Adrenergic effects on plasma lipoprotein metabolism: Speculation on mechanisms of action

Sacks, Frank M.; Dzau, Victor J.

doi:10.1016/0002-9343(86)90163-4

Cited by 80 publications

(29 citation statements)

References 65 publications

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“…Additional factors include inhibition via hormonal manipulation by epinephrine, insulin, and glucagon. 31 Studies in humans show that during periods of hypoglycemic stress, production of VLDL and triglycerides is reduced. 35 The extent to which the triglyceride levels are reduced correlates with urinary epinephrine release but not norepinephrine.…”

Section: The Effects Of Adrenergic Agents On Plasma Lipoprotein Metabmentioning

confidence: 99%

Alpha‐adrenergic blockers: Mechanism of action, blood pressure control, and effects on lipoprotein metabolism

Nash

1990

Clinical Cardiology

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Summary: The sympathetic nervous system plays a major role in the pathogenesis of essential hypertension and is mediated by the a and P receptors. The a receptor is divided into two types, aI and a2, based on response to epinephrine and norepinephrine. a ,-Adrenergic receptors have a high affinity for drugs such as pmzosin, doxazosin, and terazosin, which act to reduce blopd pressure by selective blockade of the receptor. These agents provide a rational approach to the treatment of hypertension by correcting elevated total peripheral resistance, the fundamental hemodynamic abnormality in essential hypertension. In contrast, early a-adrenergic receptor blockers nonselectively blocked both a I and a2 receptors and were unsuitable as antihypertensive agents because they induced tachycardia and patients developed a tolerance to them rapidly. a,-Adrenergic blockers also have beneficial effects on plasma lipoproteins, tending to decrease levels of triglycerides and cholesterol and increase levels of highdensity lipoprotein (HDL) cholesterol and the HDL cholesterol/total cholesterol ratio. P-Adrenergic blockers, such as propranolol and atenolol, have been shown to have an adverse effect on the lipid profile by tending to increase levels of triglycerides and decrease HDL cholesterol. A number of mechanisms contribute to these effects, in particular, adrenergic modulation of lipoprotein lipase and the triglyceride secretion rate. Doxazosin has been shown to increase the activity of LDL receptors, which may be partly responsible for its beneficial effect on plasma lipids and lipoproteins. Doxazosin is different from other aIadrenergic inhibitors in that its maximal hypotensive effect occurs within 5 or 6 hours after administration in acute dosing studies, making first-dose postural hypotension unlikely, and its long half-life provides 24-h blood pressure control with once-daily dosing.

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Section: The Effects Of Adrenergic Agents On Plasma Lipoprotein Metabmentioning

confidence: 99%

Alpha‐adrenergic blockers: Mechanism of action, blood pressure control, and effects on lipoprotein metabolism

Nash

1990

Clinical Cardiology

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“…0-Blockers decrease hepatic and lipoprotein lipase activity, thus accounting for the increases in plasma trigryceride levels. 77 Although less extensively studied, /3-blockers with intrinsic sympathomimetic activity and those with combined a-adrenergic and 0-adrenergic receptor blocking properties do not appear to exhibit these adverse 72 Despite an adverse effect on the lipid profile, propranolol treatment was shown to decrease plaque formation in cholesterol-fed rabbits. 16 The relevance of this observation to human atherogenesis remains to be defined.…”

Section: Antihypertensive Therapy and Ljpidsmentioning

confidence: 99%