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Acute lipoprotein changes associated with atenolol therapy for hypertension in non-insulin dependent diabetes

M D Feher1, D J Torrens, W Richmond

  • 1Department of Clinical Pharmacology, St. Mary's Hospital Medical School, London, UK.

Journal of Human Hypertension
|December 1, 1988
PubMed

Insights

Beta-blocker withdrawal in diabetic patients significantly altered lipid profiles, increasing HDL cholesterol and decreasing triglycerides. These changes reversed upon atenolol reintroduction, showing short-term reversibility without affecting blood pressure control.

Area of Science:

  • Cardiology
  • Endocrinology
  • Pharmacology

Background:

  • Hypertension and diabetes often coexist, necessitating careful medication management.
  • Beta-blockers are commonly used for hypertension, but their effects on lipid profiles in diabetic patients require further investigation.

Purpose of the Study:

  • To assess the influence of atenolol withdrawal and reintroduction on lipid and lipoprotein profiles in hypertensive, non-insulin dependent diabetic subjects.
  • To determine if atenolol-induced lipid changes are reversible and if they occur independently of blood pressure control.

Main Methods:

  • A study involving 11 stable hypertensive non-insulin dependent diabetic subjects.
  • A three-week placebo phase followed by atenolol (100mg) reintroduction.
  • Monitoring of pulse rate, blood pressure, weight, and lipid/lipoprotein parameters (cholesterol, triglycerides).

Main Results:

  • Withdrawal of atenolol led to significant increases in pulse rate, HDL-cholesterol, and HDL2-cholesterol, with a significant decrease in triglycerides.
  • Reintroduction of atenolol reversed these lipid and lipoprotein changes.
  • Weight and blood pressure remained stable throughout the study.

Conclusions:

  • Atenolol-induced lipid and lipoprotein alterations in non-insulin dependent diabetes are reversible in the short term.
  • These reversible changes occur without significant alterations in blood pressure control.
  • Future research should consider beta-blocker-induced lipoprotein changes in the context of diabetic macrovascular complications.

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