Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renin-angiotensin system has a wide range of physiological actions, and thus interference with the system has attractive therapeutic potential. The orally active angiotensin converting enzyme (ACE) inhibitors have so far been the most successful drugs in this area. They lower arterial pressure both in renovascular and essential hypertension, and their effects are enhanced by concomitant diuretic therapy or dietary salt restriction. Since, in renovascular hypertension, the affected kidney depends on enhanced local generation of angiotensin II to help preserve its function, the circulation and excretory capacity of this kidney may be compromised with ACE inhibition. ACE inhibitors can improve exercise tolerance and diminish cardiac ventricular arrhythmias in patients with heart failure. Because these drugs lower plasma aldosterone, they tend to correct potassium deficiency and hypokalemia, which may have been induced by diuretic treatment. Hypotension can occur with the first dose of ACE inhibitor, especially in sodium-depleted subjects; in patients on prior antihypertensive therapy, particularly if this includes a diuretic; and in the elderly. Not all of the actions of ACE inhibitors are necessarily due to lowering of plasma angiotensin II: accumulation of kinins may be responsible for some of the effects and side effects. Common to all ACE inhibitors are occasional rashes, cough, and, more rarely, angioedema. Apparently peculiar to captopril, and less often seen with the lower doses now employed, are taste disturbance, proteinuria, and marrow depression. ACE inhibitors, should not be used in pregnant women.
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PMID:Converting enzyme inhibitors in the treatment of hypertension. 248 62

To investigate the significance of the electrocardiographic (ECG) pattern of left ventricular hypertrophy and strain, two groups of asymptomatic patients with essential hypertension were compared. The patients were similar in terms of age, smoking habit, serum cholesterol and blood pressure levels, but differed in the presence (Group I, n = 23) or absence (Group II, n = 23) of the ECG pattern of left ventricular hypertrophy and strain. Group I patients had significantly more episodes of exercise-induced ST segment depression (14 versus 4, p less than 0.05) and reversible thallium perfusion abnormalities (11 of 23 versus 3 of 23, p less than 0.05) despite similar exercise capacity and absence of chest pain. Nonsustained ventricular tachycardia was detected on 24 h ambulatory ECG monitoring in two patients in Group I, but no patient in Group II. Coronary arteriography performed in 20 Group I patients demonstrated significant coronary artery disease in 8 patients. This study has shown that there is a subgroup of hypertensive patients with ECG left ventricular hypertrophy and strain who have covert coronary artery disease. This can be detected by thallium perfusion scintigraphy, and may contribute to the increased risk known to be associated with this ECG abnormality.
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PMID:Pathophysiologic assessment of left ventricular hypertrophy and strain in asymptomatic patients with essential hypertension. 252 59

Microvascular angina - chest pain syndrome in the presence of angiographically normal epicardial coronary arteries and reduced flow reserve - has been also described in patients with essential hypertension and it has been linked to the development of left ventricular hypertrophy. Dipyridamole-Echocardiography Test (DET: 2D-echo and 12 lead ECG monitoring with dipyridamole infusion, up to 0.84 mg/kg over 10') was performed in 28 essential hypertensives meeting the following inclusion criteria; 1) history of chest pain; 2) angiographically normal coronary arteries; 3) normal resting regional and global left ventricular function. A group of 12 (age and sex matched) normotensives with the same inclusion criteria, as well as with negative exercise stress test, was also evaluated. During DET, none, either in essential hypertensives or in control group, developed a regional dyssynergy of contraction; 15 in essential hypertensives, and 2 in control group had a diagnostic (greater than 0.1 mVolt from baseline) ST segment depression on ECG tracing (54 vs 17% p less than 0.01); 16 in essential hypertensives and 2 in control group had chest pain (57 vs 17%, p less than 0.01). None of the control group and 9 of the essential hypertensives had echocardiographically assessed left ventricular hypertrophy. In the essential hypertensives group, ventricular hypertrophy was present in 7/20 patients with and in 2/8 patients without dipyridamole induced chest pain and/or ST segment depression (35 vs 25%, p = ns). In conclusion, essential hypertensives patients with chest pain and angiographically normal coronary arteries frequently show "echocardiographically silent" angina and/or ST segment depression during DET. The presence of ventricular hypertrophy does not appear to be a prerequisite for the induction of angina in these patients.
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PMID:[The dipyridamole-echo-ECG test in hypertensives with microvascular angina]. 253 Apr 14

