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Systemic arterial hypertension is strongly linked to metabolic issues like insulin resistance, forming a hypertensive metabolic syndrome. Addressing insulin resistance through lifestyle changes can improve blood pressure management and treatment effectiveness.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Metabolic Syndrome
Context:
- Systemic arterial hypertension frequently co-occurs with metabolic abnormalities, affecting up to 80% of patients.
- This cluster of symptoms, including impaired glucose tolerance, obesity, and hyperlipoproteinaemia, is termed hypertensive metabolic syndrome, closely related to Syndrome X.
Purpose:
- To explore the common pathogenetic basis linking hypertension and metabolic deviations.
- To elucidate the role of insulin resistance and hyperinsulinism in the development and progression of hypertensive metabolic syndrome.
Summary:
- Reduced tissue sensitivity to insulin (insulin resistance) leads to compensatory hyperinsulinism.
- Hyperinsulinism contributes to hypertension via sympathetic nervous system activation, sodium retention, altered electrolyte transport, vascular remodeling, and accelerated atherosclerosis.
- Hyperinsulinemia is associated with resistance to antihypertensive treatments, which can be overcome by reducing insulin resistance through non-pharmacological interventions.
Impact:
- Understanding the link between insulin resistance and hypertension is crucial for managing metabolic syndrome.
- Non-pharmacological interventions targeting insulin resistance can enhance the efficacy of antihypertensive therapies.
- This research highlights the genetic basis of insulin resistance and its diverse phenotypic manifestations in cardiovascular and metabolic diseases.
Abstract:
Systemic arterial hypertension is not merely a simple haemodynamic abnormality. It is as frequently as in 80% associated with metabolic deviations such as impaired glucose tolerance or NIDDM, obesity, hyperuricaemia, hyperlipoproteinaemia, rapid development of atherosclerosis. This cluster of different symptoms with higher BP readings is too frequent to be incidental. We speak therefore of hypertensive metabolic syndrome which is close to or identical with Reaven's syndrome X or familial dyslipidaemic hypertension. The common pathogenetic basis of the listed metabolic deviations and hypertension is probably genetic or acquired reduction of tissue sensitivity, in particular striated muscle sensitivity to the physiological action of insulin. The consequence of this insulin resistance and the effort to maintain euglycaemia is a compensating adaptational risk of plasma insulin. Hyperinsulinism in addition to an increased synthesis of triacylglycerols, VLDL and LDL lipoproteins can promote the rise of BP by a complex mechanism: it stimulates the activity of the sympathetic nervous system, it promotes sodium retention in the kidneys, it affects transmembrane transport mechanisms for electrolytes and an increase of intracellular sodium and calcium, it stimulates hypertrophy and remodelling of the vascular wall and hastens the development of atherosclerosis. Hyperinsulinaemia is also associated with resistance of hypertonic patients to antihypertensive treatment. Its reduction by non-pharmacological procedures (reduction of body weight, physical activity etc.) restore the effectiveness of antihypertensive drugs. Insulin resistance is most probably a genetically conditioned abnormality which has multiple phenotypic manifestations, depending how this congenital disposition is amplified or associated with other genetic abnormalties or external and internal factors.(ABSTRACT TRUNCATED AT 250 WORDS)