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This Article Full Text Full Text (PDF) All Versions of this Article: 290/3/R741    most recent 00660.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Possas, O. S. Articles by Lewis, S. J. Search for Related Content PubMed PubMed Citation Articles by Possas, O. S. Articles by Lewis, S. J.

NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Role of nitrosyl factors in the hindlimb vasodilation elicited by baroreceptor afferent nerve stimulation

Departments of ¹Pharmacology and ²Psychology and ³The Cardiovascular Center, University of Iowa, Iowa City, Iowa; and ⁴Department of Physiology and Pharmacology, University of Georgia, Athens, Georgia

Submitted 9 September 2005 ; accepted in final form 26 October 2005

This study determined whether electrical stimulation (ES) of the baroreceptor afferent fibers in the aortic depressor nerve (ADN) produces hindlimb vasodilation in pentobarbital-anesthetized rats via the release of nitric oxide (NO)-containing (nitrosyl) factors from NO synthase-positive lumbar sympathetic nerve terminals. ES of the ADN (1–10 Hz for 15 s) produced frequency-dependent reductions in mean arterial blood pressure (MAP) and mesenteric and hindlimb vascular resistance (MR and HLR, respectively). The falls in resistance were substantially smaller in hindlimb beds in which the ipsilateral lumbar sympathetic chain had been transected 7–10 days previously. The maximal falls in MR and hindquarter vascular resistance (HQR) produced by 1- to 10-Hz ES of the ADN were unaffected by the specific inhibitor of neuronal NO synthase 7-nitroindazole (7-NI, 45 mg/kg iv). However, the total falls in HQR (mmHg·kHz^–1·s) produced by these stimuli were significantly diminished by 7-NI, whereas the total falls in MR were not affected. Four successive episodes of 10-Hz ES produced equivalent reductions in MAP, MR, and HQR. The peak changes in these parameters were not affected by 7-NI. However, the total falls in HQR progressively diminished with each successive stimulus, whereas the total falls in MR remained unchanged. These results provide evidence that the hindlimb vasodilation produced by ES of baroreceptor afferents within the ADN may involve the activation of postganglionic lumbar sympathetic vasodilator fibers, which release newly synthesized and preformed nitrosyl factors.

aortic depressor nerve; nitric oxide; rat

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