Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. A double-blind cross-over evaluation of the anti-hypertensive effect of metoprolol vs placebo was carried out in a series of twenty-three patients with mild or moderate essential hypertension who were receiving 25 mg of chlorthalidone daily as their basic treatment. An individually determined dose of metoprolol (75-300 mg) was used. 2. Metoprolol, as compared with placebo, produced a statistically significant reduction of blood pressure, both in supine and standing positions. 3. During the double-blind cross-over study mild side effects were more common at the beginning of metoprolol/chlorthalidone treatment than during placebo/chlorthalidone, but these tended to diminish or disappear with time. 4. Metoprolol in combination with chlorathalidone appears to be an effective and well-tolerated treatment for mild and moderate hypertension in patients not responding to chlorthalidone alone.
Clin Sci Mol Med Suppl 1976 Dec
PMID:A controlled study on the anti-hypertensive effect of a new beta-adrenoreceptor-blocking drug, metoprolol, in combination with chlorthalidone. 79 61

1. The beta1-adrenoreceptor-blocking agent atenolol was studied in the treatment of twelve out-patients with essential hypertension. 2. With a mean dose of 110 mg of atenolol daily (range 75-200 mg/day) we observed a pronounced decrease in blood pressure. 3. Only minimal side effects were seen. 4. Cardiac output decreased from 4-6 to 3-4 l/min during treatment. This decrease did not correlate with the decrease in blood pressure but correlated well with the changes in calculated total peripheral resistance.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Clinical and haemodynamic study of atenolol (Tenormin) in essential hypertension. 79 62

1. The effects of timolol alone and in combination with a fixed dose of hydrochlorothiazide and amiloride have been studied in a double-blind, controlled study in fifty-four patients with mild to moderate essential hypertension. 2. After a 4 weeks placebo period patients were randomly assigned to enter groups receiving timolol alone (group A), hydrochlorothiazide + amiloride (group B) or timolol + hydrochlorothiazide + amiloride (group C). Each treatment was carried out for 6 weeks. 3. The use of timolol (10 mg), hydrochlorothiazide (25 mg) and amiloride (2-5 mg) in a combination tablet given twice daily gave better control of blood pressure in patients with mild to moderate essential hypertension than did equivalent dosages of timolol alone or of hydrochlorothiazide and amiloride. 4. Clinical and laboratory side effects were minimal.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Evaluation of the effect of timolol alone and in combination with hydrochlorothiazide and amiloride in the treatment of mild to moderate arterial hypertension: a double-blind, controlled study. 79 63

1. Serial measurements of plasma renin activity (PRA), plasma aldosterone concentration (PA) and blood pressure were performed overnight in patients with borderline (group 1) and sustained essential hypertension (group 2) before and after acute and chronic administration of either propranolol or pindolol. 2. Group 1 patients exhibited a typical rhythm of recumbent PRA with low values before midnight and large increases early in the morning. 3. In contrast, no rhythm and very low PRA values were observed in patients of group 2. Blood pressure was higher in group 2 than in group 1. There was a significant correlation between the hyporeninaemic and hypotensive effect of either acute (r = 0-79) or chronic (r = 0.4) beta-receptor blockade. 4. In group 1, after beta-receptor blockade the day-night profile of renin was similar to that observed in group 2 before treatment. Thus, in this latter subgroup, low-renin profiles might reflect reduced beta-adrenoreceptor activity. 5. Plasma aldosterone was lower in group 2 but appeared to be inappropriately high relative to renin. 6. The data suggest that in hypertensive patients classified according to their blood pressure and recumbent PRA profiles a significant relationship exists between changes in PRA and arterial pressure. Thus patients with high PRA respond better to treatment than patients with low renin. We conclude that in the patients studied sympathetic nervous system activity mainly determined renin values as well as anti-hypertensive effectiveness of the beta-blocking drugs.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Differential effects of acute and chronic beta-adrenoreceptor blockade on blood pressure and the renin-angiotensin-aldosterone system in essential hypertension. 79 64

1. Twelve patients with essential hypertension were treated aggressively with minoxidil in order to achieve blood pressure control as rapidly as possible. 2. After an initial dose of 5 mg, dose increments were administered 6 hourly until a fall in blood pressure was observed. 3. The size of additional doses was determined by the magnitude of and response to the lowest effective dose and the therapeutic objective. 4. Over a time-interval of 24-42 h blood pressure was reduced to normal or near normal in each case. 5. Analysis of the relationship between blood pressure response and cumulative dose indicates that at sub-optimum blood pressure responses it is safe and efficacious to give half the antecedent cumulative dose as a single dose in arriving at the therapeutic objective.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Technique for rapid control of hypertension with oral minoxidil. 80 34