In a double-blind study of 30 elderly patients with mild to moderate essential hypertension, the antihypertensive effects of ketanserin and methyldopa were compared. The patients were randomly assigned to receive 20 mg of ketanserin or 250 mg of methyldopa twice daily for two weeks; the dose was then doubled for the rest of the three-month period. Two of the ketanserin group dropped out of treatment, one because of psychic depression, the other because of epigastric pain. After three months of therapy with ketanserin, systolic blood pressure decreased in a dose-dependent manner from 190 +/- 20 to 175 +/- 20 mmHg (P less than 0.05) and diastolic blood pressure from 106 +/- 8 to 91 +/- 9 mmHg (P less than 0.001). Blood pressure was reduced to 160/90 mmHg or less in eight of the 13 ketanserin patients and in five of the 15 methyldopa patients. In both groups heart rate and body weight remained constant. No orthostatic hypotension or hypertensive rebound after ketanserin withdrawal was recorded. It is concluded that 40 mg of ketanserin twice daily can control hypertension in the elderly.
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PMID:Ketanserin in mild to moderate hypertension in the elderly: a double-blind study versus methyldopa. 266 64

Forty patients with sick sinus syndrome, 15 women and 25 men with a mean age of 53.83 +/- 13.34 years, were studied using a maximal graded bicycle stress test. None of the patients were using a pacemaker or being treated with drugs that would interfere with the sinus node function; one patient had family myocardiopathy and eight suffered from essential hypertension. All patients, including those suffering from very marked bradycardia (less than 40 beats/min) responded to the increased effort with increased heart rate. The exercise test was stopped in 22 patients (55%) after the appearance of clinical signs and in 4 (10%) after ST-segment depression greater than 1 mm. Eight (20%) finished the stress test after reaching the maximal heart rate according to age, due to an increase in sinus rate. The exercise produced or increased extrasystoles in five patients (12.5%), but only one was forced to suspend the test. The Q-T interval, corrected for heart rate according to Bazett's formula (QTc), was measured on the resting ECG before the start of the test and on the ECG recorded immediately following the end of the exercise in all patients, except one with atrial fibrillation. In 24 patients (60%), a QTc mean increase of 0.040 +/- 0.022 sec was observed at the end of the stress test. Fourteen (35%) had the usual shortening due to the increase in heart rate. One patient showed no variation of the QTc. A lengthening of the QTc at the end of the exercise in more than half of the patients was the most intriguing electrocardiographic change.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postexercise electrocardiographic and clinical changes in patients with sick sinus syndrome. 270 31

The side-effect profile of labetalol was assessed in 34 patients with mild to moderate essential hypertension who had previously experienced side effects during beta-blocker therapy. The most frequently reported beta-blocker side effects were fatigue, impotence, cold extremities, and depression. After discontinuing their previous beta-blocker for 4 weeks, labetalol was titrated (100-400 mg b.i.d.) to achieve blood pressure control. Twenty-seven of 34 patients did not have a recurrence of a beta-blocker related side effect while receiving labetalol. The most common new side effect with labetalol was dizziness (3 patients). As judged by the attending physician and the patient, labetalol was better tolerated than conventional beta-blocker therapy in 30 of 34 patients (88%). Twenty-four of 34 patients (71%) preferred labetalol over previous therapy. Labetalol controlled blood pressure in 30 of 34 patients (88%). At equal antihypertensive doses, some side effects common to beta-blockers are seen less frequently with labetalol.
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PMID:Comparative tolerability of labetalol versus propranolol, atenolol, pindolol, metoprolol, and nadolol. 287 65

A double-blind, multicenter study compared the safety and efficacy of oral betaxolol 10 to 40 mg once daily (n = 68) with propranolol 40 to 160 mg twice daily (n = 73) in the treatment of mild to moderate essential hypertension. Both agents produced significant (P less than 0.01) and comparable reductions in mean supine systolic and diastolic blood pressures (7/11 mm Hg on betaxolol and 9/10 mm Hg on propranolol). Both betaxolol and propranolol significantly (P less than 0.01) reduced mean supine heart rate by 9 beats per minute. Patients achieved a more significant (P less than 0.01) reduction in blood pressure earlier (weeks 2 and 4 of the titration period) with betaxolol. By the end of treatment there was no significant difference in response between treatment groups. A higher incidence of central nervous system side effects (insomnia, bizarre dreams, depression, hallucinations, dizziness), however, was seen with propranolol than with betaxolol. Overall, the data show that in patients with mild to moderate essential hypertension, betaxolol 10 to 40 mg administered once daily is as effective as and better tolerated than propranolol 40 to 160 mg administered twice daily.
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PMID:Comparison of betaxolol, a new beta 1-adrenergic antagonist, to propranolol in the treatment of mild to moderate hypertension. 290 Dec 66

