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Jenna R. Disser MS, Doctoral Candidate & Robert A. Larson MS, PhD Assistant Professor—Human Biology

Department of Biological Sciences, Michigan Technological University

Disser's Abstract:

Familial hypertrophic cardiomyopathy (HCM) is the most common genetic heart disease with an estimated prevalence of 1:500 individuals in the general population. Sarcomere gene mutations result in the characteristic features of HCM include left ventricular (LV) hypertrophy, myocyte disarray, interstitial fibrosis, diastolic dysfunction, and high risk of cardiac arrhythmias and sudden death. Human studies in patients with HCM have demonstrated increased cardiac norepinephrine (NE) spillover partly due to reduced neuronal NE reuptake through the neuronal norepinephrine transporter. Our lab has previously reported that conscious alpha-tropomyosin mutant HCM mice have increased cardiac sympathetic tone compared to littermate wild-type (WT) controls. In this study we examined NE levels with an ELISA in the right atrium, left ventricle and the stellate ganglia (cell bodies for the cardiac nerves) in WT and HCM mice. In addition, we will discuss the influence of endogenous neuronal vesicular NE release with tyramine on cardiac function in WT and HCM mice.

Larson's Abstract:

Sympathetic nerve activity (SNA) is known to demonstrate rhythmic activity that is synchronized with the respiratory and the cardiac cycles. These oscillations arise through integration of signals from lung inflation afferents, baroreceptor afferents, and respiratory neurons in the brainstem that influence presympathetic neurons in the rostral ventrolateral medulla (RVLM). The hypothalamic paraventricular nucleus (PVN) is a prominent regulatory center for SNA and PVN neurons have axon projections to the RVLM. Blockade of small conductance calcium-activated potassium (SK) channels in the PVN significantly increases splanchnic and renal SNA and dysfunction of SK channels contributes to the pathogenesis of hypertension. In this study, we analyzed SNA in the frequency domain by calculating power spectral density on 5-minute segments of data. We will discuss similarities and differences in power spectral density in the low (0-2Hz) and high (5-7Hz cardiac) frequency bands at baseline, and after PVN microinjection of the SK channel blocker apamin in control and angiotensin II-infused rats.