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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-two patients with primary hypertension were studied in a double-blind cross-over comparison between the cardioselective beta 1-blocking agent atenolol and the combined alpha- and beta-blocking agent labetalol. The doses used were atenolol 50--150 mg twice daily and labetalol 200--600 mg twice daily. Both drugs effectively reduced blood pressure and heart rate. Dose increments every second week resulted in a higher proportion of patients with normal blood pressure (les than or equal to 150/90 mm Hg) with both drugs. Labetalol was somewhat more effective in lowering upright blood pressure while atenolol caused a more pronounced heart-rate reduction. Both agents decreased plasma renin activity and urinary aldosterone excretion. Scalp tingling on labetalol (2 patients) and cold fingers with atenolol (1 patient) caused withdrawal of the drugs. Cold fingers were reported in another four patients during treatment with atenolol and in one when on labetalol. Tiredness and postural symptoms were more common during intake of labetalol.
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PMID:Antihypertensive and metabolic effects of increasing doses of atenolol and labetalol. A comparative study in primary hypertension. 676 Jun 79

1. Twenty-two patients with moderately severe essential hypertension were treated for a period of 12 months with guanfacine (BS 100-141), a new centrally-acting antihypertensive agent. A twice daily schedule was followed and the dose range of guanfacine was 1-8 mg daily. 2. In twenty patients satisfactory blood pressure responses (diastolic pressure below 95 mmHg) were achieved in both the supine and the standing position. Pulse rate decreased slightly, though not significantly. 3. Tolerance to the pressure-lowering effect of the drug developed during the third or fourth month of therapy. This could be overcome by either increasing dosage or adding a diuretic. 4. All patients reported side-effects, mainly dryness of the mouth and fatigue. These side-effects became less or disappeared at the end of 3 months. Rebound hypertension on discontinuation of therapy occurred in two patients. 5. Plasma concentrations of noradrenaline and adrenaline as well as plasma renin activity were decreased after 1 week of treatment with the drug. 6. Guanfacine in conjunction with a diuretic is a useful drug in the long-term treatment of hypertension. Reduced central sympathetic outflow may be the major mechanism underlying the antihypertensive effect of the drug.
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PMID:Evaluation of long-term treatment of essential hypertension with guanfacine. 699 80

1. Prizidilol (SKF 92657), a new antihypertensive drug with combined precapillary vasodilator and non-selective beta-adrenoceptor-blocking actions, was given to 24 patients with essential hypertension in a placebo-controlled, dose-titration study, Incremental doses from 200 to 800 mg were given once daily. Supine and standing blood pressure measured 24--27 h after drug intake was reduced during treatment with prizidilol (400--800 mg/day). Slight but significant decreases in heart rate were seen after moderate doses (mean: 447 mg once daily) of prizidilol. A more pronounced blood pressure reduction was noticed 2--7 h after drug administration. 2. Maximal blood pressure reduction coincided with peak plasma concentration of prizidilol, which was measured by a newly developed assay. 3. Plasma renin activity and 24 h urinary excretion of aldosterone and methoxycatecholamines were reduced after the highest doses (mean: 700 mg once daily) of prizidilol. 4. Prizidilol was well tolerated, although dizziness and tiredness were reported by four patients and oedema by two.
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PMID:Prizidilol (SKF 92657) in primary hypertension. 718 85

