Exercise training increases GAD65 expression, restores the depressed GABAA receptor function within the PVN and reduces sympathetic modulation in hypertension
We applied physiological and molecular techniques to uncover the potential benefits of exercise training to rescue the autonomic dysfunction that characterizes the chronic phase of spontaneous hypertension. The main focus of the study was the GABAergic neurotransmission within the PVN. We observed that training augments the expression/activity of GABAergic neurotransmission within presympathetic PVN neurons and restores GABAA receptors ´ function, therefore strengthening GABAergic inputs which inhibit the sympathetic outflow in hypertension. AbstractGABAergic inhibitory input within the paraventricular hypothalamic nucleus (PVN) plays a key role in restraining sympathetic outflow. Although experimental evidence has shown depressed GABAA receptor function plus sympathoexcitation in hypertension and augmented GABA levels with reduced sympathetic activity after exercise training (T), the mechanisms underlying T ‐induced effects remain unclear. Here we investigated in T and sedentary (S) SHR and WKY: (1) time‐course changes of hemodynamic parameters and PVN glutamic acid decarboxylase (GAD) isoforms’ expression; (2) arterial pressure (AP) and heart rate (HR) responses, sympathetic/parasympathetic modu lation of heart and vessels and baroreflex sensitivity to GABAA receptor blockade within the PVN. SHR ‐S versus WKY‐S exhibited higher AP and HR, increased sympathetic reduced parasympathetic modulation, smaller baroreflex sensitivity, and reduced PVN GAD65 immunoreactivi...
Source: Physiological Reports - Category: Physiology Authors: Nilson C. Ferreira ‐Junior,
Adriana Ruggeri,
Sebastião D. Silva,
Thais T. Zampieri,
Alexandre Ceroni,
Lisete C. Michelini Tags: Original Research Source Type: research
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