Effects of atenolol, doxazosin, and enalapril on measures of insulin metabolic syndrome and cardiovascular function at rest and in response to stress in hypertension

Date of Award




Degree Name

Doctor of Philosophy (Ph.D.)



First Committee Member

Barry Hurwitz - Committee Chair


The purpose of the current investigation was to gain a clearer understanding of the cardiovascular changes which occur as treatment effects of doxazosin, atenolol and enalapril. A randomized, double blinded crossover design with a placebo condition was used in this design. Assessment of cardiac output (Q), total peripheral resistance (TPR), and the contractility estimate Heather Index (HI) were examined in the context of treatment differences both at rest and in response to two behavioral stressors.When the entire sample was examined, treatment with atenolol, doxazosin, and enalapril produced few changes in Insulin Metabolic Syndrome (IMS) risk factors relative to placebo condition. Blood pressure reductions were achieved primarily through decreases in peripheral resistance during treatment with doxazosin, atenolol, and enalapril. All tasks produced significant reactivity during all conditions, and speech delivery consistently produced the greatest change in cardiovascular functioning. Treatment with atenolol produced a decrease in heart rate reactivity to mirror tracing, speech preparation, and speech delivery tasks relative to heart rate reactivity observed during treatment with placebo, doxazosin, and enalapril.When IMS and cardiovascular measures were examined in the context of blood pressure response to medication and blood pressure determinant decrease, differences between groups were uncovered. Specifically, individuals who responded to a medication with a greater decrease in Q relative to TPR displayed greater negative metabolic changes in response to medications, especially in regard to glycemic control. This group was also was less able to respond to the anti-hypertensive effects of the medications, as decreases in Q were countered by compensatory increases in TPR, and relatively greater increases in TPR to vascularly-challenging stressors.The investigation of change in IMS measures was aided by the identification of subgroups based on underlying hemodynamic regulation. Specifically, relationships which were difficult to interprete were clarified somewhat when interpreted in the context of blood pressure response, and clarified still more when interpreted in the context of blood pressure determinant changes. The validity of the conclusions about IMS changes is supported when such changes can be identified consistently and associated with known metabolic and physiological processes. These findings are consistent with the model proposed by Hurwitz and Schneiderman (1998), and support the assertion that risk factors for cardiovascular disease are complexly interwoven and likely cannot be addressed through only modifying disease midpoints such as high blood pressure.


Psychology, Physiological

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