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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

White blood cell (WBC) Na+ and K+ concentrations, plasma (Na+ + K+)ATPase inhibition and blood pressure were determined in normotensive control subjects and patients with essential hypertension. While the untreated hypertensive group had significantly lower WBC K+ concentrations than the normotensive group (mean +/- SEM, 121.6 +/- 4.4 vs. 134.7 +/- 2.8 mEq/kg, p less than 0.05), no significant difference was observed in WBC Na+ concentrations between the 2 groups. The mean of plasma (Na+ + K+)-ATPase inhibition in untreated hypertensive patients was higher than that in normotensive controls (14.8 +/- 1.7 vs. 7.2 +/- 1.8%, p less than 0.05). The correlations between (Na+ + K+)ATPase inhibition and mean blood pressure and between WBC Na+/K+ ratio and mean blood pressure were significant (r = 0.278, p less than 0.05 and 0.270, p less than 0.05, respectively), but both were weak. However, untreated hypertensive patients with higher (Na+ + K+)ATPase inhibition had significantly higher WBC Na+/K+ ratios than untreated patients with less (Na+ + K+)ATPase inhibition. These results suggest a contribution of plasma (Na+ + K+)ATPase inhibition in the production of high blood pressure in a subset of patients with essential hypertension, which results in altered intracellular K+ concentrations.
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PMID:(Na+ + K+) ATPase inhibitors and intracellular electrolytes in essential hypertension. 282 6

In nine young normotensive subjects with no family history of hypertension and nine age-matched normotensive subjects with one parent with essential hypertension, effective renal plasma flow (p-aminohippuric acid clearance), glomerular filtration rate (inulin clearance), and excretion of sodium and exogenously administered lithium were measured for 90 minutes before and after administration of a single 20-mg oral dose of the calcium entry blocker nifedipine. Segmental tubular handling of fluid and sodium was estimated using lithium clearance as a marker of proximal tubular reabsorption. Nifedipine did not cause any change in subjects with no family history of hypertension, but in those with one hypertensive parent there was a marked increase in effective renal plasma flow (from 644 +/- 39 to 847 +/- 42 [SEM] ml/min x 1.73 m2; p less than 0.001) and a decrease in filtration fraction (from 17.6 +/- 1.0 to 12.6 +/- 0.4%; p less than 0.001), while the glomerular filtration rate was unchanged, thus suggesting a prevailing efferent vasodilation. Sodium excretion rate (p less than 0.02) and fractional sodium excretion (p less than 0.025) increased slightly but significantly in subjects with one hypertensive parent, but not in normotensive subjects with no family history of hypertension. Lithium clearance also rose (from 29.0 +/- 2.0 to 32.8 +/- 1.9 ml/min, p less than 0.001), and the derived value of fractional proximal reabsorption diminished (from 75.8 +/- 1.0 to 71.3 +/- 1.2%, p less than 0.001). Estimated distal delivery of sodium and absolute distal sodium reabsorption both increased significantly (p less than 0.005), while fractional distal sodium reabsorption was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormal renal responses to calcium entry blockade in normotensive offspring of hypertensive parents. 284 83

The effects of selective alpha 1-adrenergic blockade with terazosin on blood pressure and cardiovascular pressor responsiveness were assessed in 17 subjects with mild to moderate essential hypertension (mean age, 48 +/- 2 [SEM] years). As compared with a 2-week placebo period, 8 weeks of terazosin treatment (mean dose, 10.5 +/- 1.7 mg/day) caused a fall of supine (from 153/103 +/- 3/2 to 143/96 +/- 4/2 mm Hg; p less than 0.025) and upright (from 145/106 +/- 4/2 to 131/94 +/- 5/3 mm Hg; p less than 0.01) arterial pressure; a marked blunting of cardiovascular pressor responsiveness to norepinephrine, as judged from the pressor dose (from 73 +/- 9 to 2156 +/- 496 ng/kg/min; p less than 0.02) and from the rightward shift (p less than 0.01) of the plasma concentration-blood pressure response curve; and a slight increase in plasma norepinephrine concentration (from 37.7 +/- 3.3 to 52.2 +/- 7.8 ng/dl; p less than 0.01). Heart rate, body weight, exchangeable sodium, blood volume, and norepinephrine plasma clearance; plasma epinephrine, renin, angiotensin II, and aldosterone levels; the relationships between angiotensin II-induced increases in arterial pressure or plasma aldosterone and the concomitant increments of plasma angiotensin II; and heart rate responsiveness to isoproterenol did not change significantly after terazosin treatment. These findings suggest that the fall of arterial pressure induced by selective alpha 1-adrenergic blockade in subjects with essential hypertension is associated with, and probably explained by, inhibition of alpha 1-mediated, noradrenergic-dependent vasoconstriction. alpha 1-Adrenergic receptor antagonism did not modify body sodium concentration, the adrenomedullary component of the sympathetic nervous system, angiotensin II levels, or beta-adrenergic dependent mechanisms.
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PMID:Alpha 1-adrenergic blockade and cardiovascular pressor responses in essential hypertension. 287 Sep 84

