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 interaction of the benzothiazolamine R 56865 with the nifedipine-sensitive component of the serotonin (5-HT)-, angiotensin II (AII)- and arginine-vasopressin (AVP)-induced contractions was studied in the isolated rat aorta. Nifedipine caused concentration-dependently (10(-9)-10(-6) mol/l) a slight rightward shift accompanied by a limited depression of the maximum of the concentration-response curves for 5-HT-, AII- and AVP-induced contractions. R 56865 (10(-5) mol/l) antagonized the contraction elicited by 5-HT and AII in a similar manner as nifedipine. The effect of R 56865 on 5-HT- and AII-induced contractions was no longer observed after pretreatment with nifedipine. The AVP-induced contraction was not affected by R 56865 (10(-5) mol/l). As shown previously, R 56865 is a weak inhibitor of potential-operated channels but inactive on Ca2+ channels activated by NA. In conclusion, R 56865 does not only differentiate between depolarization and receptor-stimulation, but also between the activation of Ca2+ channels by different types of receptors. We propose that R 56865 may interact with Ca2+ channels at a site which plays a role in their activation.
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PMID:R 56865 differentiates between contractile agents with respect to the nifedipine-sensitive component in the isolated rat aorta. 255 25

The Nifedipine-Total Ischemia Awareness Program was designed to evaluate the prevalence, prognostic implications and effect of therapy on painful and painless myocardial ischemic episodes in a nationwide study of patients with angina pectoris. Three hundred forty-eight patients with at least 2 anginal attacks/week while taking antianginal medications were enrolled at 53 participating centers between September 1, 1986 and March 31, 1988; 312 of the 348 patients formed the study group, while 36 patients formed the control group. At least 1 episode of ST-segment depression during two 48-hour periods of Holter monitoring was present in 136 of the 312 patients in the study group. In these 136 patients, there was a total of 372 episodes of ST-segment depression, of which only 69 (18%) were painful; 85% of the 136 patients had either painless episodes only or both painless and painful episodes. Despite apparently adequate antianginal therapy, 48 patients had greater than or equal to 3 episodes of ST-segment depression/48 hours of ambulatory electrocardiographic monitoring, and 38 patients greater than 60 minutes of ST-segment depression. After nifedipine was administered, there was a 23% reduction in the mean number of episodes of ST-segment depression (2.7 +/- 0.3 to 2.1 +/- 0.2, p less than 0.01). The most pronounced effects were found in the 48 patients with greater than or equal to 3 episodes of ST-segment depression and the 38 patients with greater than or equal to 60 minutes of total ischemic time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The Nifedipine-Total Ischemia Awareness Program: a national survey of painful and painless myocardial ischemia including results of antiischemic therapy. 256 24

A placebo-controlled, double-blind, crossover study was conducted to determine the effects of nifedipine (60 to 90 mg per day) monotherapy and propranolol (240 mg per day) monotherapy on symptoms, angina threshold, and cardiac function in patients with chronic stable angina. Following a two-week placebo period, patients were randomly assigned to receive either nifedipine or propranolol for a five-week treatment period, after which they crossed over to the alternative regimen. All 21 patients were men with chronic stable angina pectoris, 13 of whom had symptoms both at rest and on exertion. New York Heart Association functional class improved in patients taking either nifedipine or propranolol, and nitroglycerin consumption decreased with both treatments compared with placebo. Nifedipine significantly delayed the onset of chest pain and 1 mm of ST-segment depression during bicycle exercise; increases with propranolol were smaller and not statistically significant. Nine patients had a preferential clinical response to nifedipine compared with six patients to propranolol; this was unrelated to the presence or absence of pain at rest or to any baseline hemodynamic finding. Nifedipine and propranolol were equally effective in relieving exertional ischemia as shown by improvement in radionuclide ejection fraction at identical work loads. Exercise wall motion, assessed by a semiquantitative wall motion score, also improved with both drugs. Propranolol treatment decreased exercise cardiac output by 14 percent (p = 0.01) through its effect on heart rate. In contrast, nifedipine treatment had no effect on cardiac output. Thus, nifedipine is more effective on several measurements than propranolol when administered as single drug therapy in stable angina and has the advantage of preserving cardiac output during exercise.
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PMID:Chronic stable angina monotherapy. Nifedipine versus propranolol. 264 28

