Gene/Protein Disease Symptom Drug Enzyme Compound
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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rate of red blood cell sodium-lithium countertransport is elevated only in a subgroup of patients with essential hypertension. We have therefore compared renal and cardiac function and morphology in two groups of hypertensive patients with high (n = 23) or normal (n = 22) sodium-lithium countertransport (mean +/- SEM: 0.61 +/- 0.10 versus 0.29 +/- 0.07 mmol/l red blood cells.hr). The two groups were similar in age, sex distribution, body mass index, smoking habit, duration of hypertension, and actual levels of untreated blood pressure. Hypertensive patients with elevated sodium-lithium countertransport activity showed elevated glomerular filtration rate (118 +/- 2 versus 109 +/- 2 ml/min.1.73 m2; p less than 0.001), albumin excretion rate (23 +/- 3 versus 14 +/- 2 micrograms/min; p less than 0.001), larger kidney volume (250 +/- 15 versus 203 +/- 13 ml.1.73 m2; p less than 0.01), lower lithium clearance rate (26.7 +/- 0.3 versus 28.9 +/- 0.3 ml/min.1.73 m2; p less than 0.01), and higher total body exchangeable sodium (2,716 +/- 33 versus 2,485 +/- 41 mmol.1.73 m2; p less than 0.01). Left ventricular mass index (139 +/- 6 versus 119 +/- 6 g/m2; p less than 0.05), relative wall thickness (0.39 +/- 0.05 versus 0.29 +/- 0.04 cm; p less than 0.001), and left posterior wall plus intraventricular septum thickness (2.02 +/- 0.04 versus 1.76 +/- 0.03 cm; p less than 0.05) were also higher in patients with high sodium-lithium countertransport. Hypertensive patients with normal sodium-lithium countertransport had renal and cardiac parameters similar to those of a normotensive control group (n = 21) except for a higher glomerular filtration rate and left ventricular mass index.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sodium-lithium countertransport and cardiorenal abnormalities in essential hypertension. 188 27

A multicenter, randomized, double-blind, parallel-group trial of 8 weeks' duration was designed to compare the efficacy and safety of once-daily carvedilol with that of twice-daily labetalol in patients with essential hypertension. A total of 61 patients (13 women and 48 men) aged 26-64 years (mean +/- SEM = 49.6 +/- 1.3 years) were enrolled. All patients had mild to moderate hypertension, defined as diastolic blood pressure (DBP) of 95-114 mm Hg at the end of a 1- to 2-week single-blind placebo period. In all, 30 patients received carvedilol (25 mg once daily) and 31 received labetalol (200 mg twice daily). The initial dose could be doubled for both treatment groups at day 29 if the DBP was greater than 90 mmHg on days 28 and 29. Hemodynamic parameters, including supine and standing DBP, systolic blood pressure (SBP), and heart rate (HR), were measured and safety was evaluated at baseline and at days 14, 28, and 56 at the end of the dosing interval. In all, 3 patients on carvedilol and 4 patients on labetalol required upward dose titration after 1 month. At the end of the trial, 26 of 30 carvedilol-treated patients and 27 of 31 labetalol-treated patients (87% of each group) had a supine DBP of less than or equal to 90 mm Hg. On day 56, mean decreases in supine DBP, SBP, and HR in the carvedilol group were 18.5 and 23.4 mm Hg and 11 beats/min, respectively, from baseline values of 101.6 and 163.8 mm Hg and 80 beats/min, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety and efficacy of once-daily carvedilol vs twice-daily labetalol in mild to moderate hypertension. 197 9

When the function of the renin system is inhibited, blood pressure becomes more dependent on changes in sodium and water balance. Diuretics alone and sodium restriction alone are additive to converting enzyme inhibitor therapy. However, it is not known if these two ways of reducing sodium balance are additive in the presence of established converting enzyme inhibition. We therefore performed a double-blind crossover study of the effects of moderate sodium restriction in 21 patients with essential hypertension who were already being treated with the combination of a converting enzyme inhibitor and a diuretic. After 1 month of captopril (50 mg twice daily) and hydrochlorothiazide (25 mg once daily) therapy, with their usual sodium intake, average supine blood pressure was 147/96 +/- 5/3 (SEM) mm Hg 2 hours after treatment. Patients then reduced their sodium intake to around 80-100 mmol/day for the remainder of the study. After 2 weeks of sodium restriction, they entered a double-blind, randomized, crossover study of Slow Sodium (100 mmol sodium/day) compared with Slow Sodium placebo, while continuing sodium restriction and the above treatment. During the double-blind study, after 1 month of treatment with captopril (50 mg twice daily), hydrochlorothiazide (25 mg once daily), and Slow Sodium placebo, supine blood pressure 2 hours after treatment was 138/88 +/- 4/2 mm Hg (24-hour urinary sodium 104 +/- 11 mmol). After 1 month of captopril (50 mg twice daily), hydrochlorothiazide (25 mg once daily), and Slow Sodium tablets, supine blood pressure 2 hours after treatment was 147/91 +/- 5/2 mm Hg (p less than 0.05; 24-hour urinary sodium 195 +/- 14 mmol).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sodium restriction in hypertensive patients treated with a converting enzyme inhibitor and a thiazide. 204 42

