Induction of c-fos in forebrain circumventricular organs after renal artery stenosis.
Experiments were done in the anaesthetized rat to determine the effect of activation of renal receptors following renal arterial occlusion (RAO) on the induction of c-fos in neurons of the lamina terminalis in the forebrain. Following RAO, fos labeled neurons were found in both the subfornical organ (SFO) and the organum vasculosum of the lamina terminalis (OVLT). Transection of the renal nerves ipsilateral to RAO reduced ( approximately 61%) the number of fos labeled neurons in the SFO and prevented the fos labeling in the OVLT. Similarly, administration of the angiotensin II converting enzyme inhibitor enalapril maleate prior to RAO also reduced ( approximately 27%) the number of fos labeled neurons in the SFO to RAO. However, the number of fos labeled neurons was not altered in the OVLT. The number of fos labeled neurons in the SFO of the intact animals after RAO was found to be greater than the algebraic sum of the number of fos labeled neurons in the renal nerve transected and enalapril treated animals. These results suggest that neurons in the SFO are activated by at least two different mechanisms following renal artery occlusion; those involving the activation of afferent renal nerves and those due to changes in circulating levels of angiotensin II. In addition, afferent renal nerve inputs combined with the effect of increased circulating levels of angiotensin II produce a greater activation of the SFO than either input alone. On the other hand, the OVLT appears to be selectively activated by afferent renal nerve inputs following RAO. Taken together, these data suggest that neural inputs from the kidney may play an important role in controlling body fluid balance and arterial pressure (AP) by influencing the activity of forebrain circumventricular organs neurons that function in the detection of blood borne signals associated with changes in extracellular fluid volume.
Ciriello
John
J
Department of Physiology and Pharmacology, Health Sciences Centre, University of Western Ontario, London, ON, Canada N6A 5C1. john.ciriello@fmd.uwo.ca
Rosas-Arellano
M Patricia
MP
Solano-Flores
L Pastor
LP
D000804:Angiotensin II / Q000378:metabolism; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001810:Blood Volume / Q000502:physiology; D004656:Enalapril / Q000494:pharmacology; D006439:Hemodynamics / Q000502:physiology; D006706:Homeostasis / Q000502:physiology; D007031:Hypothalamus / Q000166:cytology / Q000502:physiology*; D007150:Immunohistochemistry; D007668:Kidney / Q000294:innervation* / Q000502:physiology; D008297:Male; D009474:Neurons / Q000166:cytology / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D013356:Subfornical Organ / Q000166:cytology / Q000502:physiology*; D015854:Up-Regulation / Q000502:physiology; D017833:Visceral Afferents / Q000502:physiology*; D014882:Water-Electrolyte Balance / Q000502:physiology
D000806:Angiotensin-Converting Enzyme Inhibitors; D016760:Proto-Oncogene Proteins c-fos; D000804:Angiotensin II; D004656:Enalapril