Despite decreasing cardiac mortality rates in the elderly since 1968, rates of health care service use by persons over age 65 years have progressively increased. The growing availability of potent and effective cardiovascular drugs, together with the high prevalence of untoward side effects in the elderly, make it important that we consider the influence of age on cardiovascular response to the calcium entry blockers. The age-related structural, functional, pharmacokinetic, and pharmacodynamic changes that occur in elderly patients suggest that careful monitoring, adjustment, and frequent reassessment of the medical regimen should be performed to minimize untoward effects. Nifedipine, diltiazem, and verapamil are all well absorbed orally, are extensively protein bound, and are metabolized by the liver. The age-associated attenuation in rates of hepatic metabolism and hepatic blood flow contribute to the decreased clearance and prolonged elimination half-lives of these drugs in the elderly. Advanced age can be associated with increased susceptibility to sinoatrial depression, fatigue, constipation, hypotension, and peripheral edema after calcium entry blockade, even at modest doses. It would be prudent, therefore, to administer these agents at lower doses and at less frequent intervals.
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PMID:Use of calcium entry blockers in elderly patients. Special considerations. 268 81

The influence of a 6-week treatment of female Wistar rats with one-kidney, one clip (1-K, 1 C) renal hypertension, with the calcium antagonist nifedipine on plasma volume, red cell Na+ handling and plasma atrial natriuretic peptide immunoreactivity (ANP-IR) was studied. Measurements were performed at 2 and 6 weeks after surgery. In 1-K, 1 C rats plasma volume was increased and red cell Na+ pump activity was reduced only after 2 weeks. Blood pressure, heart weights and plasma ANP were massively increased after both 2 and 6 weeks. 1-K, 1 C-rats treated with nifedipine had normal plasma volume, plasma ANP, and red cell Na+ pump activity in comparison with sham-operated rats. Increases in blood pressure and heart weights were attenuated. It is concluded that 1-K, 1 C hypertension in the rat is associated with cardiomegaly, rise in plasma ANP, initial hypervolemia and depression of the membrane Na+ pump. Nifedipine prevents the occurrence of hypervolemia and secondary phenomena such as rises in plasma ANP and cardiomegaly. This may play an important contributory role in the prevention of pathological sequelae.
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PMID:Modulation by chronic nifedipine of plasma atrial natriuretic peptide, cell Na+ transport and plasma volume in rats with renal hypertension. 284 89

Combined nitrate/beta-blocker/nifedipine therapy is commonly used to treat refractory angina pectoris. We have observed "paradoxical" myocardial ischemia in ten patients with refractory angina (seven receiving combined beta-blocker and nitrate therapy, and three receiving nitrate treatment alone) in whom nifedipine (mean dosage, 92 mg/day; range, 60 to 120 mg/day) induced a decrease in blood pressure, angina pectoris (10/10 patients), and ischemic ECG changes (7/10 patients). These ten patients, all of whom regularly reported angina within 20 to 30 minutes of nifedipine ingestion, were prospectively studied before and after usual nifedipine dose administration, while blood pressures, heart rate, and ECGs were recorded. Mean systolic BP fell from 109 to 94 mm Hg after nifedipine (P less than .001, paired t test); mean heart rate increased from 64 to 68 beats per minute (P less than .05); seven patients developed transient ECG changes (five with ST-T wave depression and two with ST-T wave elevation) during the hypotensive period. Nifedipine may provoke angina and myocardial ischemia in certain patients with refractory angina pectoris receiving concomitant beta-blocker and nitrate therapy.
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PMID:Nifedipine-induced hypotension and myocardial ischemia in refractory angina pectoris. 285 6

The ergometric effects of different vasodilator drugs in 5 series of 10 patients with stable angina and persistent effort ischaemia despite beta-offckade, were compared two by two in a random, single blind cross-over study under basal conditions on betablocker therapy and at the peak of their action, the second measurement being performed after a 2 to 7 day interval. The principal criteria of assessment were the work required to induce 1 mm ST depression (WST1), and the maximum ST depression (ST max) at comparable work loads. Molsidomine (2 mg), Risordan 20 mg) and Nifedipine (10 mg) significantly improved both parameters (p less than 0.001). Lenitral (7.5 mg), Langoran (40 mg), Trinitrin skin patch (10 mg) did not produce a significant improvement. Corditrine improved WST1 (p less than 0.05) and slow release Trinitrin (2.5 and 5 mg) improved WST1 at 3 hours (p less than 0.05) and ST max at 15 minutes (p less than 0.001) and 3 hours (p less than 0.05). The fall in resting blood pressure was parallel to the ergometric changes. These results suggest that Molsidomine, Nifedipine, Risordan and slow release Trinitrin (2.5 mg) are the most effective vasodilators when used in association with betablockers.
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PMID:[Randomized ergometric study of vasodilators combined with betablockaders]. 287 18