Nine mild-to-moderate hypertensive patients (HT), aged 41 +/- 0.6 years (mean +/- SEM) and nine age-matched normotensive control subjects (NT) were tilted to 60 degrees for 10 min. During tilt, both systolic (S) blood pressure (BP) (p less than 0.01) and diastolic (D) BP (p less than 0.05) increased in HT, but not in NT. At supine rest renal blood flow was higher in HT than in NT and increased by 17% in HT during tilt, while a decrease of 13% was observed in NT (p less than 0.05). Renal vascular resistance was unchanged in HT during tilt, while a significant increase (p less than 0.01) was observed in NT. Arterial plasma noradrenaline increased in both groups (p less than 0.05) during tilt, significantly more in HT than in NT (p less than 0.05). No statistically significant difference was observed between the groups in renal catecholamine uptake or release. Our data indicate enhanced general sympathetic and circulatory responses to tilt in subjects with mild-to-moderate essential hypertension. However, the enhanced haemodynamic and sympathetic responses were not shared by hypertensive kidneys and renovascular resistance remained unaffected by tilt.
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PMID:Renal haemodynamic and sympathetic responses to head-up tilt in essential hypertension. 208 19

The captopril test was performed in 49 children of whom 36 were hypertensive, and the remainder were normotensive but at risk for developing hypertension because of scarred kidneys secondary to vesicoureteral reflux. The blood pressure was monitored in fasting supine patients throughout the duration of the test. Blood was taken for measurement of plasma renin activity (PRA), then captopril (0.7 mg/kg body weight) was administered orally. A second blood sample was taken for PRA measurement 90 min after captopril administration. The mean PRA at 90 min was 11.90 +/- (SEM) 4.01 ng/l/s (42.84 +/- 14.44 ng/ml/h) in 7 patients with renovascular disease. In 4 patients with essential hypertension, the corresponding value was 0.88 +/- 0.38 ng/l/s (3.17 +/- 1.37 ng/ml/h). Patients with other renal diseases showed variable values. Some individuals had PRA values as high as those of patients with renovascular disease, but the etiology of their hypertension was usually clinically evident. Our preliminary data would suggest that the captopril test may help differentiate between patients with essential hypertension and those with renovascular disease or may help select patients that should be followed up by more definitive diagnostic procedures.
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PMID:Use of the captopril test to assess renin responsiveness in children with hypertension and renal disease. 208 87

A placebo-controlled study of Ramipril on total and intrarenal flow distribution was carried out in 7 patients with essential hypertension. Cortical nephron flow was measured using radiolabelled tubular secreted radiopharmaceuticals 123I orthoidohippurate or 99mTc mercaptoacetyl triglycine by the transit time distribution technique. Both systolic and diastolic blood pressure were reduced significantly by Ramipril without significant changes in an index of cardiac output or in effective renal plasma flow. Cortical nephron flow increased from 207 +/- 7 to 257 +/- 21 ml/min (mean +/- SEM) p less than 0.05 and the percentage of flow to cortical nephrons increased by 6% (p = 0.05). Ramipril corrects the reduced cortical nephron flow found in essential hypertension.
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PMID:The effect of ramipril, a new angiotensin-converting enzyme inhibitor on cortical nephron flow and effective renal plasma flow in patients with essential hypertension. 213 39

To study the cardiac determinants of regression of left ventricular hypertrophy in hypertension, left ventricular mass, fractional shortening and end-systolic wall stress were measured echocardiographically in 36 patients with essential hypertension and left ventricular hypertrophy. The patients were classified into two groups. Group I consisted of 15 patients with subnormal end-systolic wall stress, and Group II consisted of 21 patients with normal end-systolic wall stress. There were no significant differences between groups in systolic or diastolic blood pressure. After treatment for 4.4 +/- 1.7 years, echocardiographic studies were repeated. There were no significant differences between groups in the duration of the follow-up period and the kinds of antihypertensive drugs. After treatment, blood pressure decreased significantly in both groups (p less than 0.001 for both), with no significant difference between groups. Left ventricular mass increased significantly in Group I (from 331 +/- 7 to 363 +/- 24 g, mean +/- SEM, p less than 0.05), whereas it decreased significantly in Group II (from 318 +/- 16 to 268 +/- 17 g, p less than 0.001). Myocardial contractility (the relation between end-systolic wall stress and fractional shortening) remained almost the same as before treatment. In conclusion, in patients with hypertensive ventricular hypertrophy with subnormal end-systolic wall stress (inappropriate hypertrophy, probably induced by a neurohumoral factor), a decrease in blood pressure with antihypertensive treatment does not lead to regression of left ventricular hypertrophy, but rather to an increase in left ventricular mass.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiac determinants of regression of left ventricular hypertrophy in essential hypertension with antihypertensive treatment. 213 79

