PSIO 303A Lecture 13: Lecture 13 - Cellular basis for hypertension in the Metabolic Syndrome_AF

• School: University of Arizona
• Department: Physiology
• Course: PSIO 303A
• Professor: Eric Price, Steven Wright, Nick Delamere

Document Summary

Lecture 13 - cellular basis for hypertension in the. Lecture objectives for the cellular basis for hypertension in the metabolic syndrome: Describe in general terms the prevalence of insulin resistance in individuals with hypertension, which can co-exist in the metabolic syndrome. Describe the mechanistic pathway of hyperinsulinemia and sns overactivity to long term adaptations in the vasculature than can lead to a hypertensive state in the metabolic syndrome. Defend the concept sns overactivity can lead to upregulation of the renin-angiotensin system and can contribute to hypertension and insulin resistance in the metabolic syndrome. Is there a connection between hyperinsulinemia and the onset and worsening of hypertension in the. During visceral adiposity (first thick band in yellow), there"s an increased level of bad adipokines and decreased levels of good adipokines (e. g. adiponectin) A insulin secretion increases, it eventually leads to hypertension. However, the transition at the beginning is a benign physiological response.