sodium replete normal volunteers. Facilitation of sodium excretion by human ANF may be an additional diuretic mechanism of calcium entry blockers.
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PMID:The diuretic effect of calcium entry blockade in normals and hypertensive patients. 141 40

Increased blood viscosity has been previously noted in a subgroup of patients with essential hypertension with concomitant high plasma renin activity (PRA). It has been suggested that the cause of hyperviscosity in hypertensives is the presence of circulating red blood cells (RBCs) that were rendered less deformable by significant alterations in their cationic milieu, namely an increase in intracellular concentration of calcium and sodium. The relation between RBC deformability and PRA however is not clear. Our study was conducted to examine this issue. RBC deformability was reduced experimentally, and its effects on renal blood flow, renal artery resistance, glomerular filtration rate and PRA were investigated in experimental (n = 8) and control (n = 4) groups of dogs. Blood was collected from the animals before the experiments and incubated with 0.025% glutaraldehyde. These hardened RBCs were administered to the animals through exchange transfusions. Following the exchange transfusion with the hardened RBCs, there were no changes in renal blood flow, renal artery resistance, and the creatinine clearance. The only change observed was an increase in PRA. In the control group, all parameters that were determined remained unchanged. The data are consistent with the notion that the presence of circulating hardened RBCs may by itself increase PRA, and this effect can be important in some types of hypertension and some other disorders in which impaired deformability of RBCs have been reported.
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PMID:Effect of erythrocyte deformability on renal hemodynamics and plasma renin activity. 141 63

Alterations in intracellular cation metabolism have been implicated in the pathophysiology of essential hypertension. Total magnesium, calcium, sodium and potassium levels were studied in serum erythrocytes and platelets, from 154 subjects (76 hypertensive and 78 normotensives; 104 blacks and 50 whites). In the combined black and white hypertensive group, platelet sodium and calcium and erythrocyte calcium were elevated and serum potassium, serum magnesium and platelet magnesium decreased. In the black hypertensive patients, platelet sodium and calcium and erythrocyte calcium were increased, whereas serum magnesium, serum potassium, platelet magnesium and erythrocyte magnesium were decreased. In the white hypertensive group, platelet sodium and erythrocyte calcium were raised and platelet magnesium was decreased. In the black hypertensive patients, serum and platelet magnesium and serum calcium were negatively and erythrocyte and platelet calcium positively correlated with mean arterial pressure. In the white hypertensive patients platelet sodium was directly related to mean arterial pressure. These results suggest that intracellular sodium and calcium overload and magnesium depletion may be important in the pathophysiology of hypertension. Magnesium disturbances are more consistent and widespread in black hypertensive patients than in white hypertensive patients.
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PMID:Intracellular Mg2+, Ca2+, Na2+ and K+ in platelets and erythrocytes of essential hypertension patients: relation to blood pressure. 142 23

Essential hypertension has been associated with disturbed calcium metabolism, but the available data are controversial. We measured parameters of calcium metabolism in groups of untreated male subjects (n = 78) with elevated diastolic blood pressure (101 +/- 6 mmHg, mean +/- SD) and age-matched male subjects (n = 79) with low diastolic blood pressure (62 +/- 4 mmHg). The participants of the study were drawn from a random population sample. Subjects with high diastolic blood pressure had significantly higher carboxy-terminal parathyroid hormone (PTH) plasma concentrations than controls with low diastolic blood pressure (median 114 vs. 43 pmol/l, P less than 0.01). The 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D concentrations were comparable in both groups. Individuals with high diastolic blood pressure had significantly lower total serum calcium (2.41 +/- 0.10 vs. 2.47 +/- 0.10 mmol/l, mean +/- SD; P less than 0.01). PTH concentrations were correlated with diastolic pressure (r = -0.39, P less than 0.001). The data are compatible with increased parathyroid activity despite unchanged concentrations of vitamin D metabolites in human hypertension.
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PMID:Disturbed calcium metabolism in subjects with elevated diastolic blood pressure. 848 30

The clinical linkage of hypertensive cardiovascular disease, left ventricular hypertrophy, and accelerated atherosclerosis with a spectrum of metabolic disturbances including peripheral insulin resistance, hyperinsulinemia, obesity, and frank non-insulin dependent diabetes mellitus, has been increasingly appreciated. However, the underlying biologic basis mediating this clinical association remains unclear. Nuclear magnetic resonance techniques have been used to measure various intracellular ion species in human erythrocytes and have found that common, shared intracellular abnormalities of cytosolic free calcium, free magnesium, and pH occur in each of these clinical syndromes. Specifically, essential hypertension is characterized by higher fasting free cytosolic calcium concentrations and reciprocally lower intracellular free magnesium and pH levels compared with those of normotensive control subjects. Furthermore, for all subjects, free calcium and free magnesium levels were closely related both to the left ventricular mass and to the degree of insulin resistance present. Moreover, these same intracellular ionic lesions were found in normotensive obese and/or non-insulin diabetic individuals. Last, evidence has recently been provided that the cardiovascular consequences of increased dietary sugar and salt intake may well be determined by their concurrent influence on cellular ion metabolism. These data led to a hypothesis for a central role for altered cellular ion homeostasis in mediating the clinical linkage of cardiovascular and metabolic disease. According to this ionic hypothesis, essential hypertension, non-insulin dependent diabetes, and their frequently associated features of obesity, left ventricular hypertrophy, and accelerated atherosclerosis all derive from and reflect different clinical manifestations of the same underlying cellular lesion, characterized at least in part by elevated cytosolic free calcium and suppressed free magnesium levels.
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PMID:Cellular ions in hypertension, insulin resistance, obesity, and diabetes: a unifying theme. 145 64

The efficacy and tolerability of nicardipine retard and captopril were assessed in 174 over-60-year-olds suffering from slight or moderate essential hypertension. After 2-3 weeks of wash out the patients were randomly assigned to calcium antagonist (40 mg twice a day) or ace-inhibitor (25 mg twice a day) treatment which continued for 180 days. Monotherapy was combined with hydrochlorothiazide (12.5 mg/day) after 2 months in the event of an unsatisfactory reduction of arterial pressure in relation to basal values. Systolic and diastolic blood pressure was measured (1st and 5th Korotkoff's tone) at monthly intervals while lying and standing; heart rate was also measured using a palpatory method. Both nicardipine retard (no. 86) and captopril (no. 88) caused a significant reduction of clino- and orthostatic systolic and diastolic arterial pressure during the first two months of treatment. Respectively 70% and 51% of patients responded to treatment and the blood pressure reductions achieved using monotherapy remained unchanged during the course of the study. The association of hydrochlorothiazide resulted in a significant decrease in arterial pressure in non-responders, an effect which was observed with both nicardipine retard and captopril. No significant variation in heart rate was recorded between the two groups. Twenty-one patients in the nicardipine retard group and 16 in the captopril group suffered from slight to moderate side effects. Six patients dropped out of the nicardipine retard group and 15 patients out of the captopril group, an event for which side-effects were responsible in 1 and 3 cases respectively. In conclusion, nicardipine retard and captopril represent an efficacious form of treatment for geriatric hypertension and possess a satisfactory level of tolerability.
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PMID:[Efficacy and tolerability of nicardipine retard and captopril in hypertension in the aged. Results of a multicenter study]. 146 44


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