Calcium channel blocking agents function as negative inotropic agents when they are administered in vitro directly to the myocardium. In patients with coronary artery disease, however, such direct effects are attenuated by a number of other factors, including decreased afterload and resultant reflex sympathetic stimulation, increased coronary blood flow with improved myocardial perfusion, and protection of mitochondria. Nifedipine has not been observed to cause significant left ventricular depression in patients with angina pectoris; this is primarily due to peripheral arteriolar vasodilatation, which reduces impedance of left ventricular ejection. In addition, the relief of myocardial ischemia by nifedipine plays a major role in improving systolic and diastolic function. The clinical response to calcium channel blockers may differ in patients with idiopathic dilated cardiomyopathy, for whom the factor of fluctuating ischemia is less important.
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PMID:Effect of nifedipine on left ventricular function in patients with angina pectoris. 287 35

The effects of nifedipine (60 to 90 mg/day) and propranolol (240 mg/day) on symptoms, angina threshold and cardiac function were compared in a placebo-controlled, double-blind, crossover study. Five-week treatment periods with nifedipine and propranolol were compared with 2 weeks of placebo treatment in 21 men with chronic stable angina pectoris, 13 of whom had symptoms both at rest and on exertion. Compared with placebo, New York Heart Association functional class improved in patients equally with nifedipine (p = 0.001) and propranolol (p = 0.006). Frequency of chest pain decreased with nifedipine (p = 0.001) and propranolol (p = 0.01), and nitroglycerin consumption similarly decreased with both treatments. Nifedipine significantly delayed the onset of chest pain (p = 0.01) and 1 mm of ST-segment depression (p = 0.002) during bicycle exercise; smaller increases with propranolol were not statistically significant. A preferential clinical response to nifedipine (9 patients) or propranolol (6 patients) was unrelated to the presence or absence of pain at rest or to any baseline hemodynamic finding. Nifedipine and propranolol were equally effective in relieving exertional ischemia as shown by improvements in ejection fraction at identical workloads, from 0.48 +/- 0.11 to 0.58 +/- 0.12 (p less than 0.001) and 0.56 +/- 0.14 (p less than 0.001), respectively. Exercise wall motion, assessed by a semiquantitative wall motion score, also improved with both drugs. Propranolol treatment decreased exercise cardiac output by 14% (p = 0.01) through its effect on heart rate. In contrast, nifedipine treatment had no effect on cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of nifedipine alone with propranolol alone for stable angina pectoris including hemodynamics at rest and during exercise. 308 64

The effects of intracoronary injection of nitroglycerin, adenosine, nifedipine and prostacyclin on restoring coronary perfusion during flow-reducing partial coronary obstruction in anesthetized dogs were studied. Coronary obstruction was obtained by inflation of an intraluminal balloon to decrease coronary blood flow and rate of rise in left ventricular pressure (dP/dt) by approximately 30 to 40 and 10%, respectively. Nitroglycerin (0.01 to 10 micrograms/kg per min) increased coronary blood flow and distal coronary pressure and decreased stenosis resistance associated with improved left ventricular dP/dt depending on its dose. In contrast, adenosine (0.3 to 1.0 micrograms/kg per min) decreased coronary blood flow and distal coronary pressure and intensified stenosis resistance associated with depression of left ventricular dP/dt. Nifedipine and prostacyclin caused divergent effects on the coronary circulation related to each dose. Nifedipine (0.01 and 0.1 micrograms/kg per min) and prostacyclin (0.01 micrograms/kg per min) increased coronary blood flow and distal coronary pressure and reduced stenosis resistance. Nifedipine (1.0 micrograms/kg per min) and prostacyclin (0.3 micrograms/kg per min) did not increase coronary blood flow, but reduced distal coronary pressure and intensified stenosis resistance. Thus, the vasodilators produced different effects on restoration of coronary perfusion during pliable severe coronary stenosis. Nitroglycerin and lower doses of nifedipine and prostacyclin improved coronary perfusion due to selective or preferential dilation of large coronary arteries. Adenosine and higher doses of nifedipine and prostacyclin had deleterious effects on the coronary circulation due to potent arteriolar vasodilation.
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PMID:Comparative effects of intracoronary vasodilators on restoring coronary perfusion during flow-reducing coronary stenosis in the dog. 309 16


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