Excess Catecholamine Syndrome and metabolic syndrome
Hypertension is often associated with metabolic disorders involving particularly insulin resistance. This decreased insulin sensitivity leads to a compensatory hyperinsulinemia that is commonly accompanied with hypertriglyceridemia and a raised sodium and uric acid re-absorption of the kidney. In the last years, these symptoms have been referred to as " metabolic syndrome" or "syndrome X" (1). Characteristics of the metabolic syndrome are hypertension, insulin resistance, hyperinsulinemia, hypertriglyceridemia, hyperuricemia and reduced HDL-cholesterol.
    The majority of persons with symptoms of the metabolic syndrome are overweight. The PROCAM study has shown (2) that in parallel to the increase in body mass index those parameters are increased that have been summarized under the term metabolic syndrome.
A prolonged hypercaloric diet intake is expected to induce insulin resistance and hyperinsulinemia. An increased sympathetic tone can amplify insulin resistance involving several mechanisms, i.e. acute and chronic reactions. An acutely raised sympathetic activity increases the glucose output of the liver while the insulin secretion of the beta-cells of the pancreas becomes relatively diminished. If a teleological viewpoint would be justified  then one could argue that this mechanism garantuees the supply of glucose for the insulin-independent glucose use of the brain that is mobilized by epinephrine when food shortage occurs. At the same time, the lipolysis induced increase in plasma fatty acids causes a further reduction of peripheral glucose utilization ("Randle cycle").
    Chronic modifications in the morphology of skeletal muscle contribute to a further reduction in insulin sensitivity. The arteriolar density of skeletal muscle becomes reduced ("rarefaction") leading to increased diffusion distances for oxygen and probably also glucose (3) after a chronic beta2-adrenergic stimulation. Furthermore, the proportion of fast fibers with a lower glucose oxidation becomes increased at the expense of slow muscle fibers (4).

Although the hyperinsulinemia can initially prevent hyperglycemia, this state can frequently not be maintained and diabetes mellitus type II ensues. B-cells of the pancreas are limited in their production of insulin. Oral antidiabetic drugs lead to an increased insulin release for preventing hyperglycemia. A consequence is that organs that do not become insulin-resistant are exposed to higher insulin levels.
    The insulin resistance of the body arises predominantly from a reduced insulin sensitivity of skeletal muscle, i.e. it represents a selective insulin resistance. Organs that are not insulin resistant are influenced by the higher insulin levels. In the liver, an increased triglyceride and LDL synthesis ensues and in the kidney the re-absorption of sodium and uric acid is increased. The hyperinsulinemia associated reactions amplify, therefore, direct effects of a raised sympathetic nervous system activity.
    Since the centrally acting antihypertensive drug moxonidine ( Physiotens, Moxon, Cynt, Moxol and Normatens) was shown to increase insulin sensitivity of overweight insulin-resistant hypertensive patients (5) it is expected to reduce also other negative effects arising from hyperinsulinemia.


1. Reaven GM: Banting lecture 1988. Role of insulin resistance in human disease. Diabetes 1988;37:1595-1607
2. Assmann G, Schulte H: Results and conclusions of the Prospective Cardiovascular Münster (Procam) Study, in Assmann G (ed): Lipid Metabolism and Coronary Heart Disease. München, MMV-Verlag, 1993, pp 19-67
3. Suzuki J, Gao M, Xie Z, Koyama T: Effects of the beta 2-adrenergic agonist clenbuterol on capillary geometry in cardiac and skeletal muscles in young and middle-aged rats. Acta Physiol Scand 1997;161:317-326
4. Zeman RJ, Ludemann R, Easton TG, Etlinger JD: Slow to fast alterations in skeletal muscle fibers caused by clenbuterol, a beta 2-receptor agonist. Am J Physiol 1988;254:E726-32
5. Haenni A, Lithell H: Moxonidine improves insulin sensitivity in insulin-resistant hypertensives. J Hypertens 1999;17 Suppl 3:S29-35