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The objective of these studies was to investigate the role of arterial baroreceptors in the control of neurohypophyseal secretion. The effect of sinoaortic denervation on basal and osmoticinduced release of oxytocin and vasopressin and on blood pressure was determined. Hypertonic or isotonic saline was infused intravenously into sham-operated or denervated rats 3 days after surgery. Plasma oxytocin and vasopressin were measured at 5 and 15 minutes after the infusion. The control levels of oxytocin were increased in the denervated rats, but vasopressin levels were not significantly altered. The vasopressin and oxytocin responses to hypertonic saline were greater after baroreceptor denervation. Plasma oxytocin was increased from 4.7±0.9 to 72.2±8.7 pg/ml in the denervated rats and from 1.8±0.3 to 39.9±6.7 pg/ml in the shamoperated control group at 5 minutes after the infusion (/?<0.01). The plasma vasopressin response to hypertonic saline was 7.1 ±0.6 pg/ml in the sham-operated versus 11.1±1.6 pg/ml in the denervated rats (p<0.05). There was no difference between sham-operated and denervated rats hi the effect of hypertonic saline on plasma sodium and hematocrit. Mean arterial blood pressure was increased after sinoaortic denervation (116.3±4.2 mm Hg in the sham-operated vs. 138.2±8.3 mm Hg in the denervated rats, p<0.05); however, there was no difference in the pressor response to hypertonic saline. These results show that the baroreceptor system influences the secretion of both oxytocin and vasopressin, with effects on basal secretion as well as the response to an osmotic stimulus. These changes may be important in the regulation of cardiovascular and fluid balance under conditions of baroreceptor deficiency. {Hypertension 1989; 13:110-114) I nformation on the status of the cardiovascular system is conveyed to the central nervous system by afferent fibers in the glossopharyngeal and vagus nerves. These primary afferents terminate mainly in the nucleus tractus solitarii with secondary pathways projecting to higher brain structures. Although these pathways are not completely known, brainstem noradrenergic centers are known to receive visceral afferent information and to send projections to the paraventricular and the supraoptic hypothalamic neurohypophyseal nuclei. 1Information on the role of baroreceptor input is provided by studies of the effects caused by surgical interruption of the arterial baroreceptor nerves.From the Department of Physiology and Pharmacology, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North Carolina and the Department of Medicine, University of Southern California School of Medicine, Los Angeles, California.Supported by grants HL-19251 (to N.A.) Results show that sinoaortic denervation (SAD) has widespread effects on both the cardiovascular and endocrine systems; there are increases in blood pressure, sympathetic nerve activity, and vasopressin secretion, while plasma prolactin and atrial natriuretic peptide concentrations are reduced. 2 -7 The objective o...

Partial removal of the adult rat liver-a procedure that stimulates liver regeneration-causes arterial levels of insulin and thyroxin to fall and glucagon levels to rise. These changes are correlated with the quantity of liver tissue excised and not solely with nonspecific operative manipulations or with blood glucose levels. During regeneration (about 24 hr postoperatively), hepatic plasma membranes become partially resistant to binding glucagon; this change is specific because it is not detected in laparotomized controls and insulin binding is not significantly altered. It remains to be proven whether any one or more of these specific endocrine changes are causally related to the initiation of hepatic proliferation.The phenomenon of liver regeneration in adult rats has been investigated for many years in attempts to understand processes that control mammalian cell proliferation. After partial removal of the liver (partial hepatectomy), the remaining tissue undergoes metabolic changes which culminate in the initiation of hepatocyte DNA synthesis and mitosis about 14 and 24 hr later, respectively, and which continue until the initial cellular mass is restored (1).It has been proposed that hepatocyte proliferation is controlled by blood-borne factors, the levels of which appear to be regulated by the available liver mass (2). Indirect in vvo evidence suggests that hormones may be involved (3-8). Recently, it has been reported that in adult rats, peripheral venous perfusions of glucagon and thyroxin-but not insulinstimulate partial hepatocellular growth similar to the hyperplasia induced by partial hepatectomy (9). However, a growth regulatory role for pancreatic hormones is controversial (10-13); moreover, neither glucagon nor thyroxin appear to be specific hepatotrophic mitogens (14).A conceptual attempt to unify these apparently unrelated findings was discussed elsewhere (15, 16) and was based upon in vitro growth control studies using chemically defined medium and quiescent monolayer cultures (17) of differentiated fetal rat hepatocytes (18-21). Direct evidence from these studies suggested that many serum (22) and conditioning factors (17) contributed to the growth response, including insulin and thyroxin, which partially stimulated the initiation of DNA synthesis, and glucagon, which partially inhibited this process.These findings suggested that the in vivo induction of liver regeneration by partial hepatectomy might be accompanied by specific alterations in plasma levels of these hormones as well as in the liver's capacity for hormonal responsiveness.Accordingly, we began approaching these problems by measuring plasma levels of insulin, glucagon, and thyroxin in partially hepatectomized rats and by measuring the capacity of plasma membranes derived from regenerating liver to bind peptide hormones. Measurements were performed during the period that precedes maximal DNA replication rates (0-24 hr) because regulatory changes initiating growth would be expected to occur during this time (1). MATERIALS AND...