The antihypertensive effect of labetalol was evaluated in 18 adult black patients with mild to moderate essential hypertension previously controlled with a combination of a diuretic and a beta blocker. After a 4-week washout period, standing blood pressure had increased from 138 +/- 2.2/85 +/- 1.5 mmHg, (mean +/- SEM) to 154 +/- 1.9/100 +/- 0.6 mmHg. Labetalol was then titrated to a maximum of 600 mg BID to obtain a standing diastolic blood pressure of less than or equal to 90 mmHg and/or a decrease of greater than or equal to 10 mmHg from baseline (end of washout period). By the end of the labetalol titration period, standing blood pressure had decreased to 140 +/- 2.0/84 +/- 1.5 (p less than 0.01). Following a 2-week maintenance period, standing blood pressure was 136 +/- 1.6/80 +/- 1.5 mmHg (NS vs. titration). Labetalol therapy was well tolerated and reduced diastolic blood pressure to less than or equal to 90 mmHg in 17 of 18 patients, 13 of whom required dosages less than or equal to 300 mg BID. The average reduction in standing heart rate while on labetalol was 4 bpm (p less than 0.01). Side effects were limited to skin rash in one patient and possible mild urinary retention in another. These data indicate that labetalol is an effective antihypertensive for black patients with mild to moderate essential hypertension.
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PMID:Labetalol as monotherapy in hypertensive black patients. 287 8

Calcium antagonist monotherapy is more effective in older patients and in those with low plasma renin activity, whereas beta blockers control blood pressure better in younger patients and in those with normal or high renin activity. Monotherapy with a calcium antagonist has been shown to result in the reduction of diastolic blood pressure to equal to or less than 95 mm Hg in more than 80 percent of patients with essential hypertension. We investigated the antihypertensive efficacy of verapamil plus an angiotensin converting enzyme inhibitor and nifedipine plus a beta blocker in 24 patients (aged 41 to 68) with moderate to severe hypertension in whom monotherapy with a calcium antagonist had been ineffective. Blood pressure recorded in patients during the placebo period was 175 +/- 3/111 +/- 2 mm Hg (mean +/- SEM). Twelve patients received monotherapy with nifedipine (50.0 +/- 5.2 mg per day) and 12 others received verapamil (460 +/- 20 mg per day); neither treatment resulted in the reduction of diastolic blood pressure to less than 90 mm Hg. However, this goal was achieved when atenolol (89.5 +/- 25.7 mg per day) was added to the regimen of patients receiving nifedipine and enalapril (29.5 +/- 5.0 mg per day) was added to the regimen of those receiving verapamil; resultant blood pressures were 127 +/- 3/83 +/- 2 mm Hg and 137 +/- 5/85 +/- 1 mm Hg, respectively. It is suggested that in patients in whom hypertension is inadequately controlled by calcium antagonist monotherapy, counter-regulatory mechanisms can be blocked by the addition of a beta blocker or an angiotensin converting enzyme inhibitor to the calcium antagonist regimen, resulting in greatly improved, simple, well-tolerated, and safe control of blood pressure.
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PMID:Calcium antagonists and the second drug for hypertensive therapy. 287 44

44 men with treated essential hypertension who were moderate to heavy drinkers took part in a randomised, controlled, crossover trial of the effects of alcohol intake on blood pressure. Usual antihypertensive treatment was maintained throughout 6 weeks of normal drinking and 6 weeks of drinking only a low-alcohol beer. Self-reported changes in alcohol consumption (mean [SEM] from 452 [30] ml ethanol/week during normal drinking to 64 [8] ml/week while drinking the low-alcohol beer) were confirmed by biochemical measurements. Mean systolic and diastolic blood pressures were significantly lower during the last 2 weeks of the low-alcohol period than during the normal-alcohol period, the mean difference in the supine readings being 5.0 (1.4) and 3.0 (0.9) mm Hg, respectively. Regression analysis suggested that reduction in alcohol intake contributed to the fall in both systolic and diastolic blood pressures independently of changes in weight. Thus, curtailing alcohol intake may lead to improved blood-pressure control and may reduce the need for antihypertensive drugs.
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PMID:Regular alcohol use raises blood pressure in treated hypertensive subjects. A randomised controlled trial. 288 82