Although essential hypertension is usually defined as a hemodynamic disorder, it is expressed differently among individuals and varies during progression of the disease state. Therefore, various types of treatment can be envisioned. The use of selective I1-imidazoline-receptor agonists to modulate I1-imidazoline receptors involved in the central regulation of blood pressure has led to the introduction of a novel class of centrally acting antihypertensive drugs. Moxonidine, a representative molecule of this class, dissociates between a 10% alpha 2-adrenoceptor-agonist action linked with side effects such as fatigue or dry mouth, and a 90% specific antihypertensive action resulting from its selective agonistic action at I1-imidazoline receptors. Clinical experience is based on more than 2,000 patients and volunteers, and long-term efficacy has been demonstrated in about 500 patients who received a daily dose of moxonidine 0.2-0.4 mg. Moxonidine produces a pronounced reduction in peripheral vascular resistance without reflex tachycardia, accompanied by reduced plasma norepinephrine concentration and plasma-renin activity. Cardiovascular responses to exercise and standing remain nearly normal, and serious or life-threatening side effects, particularly the sympathetic overactivity that can occur on sudden withdrawal of other centrally acting agents, are never observed. In addition, moxonidine behaves neutrally with respect to plasma levels of cholesterol, potassium and glucose, glucose and lipid metabolism, and renal function, and can be administered without complication to patients with asthma or certain other diseases. Studies with magnetic resonance imaging have shown that moxonidine significantly reduces left ventricular mass, an indicator of left ventricular hypertrophy (LVH), within a 6-month treatment period, an effect that coincided with decreased plasma concentrations of catecholamines and renin. Comparisons between moxonidine and other well-established antihypertensive drugs such as nifedipine, atenolol, or angiotensin-converting enzyme inhibitors showed equal effectiveness in lowering blood pressure, whereas the adverse events profile always favored moxonidine. Considering its efficacy, safety, and specific effects (e.g., its ability to reduce LVH), moxonidine meets the criteria satisfied by other currently prescribed antihypertensive drugs. Because of its especially favorable benefit-to-risk ratio, moxonidine should be recommended as first-line treatment of hypertension and may also be useful in treating related problems such as LVH, coronary artery disease, and ventricular premature beats.
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PMID:I1-imidazoline-receptor agonists in the treatment of hypertension: an appraisal of clinical experience. 753 26

A twenty-one-year-old male was admitted to our hospital because of hypertension and proteinuria. He had felt general fatigue and low grade fever for one month. Blood pressure was 180/120 mmHg on admission. Laboratory findings showed 3+ proteinuria and 1+ occult blood in urinalysis; an accelerated erythrocyte sedimentation rate (ESR) of 39 mm/hr; elevation of LDH to 755 IU/l. Antinuclear antibody was positive with a titer of 1: 160, with a speckled pattern. Plasma renin activity and serum aldosterone were markedly elevated to 25.8 ng/ml/hr and 585.3 pg/ml, respectively. Renal function had declined mildly; endogenous creatinine clearance was 60 ml/min. Renal arteriogram demonstrated multiple intrarenal aneurysms in the bilateral kidneys. Aneurysms, 5-8 mm in diameter were located in the arteries from the interlobar to interlobular region. He was diagnosed as having polyarteritis nodosa (PN) and was then treated with 20 mg/day of prednisolone and monthly pulse therapy of cyclophosphamide. After steroid, cyclophosphamide and anti-hypertensive therapy, he became well and had normal blood pressure. The patient was considered a rare case of PN with multiple intrarenal aneurysms and accelerated hypertension. We discuss aneurysms in PN and accelerated or malignant hypertension documented in the literature.
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PMID:[A case of polyarteritis nodosa presenting with multiple intrarenal aneurysms and accelerated hypertension]. 769 55

The effect of carmoxirole, a presynaptic dopamine (DA2) receptor agonist, on blood pressure, plasma catecholamines, renin-aldosterone and atrial natriuretic peptide and the intracellular concentration and transmembrane fluxes of Na+ and K+, in erythrocytes and platelets was studied in 24 normal men, using a double-blind, parallel study design. After a run-in period of 1 week, the subjects were treated with either placebo (n = 8) or 0.5 mg carmoxirole (n = 16) once daily for 1 week. Blood pressure and heart rate were not changed during carmoxirole administration in these normal men. Surprisingly, no significant effect of carmoxirole was found on the circulating plasma concentration of noradrenaline, adrenaline or dopamine. Other hormones such as renin, aldosterone and atrial natriuretic peptide were also not changed during carmoxirole administration. No significant effect of carmoxirole could be demonstrated on the intracellular concentration of Na+, K+, Mg2+ and Ca2+ and on the transmembrane fluxes of Na+ and K+ in erythrocytes and platelets. In the carmoxirole-treated subjects (n = 16), 6 subjects reported spontaneously adverse events such as syncope, dizziness and vomiting tendencies and/or fatigue.
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PMID:Erythrocyte and platelet cationic concentrations and transport systems in normal volunteers treated with carmoxirole. 790 90