The predisposition of black people to salt (NaCl)-sensitive essential hypertension may relate to racial differences in cellular Na+ metabolism. This tenet was investigated by examining the Na(+)-H+ antiport in serially passed skin fibroblasts from blacks and whites. Na(+)-dependent stimulation of the Na(+)-H+ antiport by cellular acidification resulted in a greater maximal velocity (Vmax) (mean +/- SEM) of this transport system in quiescent fibroblasts from blacks than fibroblasts from whites; the Vmax for recovery from cellular pH (pHi) of 6.6 was 5.84 +/- 0.50 versus 4.39 +/- 0.34 mmol H+/l X 20 seconds for blacks and whites, respectively (p less than 0.05). Although the Na+ concentration producing 50% stimulation of the Na(+)-H+ antiport for blacks (35.1 +/- 5.7 mM) was greater than for whites (24.1 +/- 3.5 mM), this difference was not statistically significant. No racial differences were observed in the Hill coefficient (n, 1.35 +/- 0.21 for blacks and 1.46 +/- 0.28 for whites). Compared with whites, cells from blacks exhibited a greater response to cytoplasmic acidification over the range of pHi values 6.20-6.60, as exhibited by an augmented rate of recovery in the pHi. These differences were not due to different basal pHi values or cellular buffering capacities, which were similar for blacks and whites. Na(+)-H+ antiport activity was not correlated with family history of hypertension. Increased activity of the Na(+)-H+ antiport in fibroblasts from blacks was confirmed without cellular acidification by stimulating quiescent cells with 10% human serum. This study demonstrates innate racial differences in cellular membrane Na(+)-H+ antiport activity.
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PMID:Na(+)-H+ antiport activity in skin fibroblasts from blacks and whites. 215 2

The efficacy and tolerability of lisinopril administered once daily were evaluated in a 12-week open study of 60 elderly patients aged between 65 and 85 years (mean 75 years) with essential hypertension. Mean sitting blood pressure was reduced from 190/106 +/- 6.3/1.3mm Hg (mean +/- SEM) at entry to 162/89 +/- 5.5/0.9 mm Hg after 12 weeks of treatment (p less than 0.001). There was no significant alteration in heart rate, and no occurrence of postural hypotension. The median daily dose of lisinopril was 20mg (range 5 to 40 mg) and only 4 patients required the addition of a diuretic. Mean glomerular filtration rate (GFR) at entry was 61.6 +/- 3.4 ml/min and was unchanged after 12 weeks of therapy. 25 patients continued to receive treatment for 1 year, and 20 of these completed 2 years of treatment. Control of blood pressure was maintained, and heart rate, biochemical parameters and GFR remained unaltered throughout the study. Renal function was preserved and renal blood flow, measured in a group of 14 patients, was significantly increased (p less than 0.025) at the end of the first year after treatment with lisinopril. Thus, in the elderly, lisinopril was well tolerated and highly effective in lowering blood pressure, and renal function was maintained.
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PMID:Lisinopril in elderly patients with hypertension. Long term effects on renal and metabolic function. 216 Aug 84

To explore the role of the Na-H antiport in essential hypertension, we studied the kinetics of cytosolic pH and external sodium activation of this transport system in platelets from 65 normotensive and essential hypertensive subjects on and off antihypertensive medications. Subjects included both blacks and whites, as well as men and women. The fluorescent dye 2'7-bis(carboxyethyl)-5,6-carboxyfluorescein was used to monitor the cytosolic pH in these cells. Platelets from black (hypertensive and normotensive) men and hypertensive white men demonstrated a highly significant alkaline shift in the apparent cytosolic pH set point for activation of the Na-H antiport. For the hypertensive subgroups, the cytosolic pH set point values (mean +/- SEM) were: white men, 7.45 +/- 0.052; white women, 7.04 +/- 0.089; black men, 7.66 +/- 0.148; and black women, 7.20 +/- 0.082. For the normotensive subgroups, the cytosolic pH set point values were: white men, 7.13 +/- 0.034; white women, 7.05 +/- 0.036; black men, 7.50 +/- 0.110; and black women, 7.20 +/- 0.176 (p = 0.0016 for race and p = 0.0001 for gender, using a three-way analysis of variance by race, gender, and hypertension). There were no race-, gender-, or blood pressure-related differences among the various cohorts in the kinetics of sodium activation of the Na-H antiport, the cellular buffering power, and basal pH. These results suggest that at basal pH the Na-H antiport is quiescent in platelets from both black and white women and normotensive white men.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Variations in the apparent pH set point for activation of platelet Na-H antiport. 216 2


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