title: Lesions of the dorsal noradrenergic bundle augment the renin response to blood loss but do not alter hypothalamic Fos expression.
abstract: The goal of this study was to determine if the dorsal noradrenergic bundle (DNAB) plays an essential role in mediating increased plasma renin activity (PRA) and hypothalamic activation, as indicated by increased Fos expression, in response to a small volume blood loss in unanesthetized animals. Male Sprague-Dawley rats were prepared with bilateral 6-hydroxydopamine or sham lesions of the dorsal noradrenergic bundle. In both groups of animals, blood pressure decreased by only 10-15 mmHg following hemorrhage (10 ml/kg over 15 min). Plasma renin activity increased similarly in both groups after 5 ml/kg blood loss, but showed a significantly greater increase after 10 ml/kg blood loss in animals with 6-hydroxydopamine lesions than in those with sham lesions (increase of 13.8 +/- 2.0 ng/ml/h versus 8.4 +/- 1.2 ng/ml/h; P < 0.025). There were numerous Fos-immunoreactive cell nuclei in the supraoptic nucleus (SON) and parvicellular paraventricular hypothalamic nucleus (PVN) of hemorrhaged animals. The number of Fos-positive neurons did not differ between groups, indicating that the dorsal noradrenergic bundle does not convey the primary drive for supraoptic and paraventricular nucleus activation during blood loss. However, one or more of the forebrain regions innervated by the dorsal noradrenergic bundle may attenuate the sympathetic outflow that initiates renin release in response to hemorrhage.
authors.affiliation: Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave., Box 711, Rochester, NY 14642, USA.
authors.forename: Rebecca L
authors.initials: RL
authors.lastname: Jaworski
authors.forename: Martha L
authors.initials: ML
authors.lastname: Blair
mesh_terms: D018663:Adrenergic Agents / Q000633:toxicity; D000704:Analysis of Variance; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001927:Brain Diseases / Q000097:blood / Q000378:metabolism; D002452:Cell Count / Q000379:methods; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006470:Hemorrhage / Q000378:metabolism / Q000503:physiopathology; D007031:Hypothalamus / Q000378:metabolism*; D007150:Immunohistochemistry / Q000379:methods; D008297:Male; D009638:Norepinephrine / Q000378:metabolism*; D016761:Oncogene Proteins v-fos / Q000378:metabolism*; D016627:Oxidopamine / Q000633:toxicity; D011863:Radioimmunoassay / Q000379:methods; D051381:Rats; D017207:Rats, Sprague-Dawley; D012083:Renin / Q000097:blood*; D013681:Tegmentum Mesencephali / Q000293:injuries / Q000502:physiology*
chemical_list: D018663:Adrenergic Agents; D016761:Oncogene Proteins v-fos; D016627:Oxidopamine; D012083:Renin; D009638:Norepinephrine