Pasarapa Towiwat, Siripan Phattanarudee,Timothy J. Maher, Ahmmed Ally. Mol Cell Biochem DOI 10.1007/s11010-014-2218-9. The exercise pressor reflex leads to an increase in BP in response to static exercise. This reflex mediates its control over the cardiovascular system by modulating the activity of CVLM and RVLM neurons. As we already know, there are different neurotransmitters that modulate the activity neurons in the RVLM and CVLM. It has been demonstrated in the literature that microdialysis of L- arginine into the CVLM lead to enhanced pressor response during static exercise along with decreased GABA release. However, when L-arginine was infused into the RVLM blocked the cardiovascular responses to static exercise. Blockade of both nNOS and eNOS lead to enhanced GABA and decrease glu in CVLM. Blockade of both nNOS and eNOS in the RVLM lead to enhanced Glu and decrease GABA. Since it has been shown that blockade of iNOS in SHR leads to attenuation of there hypertensive state, This study wanted to further investigate the role of iNOS in the exercise pressor response. They found that blockade of iNOS by infusion into the RVLM, lead to attenuated HR and blood increase in response to activation of the exercise pressor reflex. they also showed a decrease in iNOS protein expression in the RVLM following blockade of iNOS in the RVLM and no change in CVLM. However, when the antagonist for iNOS was infused into CVLM they observed the response to activation of the exercise pressor reflex was potentiated. The protein expression of iNOS was not different when compared to controls for RVLM and CVLM. These data demonstrate that iNOS may be lead playing a role in the exciting neurons in the RVLM possibly through enhancing Glu and/or decreasing GABA release.-MD
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