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)

The effects of beta-blockade on acute exercise-induced changes in plasma lipoprotein levels were investigated in 12 healthy normotensive subjects by use of beta-blockers of three types: a nonselective agent, a beta 1-selective agent, and a nonselective agent with intrinsic sympathomimetic activity (ISA) or partial agonist activity. Each subject received each drug and a placebo for 1 wk each according to a randomized double-blind crossover design. After placebo, exercise caused 10-20% increases in total plasma cholesterol and the high-density lipoprotein (HDL)-cholesterol fraction. The total-to-HDL cholesterol ratio fell, particularly during the 30-min recovery phase. Pindolol treatment increased resting values of HDL cholesterol (from 43 +/- 4 to 48 +/- 4 mg/dl) and potentiated the response to exercise (to 59 +/- 5 vs. 51 +/- 4 mg/dl after placebo). The total-to-HDL cholesterol ratio was significantly lower after pindolol treatment than after placebo. In contrast, neither atenolol nor timolol affected exercise-induced changes in plasma lipoprotein levels. The effects of pindolol on other study parameters (exercise endurance and exercise-induced increases in systolic blood pressure, heart rate, and potassium) were similar to the effects of the nonselective agent, timolol. We conclude that the effects of pindolol on the plasma lipid profile are due to its ISA and that the process activated (possibly plasma lecithin-cholesterol acyltransferase activity) is under minimal sympathetic control and, therefore, sensitive to the expression of ISA both at rest and in response to exercise.
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PMID:Beta-blockade with intrinsic sympathetic activity modifies favorably exercise-induced changes in plasma lipoproteins. 197 31

The objective of this article is to focus on the antihypertensive agents blocking adrenergic receptors, both alpha and beta blockers, and attempt to construct potential explanations for their effects on lipids in a mechanistic manner. The essential thesis is that adrenergic control of lipid metabolism is responsible for the effect on lipids and lipoproteins of antihypertensive agents that block adrenergic receptors. Agonists and antagonists show the opposite action on lipoprotein lipase, lecithin:cholesterol acyltransferase (LCAT) and LDL-cholesterol uptake by LDL receptors in a manner that might explain the findings of increases in triglycerides and LDL cholesterol with decreases in HDL cholesterol in patients receiving beta blockers without intrinsic sympathomimetic activity and the reverse in patients on treatment with alpha adrenergic receptor blockers.
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PMID:Mechanisms of action of adrenergic receptor blockers on lipids during antihypertensive drug treatment. 809 25