Microvascular angina--chest pain syndrome in the presence of angiographically normal epicardial coronary arteries and reduced flow reserve--has been described in patients with essential hypertension (EH) and linked to the development of left ventricular hypertrophy (LVH). We performed a dipyridamole-echocardiography test (DET: 2D-echo and 12 lead ECG monitoring with dipyridamole infusion, up to 0.84 mg/kg over ten minutes) in 28 essential hypertensives meeting the following inclusion criteria: (1) history of chest pain; (2) angiographically normal coronary arteries; (3) normal resting regional and global left ventricular function. A group of 12 (age- and sex-matched) normotensives with the same inclusion criteria, as well as with negative exercise stress test, was also evaluated. During DET, none of the essential hypertensives or the control group developed a regional dyssynergy of contraction. Fifteen essential hypertensives and two in the control group had a diagnostic (greater than 0.1 mV from baseline) ST segment depression on ECG tracing (54 v 17%, P less than .01); 16 essential hypertensives and two in the control group had chest pain (57 v 17%, P less than .01). None of the control group and nine of the essential hypertensives had echocardiographically assessed LVH. In the essential hypertensive group ventricular hypertrophy was present in seven of 20 patients with and in two of eight patients without dipyridamole induced chest pain and/or ST segment depression (35% v 25%, P = NS). In conclusion, essential hypertensive patients with chest pain and angiographically normal coronary arteries frequently show echocardiographically silent angina and/or ST segment depression during DET.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dipyridamole-echocardiography test in essential hypertensives with chest pain and angiographically normal coronary arteries. 291 48

We investigated the effect of the calcium antagonist nifedipine upon the following parameters: systolic and diastolic blood pressure (SBP and DBP) heart rate (HR), electrocardiogram (ECG) and the relative rate of calcium uptake in platelets. The possible correlation between this rate and blood pressure was one of the main points we tried to establish. The subjects studied were 1) 26 patients with uncomplicated essential hypertension and 2) 13 healthy normotensive subjects. SBP and DBP were measured with the subject both in a recumbent and a sitting position. 10 mg of nifedipine were given orally. In the hypertensive patients SBP and DBP decreased significantly in both positions after receiving the drug, as expected, while HR increased significantly (P less than 0.001), also in both positions. In the normotensive subjects BP decreased too, after taking the drug, but was only significantly modified in some instances i.e. SBP recumbent, DBP recumbent and sitting. HR increased significantly in the sitting position but not in the recumbent position. The ECG post-nifedipine showed a negative depression of the ST segment in four patients from the hypertensive group. The relative rate of calcium uptake in platelets measured before the subjects had taken the drug decreased after it was administered. The difference was significant (P less than 0.05) in the hypertensive group, but not in the normotensive group. Some correlation was found between DBP and the rate of calcium uptake.
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PMID:[Effects of a calcium antagonist (nifedipine) in hypertensive and normotensive subjects]. 296 12

Nisoldipine is an orally administered calcium entry blocking drug structurally related to nifedipine. In limited clinical trials it has been shown to be effective and relatively well tolerated in the treatment of patients with chronic stable angina pectoris and mild to moderate essential hypertension. As for all dihydropyridine-calcium antagonists, its major properties include potent peripheral and coronary vasodilation and improvement in myocardial oxygen supply relative to demand. These actions occur without depression of cardiac conduction or left ventricular function. Short term clinical trials have shown nisoldipine to produce both symptomatic and objective improvements in patients with chronic angina of effort and have suggested a benefit in vasospastic angina. A small number of comparative trials indicate that nisoldipine is equally as effective as nifedipine. In addition, in combination with beta-adrenoceptor blockade nisoldipine appears to offer additional benefit compared with beta-blockade alone and is well tolerated. In patients with mild to moderate essential hypertension nisoldipine monotherapy, in 1 or 2 daily doses, has maintained blood pressure control and has also been a useful addition to diuretics and beta-adrenoceptor blocking drugs in patients with poorly controlled disease. Side effects appear to be dose related, generally mild and transient, and are primarily those resulting from potent peripheral vasodilation - headache, flushing and pretibial or ankle oedema. Although studies to date are promising, there are no published long term studies (greater than 1 year) of nisoldipine in comparison with other calcium entry blockers and other drugs currently in clinical use for the treatment of angina pectoris or hypertension. Until such studies are completed the exact place of nisoldipine in the treatment of these diseases remains to be established.
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PMID:Nisoldipine. A preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in the treatment of angina pectoris, hypertension and related cardiovascular disorders. 306 58


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