We report on diagnostic and differential diagnostic considerations in the case of a 30 year old Italian woman with hypokalemic alkalosis, fatigue and muscular weakness. The symptoms were caused by a Bartter syndrome with distinctly increased renin but almost normal aldosterone levels in the serum and increased aldosterone values in the urine.
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PMID:[Hypokalemia in the course of a Bartter syndrome]. 801

The pharmacokinetics and pharmacodynamics of the ACE inhibitor quinaprilat have been studied in six chronic haemodialysis (HD) patients and in six patients undergoing continuous ambulatory peritoneal dialysis (CAPD) after a single oral dose of 2.5 mg quinapril. Mean tmax and Cmax values (SEM) for quinaprilat in interdialytic HD patients were 4.0 (0) h and 84 (8.4) ng.ml-1 respectively, and they did not differ significantly from those in CAPD patients (4.7 (0.7) h and 64 (5.7) ng.ml-1). Elimination half lives were 30 (10.1) h (HD) and 34 (7.3) h (CAPD). Cmax, tmax, t1/2, and AUC were increased and CL was decreased compared to data reported previously after giving 2.5 mg to healthy subjects. Peritoneal clearance was calculated as 0.1 (0.1) ml.min-1, thus less than 0.5% of the dose were removed within 24 h by CAPD. ACE activity was suppressed by more than 93% between 4 and 24 h postdose (P < 0.001). It decreased in both groups with increasing plasma quinaprilat levels. Angiotensin II concentration compared to baseline was significantly decreased at 4 hours (-30.4 +/- 10%) and 24 h (-30 +/- 9.9%) (P < 0.05, n = 11), while active plasma renin concentration was still significantly increased at 48 h postdose (+ 60.2 +/- 14.5%, P < 0.01). Mean arterial pressure 24 h postdose was significantly (P < 0.05) decreased in HD (-12 mmHg) and CAPD patients (-20 mm Hg). Only two patients reported unwanted effects (fatigue, dizziness, nausea, and weakness). In conclusion, due to its long lasting effect on ACE activity and on blood pressure in terminal renal failure a starting dose of quinapril 2.5 mg o.d. may be used in hypertensive HD and CAPD patients.
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PMID:Pharmacokinetics and pharmacodynamics of quinaprilat after low dose quinapril in patients with terminal renal failure. 838 27

Hyperaldosteronism owing to aldosterone-producing adenoma (Conn syndrome) is a rare but potentially curable form of pediatric hypertension. The authors report on a 5-year-old girl who had symptoms of polyuria, polydipsia, and fatigue, and for whom the diagnosis of hyperaldosteronemia was suggested by a low serum potassium level and persistent hypertension. The diagnosis was confirmed by increased levels of plasma aldosterone and decreased levels of plasma renin. The tumor was localized with ultrasonography and computed tomography, which showed a 2-cm mass in the left adrenal gland. The left adrenal gland was excised, and pathological assessment showed an adenoma. Only 14 other pediatric cases (< 16 years of age) have been reported in the English-language literature.
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PMID:Conn syndrome in a child, caused by adrenal adenoma. 870 18

Over the past 40 years primary hyperparathyroidism (PHP) has changed from a rare, severe disease of the bones and kidneys to a common disease with hypertension, peptic ulcer, pancreatitis, easy fatigue and proximal muscle weakness. We have during these 40 years examined one of the greatest group of patients with PHP. PHP had its maximum incidence in women over the age of 40. The disease is four times frequent in women as in man. The incidence of hypertension and peptic ulcer between patients with PHP is higher as compared with the incidence of these diseases in general populations. The severity of bone changes in individual patients with PHP does not result from the direct action of a single hormone only. Parathyroid hormone (PTH) have hypotensive and vasodilator effects on various vascular beds. The resting blood flow in the limbs of our patients with PHP is increased in comparison with control subjects. PTH increases plasma renin activity in normotensive controls. This effect is partly blocked by beta adrenergic blockers.
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PMID:[Primary hyperparathyroidism]. 871 83


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