Differential recruitment of hypothalamic neuroendocrine and ventrolateral medulla catecholamine cells by non-hypotensive and hypotensive hemorrhages

We performed c-fos expression experiments in conscious rats to quantify the threshold and extent of activation of hypothalamic neuroendocrine cells in response to non-hypotensive and hypotensive hemorrhages allowing us to ass ess whether their pattern of recruitment corresponded to known oxytocin, va sopressin and ACTH release patterns. Also, because previous studies have im plicated ventrolateral medulla catecholamine cells in the generation of cer tain hypothalamic neuroendocrine cell responses, we examined the response o f ventrolateral medulla catecholamine cells to non-hypotensive and hypotens ive hemorrhages and directly tested their role in regulating neuroendocrine cell responses to hypotensive hemorrhage. Animals were subjected to hemorr hages of 0, 4, 8, 12 or 16 ml/kg BW, the latter two levels being hypotensiv e. We found that only supraoptic nucleus vasopressin cells were significant ly activated by the smallest non-hypotensive hemorrhage (4 ml/kg), which co rresponds to reports that only vasopressin is released into the plasma afte r a small hemorrhage. Hypotensive hemorrhages resulted in significant recru itment of paraventricular and supraoptic oxytocin and vasopressin cells and parvocellular cells of the medial division of the paraventricular nucleus. Vasopressin cells were recruited in much greater numbers than oxytocin cel ls, which is in agreement with previous findings that there is a,greater re lease of vasopressin than oxytocin into the plasma after hypotensive hemorr hage. In addition, medial parvocellular cells of the paraventricular nucleu s, most likely to be tuberoinfundibular-projecting corticotropin-releasing factor cells, were activated by hypotensive hemorrhage only when arterial p ressure dropped below 60 mmHg which also corresponds well with the plasma r elease response of ACTH. Ventrolateral medulla catecholamine cells were onl y recruited by hypotensive hemorrhages. While caution must be exercised in interpreting an absence of response, this certainly suggests that catechola mine cells are unlikely to have a role in the activation of supraoptic neur osecretory cells in response to non-hypotensive hemorrhages. Unilateral les ions of the ventrolateral medulla catecholamine cell column, corresponding primarily to the location of Al noradrenergic cells, significantly reduced the hypotensive hemorrhage-induced activation of hypothalamic vasopressin, oxytocin and medial parvocellular paraventricular nucleus cells. This sugge sts that Al noradrenergic cells contribute to the activation of these neuro endocrine cell populations, including oxytocin cells, which is an unexpecte d finding. More significantly, however, because the reduction in responsive ness after Al lesions was similar for all cell categories, it seems likely that other factors must determine the differential recruitment of hypothala mic neuroendocrine cells in response to a hypotensive hemorrhage. (C) 1999 Elsevier Science B.V. All rights reserved.