Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bopindolol is a nonselective beta blocker with mild intrinsic sympathomimetic activity. One of the drug's main benefits is its prolonged effect, lasting for 24 hours, which makes it possible to administer bopindolol in a single daily dose, a fact that may improve patient adherence to therapy. A double-blind study was performed in two centers, comparing bopindolol with metoprolol in 86 hypertensive patients. Baseline diastolic blood pressure (BP) was 100 to 120 mm Hg. The effects of bopindolol or metoprolol on BP and heart rate were similar: return to normal values was achieved in 70% of patients with either drug. A 6-month study at another center found that bopindolol did not affect the levels of total cholesterol, low-density and high-density lipoprotein cholesterol or triglycerides. Another 12-month study documented a decrease in total cholesterol, apolipoprotein (apo) A1 and apo B. The apo A/B ratio rose, thus improving the atherosclerotic index. No deterioration of glucose tolerance or immunoreactive insulin response to glucose was seen after 6 months of bopindolol administration. Bopindolol satisfactorily modifies not only resting but also exercise BP during isometric and isotonic load, thus reducing BP fluctuation during physical activities of the hypertensive patient. The drug exerts no effect on renal and liver function, electrolyte balance and hematologic parameters. Bopindolol is a very useful drug of first choice in mild and moderate hypertension. Bopindolol's main advantages include its prolonged action, good tolerance and a beneficial effect on risk factors of atherosclerosis (lipid and carbohydrate metabolism).
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PMID:Bopindolol: Czechoslovak experience with a new beta blocker in the treatment of hypertension. 167 80

High plasma cholesterol concentration is an important coronary heart disease risk factor, particularly in subjects less than 50 years old. Cholesterol is transported mainly by low (LDLs) and high (HDLs) density lipoproteins. High plasma levels of HDL and its apolipoprotein (A-I) are associated with low coronary heart disease risk, and the reverse is true for LDL and its apolipoprotein (B). Plasma levels of very low density lipoproteins (VLDLs) are probably not an independent risk factor, and the situation for plasma triglycerides is unclear. beta-Blockers have no significant effects on plasma concentrations of either total or LDL cholesterol, but HDL plasma concentration is reduced by about 10%, particularly by nonselective beta-blockers. Plasma triglyceride and VLDL concentrations are both raised by beta-blockade. Despite these plasma lipid changes, beta-blockers, by decreasing myocardial oxygen requirements, exhibit marked anti-ischemic properties. beta-Blockers without intrinsic sympathomimetic activity effect a 30% decrease in death from myocardial infarction (MI) in the years after an acute MI. Primary prevention of MI by beta-blockade in hypertensive persons has been well debated and probably exists (although to a lesser extent than secondary prevention) in men, particularly for nonsmokers (for nonselective beta-blockers), and despite any plasma lipid changes. beta-Blockade can inhibit the preatheromatous and atheromatous changes induced by catecholamines in the coronary arteries of animals. beta-blockers may also reduce or slow the following processes: 1) endothelial permeability to lipoproteins; 2) acylcholesterol acyltransferase activity within the arterial wall, thereby preventing cholesterol esterification and deposition in foam cells; 3) LDL precipitation with arterial wall proteoglycans; 4) calcium influx into atheromatous areas; 5) preatheromatous increased endothelial turnover; 6) heart rate; 7) blood velocity and flow disturbances; 8) atheromatous plaque rupture and consequent coronary thrombosis; and 9) platelet activity. Thus, beta-blockers may inhibit atheromatous plaque formation and reduce the likelihood of plaque beta-blockers may inhibit atheromatous plaque formation and reduce the likelihood of plaque rupture, clot formation, and coronary thrombosis.
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PMID:Beta-blockers, plasma lipids, and coronary heart disease. 197 24

Plasma lipoproteins were estimated in ten hypertensive subjects (mean age 51 +/- 11.2 yr), before, 6 wk and 6 mth following treatment with Sotalol 320 mg/day. Heart rate fell sequentially throughout the study (p less than 0.01) and although there was a sequential fall in mean blood pressure this did not reach statistical significance. There was a significant increase in plasma triglyceride concentration from a basal value of 1.87 +/- 1.064 to 2.50 +/- 0.877 mmol/l (p less than 0.005) at 6 mth. No significant change was found in very low density, low density and high density lipoprotein cholesterol or apolipoprotein concentrations (Apo A-I, Apo A-II, Apo B). We conclude that Sotalol exerts a similar influence on plasma lipoproteins as other non-cardioselective beta-adrenoceptor blockers without intrinsic sympathomimetic activity and its use does not constitute an increased risk of developing atherosclerosis, when compared with other beta-blockers.
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PMID:The effect of sotalol on plasma lipoproteins and apolipoproteins. 374 22