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Am J Physiol Regul Integr Comp Physiol 290: R1330-R1336, 2006. First published December 29, 2005; doi:10.1152/ajpregu.00150.2005
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NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Central nitric oxide modulates hindquarter vasodilation elicited by AMPA receptor stimulation in the NTS of conscious rats

Ana Carolina Rodrigues Dias1 and Eduardo Colombari1,2

1Department of Physiology, Universidade Federal de São Paulo-Escola Paulista de Medicina, São Paulo; and 2Department of Pathology and Physiology, Universidade Estadual de São Paulo, Araraquara, Brazil

Submitted 2 March 2005 ; accepted in final form 26 December 2005

Microinjection of S-{alpha}-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) in the nucleus of the solitary tract (NTS) of conscious rats causes hypertension, bradycardia, and vasoconstriction in the renal, mesenteric, and hindquarter vascular beds. In the hindquarter, the initial vasoconstriction is followed by vasodilation with AMPA doses >5 pmol/100 nl. To test the hypothesis that this vasodilation is caused by activation of a nitroxidergic pathway in the NTS, we examined the effect of pretreatment with the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 10 nmol/100 nl, microinjected into the NTS) on changes in mean arterial pressure, heart rate, and regional vascular conductance (VC) induced by microinjection of AMPA (10 pmol/100 nl in the NTS) in conscious rats. AMPA increased hindquarter VC by 18 ± 4%, but after pretreatment with L-NAME, AMPA reduced hindquarter VC by 16 ± 7% and 17 ± 9% (5 and 15 min after pretreatment, P < 0.05 compared with before pretreatment). Pretreatment with L-NAME reduced AMPA-induced bradycardia from 122 ± 40 to 92 ± 32 beats/min but did not alter the hypertension induced by AMPA (35 ± 5 mmHg before pretreatment, 43 ± 6 mmHg after pretreatment). Control injections with D-NAME did not affect resting values or the response to AMPA. The present study shows that stimulation of AMPA receptors in the NTS activates both vasodilatatory and vasoconstrictor mechanisms and that the vasodilatatory mechanism depends on production of nitric oxide in the NTS.

nitric oxide synthase; regional vascular conductance; cardiovascular regulation



Address for reprint requests and other correspondence: E. Colombari, Dept. of Physiology, Universidade Federal de São Paulo-EPM, 862 Botucatu St., São Paulo SP 04023-60, Brazil (e-mail: colombari{at}fcr.epm.br)




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Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
L. G. da Silva, A. C. R. Dias, E. Furlan, and E. Colombari
Nitric oxide modulates the cardiovascular effects elicited by acetylcholine in the NTS of awake rats
Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2008; 295(6): R1774 - R1781.
[Abstract] [Full Text] [PDF]




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