Consideration of the results obtained in studies of spontaneously hypertensive rats indicates that these animals can serve as useful models for perhaps the most common type of essential hypertension of man. Other variants of essential hypertension probably occur where the relative balance between the genetic elements predisposing to high blood pressure may be somewhat different.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Central neurohormonal mechanisms in spontaneously hypertensive rats compared with human essential hypertension. 80 37

1. Mean plasma noradrenaline concentration was elevated in forty-four patients with established essential hypertension. Eighteen of the hypertensive patients had resting plasma noradrenaline concentrations in the normal range. 2. Patients with endogenous depression had higher mean plasma noradrenaline concentrations but significantly lower blood pressure than patients with essential hypertension. 3. Patients with phaeochromocytoma had plasma noradrenaline concentrations twenty-eight times greater than those found in essential hypertension, but blood pressures were less than 20% higher. 4. It is concluded that excess of sympathetic drive only partly explains the level of the blood pressure in essential hypertension.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Plasma noradrenaline concentration and blood pressure in essential hypertension, phaeochromocytoma and depression. 80 39

1. Catecholamine plasma concentrations and urinary excretion were measured together with plasma renin activity in ten patients with essential hypertension and in five normal control subjects before and after a frusemide challenge. 2. The same procedure was repeated in the same subjects 3--4 days later after pretreatment with oxprenolol. 3. Noradrenaline plasma concentrations and urinary excretion increased significantly after frusemide in all cases, returning to normal values at 30 and 60 min. Adrenaline plasma concentrations and urinary excretion were unchanged. 4. Plasma renin activity increased significantly in seven patients with hypertension and normal renin basal values, remaining unchanged in three hypertensive patients with low-renin basal values. 5. Oxprenolol suppressed the response of noradrenaline and plasma renin activity to frusemide in all cases.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Effect of oxprenolol on catecholamines and plasma renin activity: acute response to frusemide in hypertensive patients. 80 48

1. Plasma renin concentration, intra-arterial pressure, cardiac output and total peripheral resistance have been studied in 50 patients with essential hypertension and normal renal function. 2. Total peripheral resistance and plasma renin were negatively correlated (r = -0-45), indicating that 'high-renin' essential hypertension is not necessarily associated with arteriolar vasoconstriction. 3. The inverse relation between mean arterial pressure and plasma renin (r = -0-46) suggests a role for the renal baroreceptor mechanism in the suppression of renin in 'low-renin' hypertension. 4. Cardiac output was positively related to plasma renin concentration (r = +0-42). 5. Multiple regression analysis indicates that the described relationships were independent of age.
Clin Sci Mol Med 1977 Jun
PMID:Plasma renin levels and systemic haemodynamics in essential hypertension. 88 30

1. The initial blood pressure response to saralasin (Sar1-Ala8-angiotensin II) infusion was examined in 15 normal subjects, eight patients with untreated essential hypertension and 65 patients established on chronic haemogialysis (including six anephric patients), and related to measurements of plasma renin activity (PRA), angiotensin II, plasma catecholamines (noradrenaline and adrenaline), blood volume and extracellular fluid volume ([35S]sulphate space or exchangeable sodium). 2. A transient rise in arterial pressure, maximum after 5-6 min, occurred in all normal subjects, patient with essential hypertension and anephric patients, and in 41 of the 59 dialysis patients with kidneys. 3. In the normal subjects, saralasin infusion resulted in a significant rise in plasma noradrenaline (mean increase 360%, P less than 0-02) without change in plasma adrenaline concentration. The change in noradrenaline was significantly related to the change in mean blood pressure (P less than 0-05) and was similar to the response to 5 min of a 40 degree head-up tilt. 4. An increase in plasma noradrenaline also occurred in dialysis patients (P less than 0-005) but the change in mean blood pressure with saralasin in this group was inversely related to PRA (P less than 0-001) and angiotensin II (P less than 0-001), directly related to blood volume (P less than 0-001), but unrelated to the change in plasma noradrenaline. 5. The pressor response to saralasin may be mediated not only by angiotensin-like action on vascular receptors but also by an action on the central or peripheral autonomic nervous system.
Clin Sci Mol Med 1977 Oct
PMID:Plasma catecholamines and the pressor response to Sar1-Ala8-angiotensin II in man. 91 58


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