Black people have a higher propensity than caucasians toward essential hypertension. To explore the possibility that this racial difference relates to cellular Ca2+ metabolism, we measured 45Ca2+ washout and uptake and cytosolic free concentration of Ca2+ [Ca2+]i in serially passed skin fibroblasts from normotensive black and white males. Depending on the experimental conditions, 45Ca2+ washout in these cells was described by either two or three exponential functions, whereas 45Ca2+ uptake was described only by a two-exponent function. There were no racial differences in 45Ca2+ uptake and washout of unstimulated fibroblasts. However, stimulation by human serum resulted in an increase in the 45Ca2+ washout that was higher in fibroblasts from blacks than from whites. The racial differences were expressed primarily by higher values of the apparent washout rate constant (k1) of 45Ca2+ from the largest and most rapidly exchangeable cellular pool. The effect of human serum was not related to its origin (blacks vs. whites). In 2 mM Ca2+ medium and 10% serum from blacks, the respective k1 (mean +/- SEM; x 10(-2)/min) values for fibroblasts from blacks and whites were 89.68 +/- 5.23 and 73.29 +/- 4.0; in the presence of 10% serum from whites, the k1 values for cells from blacks and whites were 84.14 +/- 2.80 and 76.36 +/- 3.23 (overall significance of P less than .01). In Ca2+-deficient medium in the presence of 10% human serum, the k1 for fibroblasts from blacks and whites were 115.57 +/- 3.76 and 102.15 +/- 3.30 (P less than .05). Serum substantially increased the 45Ca2+ uptake in fibroblasts from both blacks and whites; however, racial differences were not observed. Basal levels of [Ca2+]i were not different in fibroblasts of blacks vs. whites (46.8 +/- 6.8 and 43.2 +/- 7.1 nM for blacks and whites, respectively). However, the peak response of Cai2+ transients for cell stimulated by 5% human serum was significantly higher in blacks than whites (blacks = 963 +/- 213, whites = 481 +/- 162 nM; P = .0286). We conclude that Ca2+ regulation is different in serum-stimulated fibroblasts from blacks and whites and that, at least in part, this difference may relate to a greater agonist-induced mobilization of Ca2+ in fibroblasts from blacks.
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PMID:Differences of Ca2+ regulation in skin fibroblasts from blacks and whites. 291 38

Plasma levels of atrial natriuretic peptide (ANP) were measured in 9 patients with primary aldosteronism and 41 patients with essential hypertension (class I or II by WHO classification) using a specific and sensitive RIA. The mean plasma ANP concentration in patients with primary aldosteronism (mean +/- SEM, 67.1 +/- 10.8 pg/ml; n = 9) was significantly higher than that in healthy normotensive subjects (37.9 +/- 1.4 pg/ml; n = 108) or patients with essential hypertension (38.5 +/- 2.8 pg/ml; n = 41). During treatment with spironolactone, plasma levels of ANP declined in 6 of the 7 patients with primary aldosteronism, but no change occurred in the remaining patient who had cardiac enlargement of unknown etiology. The mean plasma ANP concentration in patients with essential hypertension, on the other hand, was not significantly different from that in normal subjects. These results indicate that plasma ANP levels are elevated in patients with primary aldosteronism, probably due to volume expansion, whereas no abnormality in ANP secretion exists in patients with uncomplicated essential hypertension.
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PMID:Plasma levels of atrial natriuretic peptide in primary aldosteronism and essential hypertension. 294 53

Plasma atrial natriuretic factor concentrations were measured in 44 patients with mild untreated essential hypertension and 48 normotensive controls. Mean venous plasma atrial natriuretic factor concentrations were 13.2 (SEM 1.5) and 13.0 (1.3) ng/l in the hypertensive patients and controls, respectively. Plasma atrial natriuretic factor concentrations were significantly correlated with age in both groups. Plasma atrial natriuretic factor concentrations were also measured during renal vein catheterisation in a group of 15 hypertensive patients; of these, eight had renovascular hypertension, and in all eight cases plasma atrial natriuretic factor concentrations were increased in the aorta and inferior vena cava. It is concluded that mild essential hypertension is not associated with increased plasma atrial natriuretic factor concentrations, whereas an age related increase in concentrations occurs in hypertensive and normotensive people.
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PMID:Plasma atrial natriuretic factor concentrations in essential and renovascular hypertension. 295 11

A sensitive and specific procedure for the measurement of atrial natriuretic peptide (ANP) in human plasma by radioreceptor assay, using bovine adrenal membranes treated with Triton-X-100, is described. Plasma levels (mean +/- SEM) of ANP in healthy subjects on a normal sodium intake were 8.4 +/- 1.4 pg/ml and could be modified by changes in sodium intake with increases in sodium intake being associated with higher levels. Mean plasma ANP was approximately 2-fold higher in patients with essential hypertension and 4-fold higher in patients with cardiac or renal disease. The values obtained were comparable in magnitude to those obtained by radioimmunoassay and there was a strong correlation (r = 0.94; p less than 0.001) between the values obtained by radioimmuno- and radioreceptor-assay. These results suggest that circulating ANP corresponds to the biologically active peptide and point to an important role of the atrial peptides in the control of sodium balance.
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PMID:Atrial natriuretic peptide in human plasma--comparison of radioreceptor versus radioimmunoassay. 295 62


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