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The Role of Endogenous Atrial Natriuretic Peptide in Resting And Proc. Nail. Acad. Sci. USA Vol. 89, pp. 11391-11395, December 1992 Physiology The role of endogenous atrial natriuretic peptide in resting and stress-induced release of corticotropin, prolactin, growth hormone, and thyroid-stimulating hormone (third ventricular I Jection/atrial natriuretic peptide antiserum) CELSO R. FRANCI*, JANETE A. ANSELMO-FRANCI*, AND SAMUEL M. MCCANNt4 *DePartamento de Fisiologia, Faculdade de Medicina de Ribeirao Preto, Universidade de Sao Paulo, 14049 - Ribeirao Preto, Sao Paulo, Brazil; and tNeuropeptide Division, Department of Physiology, The University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9040 Contributed by Samuel M. McCann, August 28, 1992 ABSTRACT Our previous studies have shown that stim- play a role in thyroid-stimulating hormone release. On the ulation of the anteroventral third ventricle region increases other hand, the endogenous peptide appears to have a physi- atrial natriuretic peptide (ANP) release, whereas lesions of the ologically significant inhibitory role in suppressing ACTH anteroventral third ventricle or median eminence block the release during stress, mediated at least partly by suppression of release of ANP from blood volume expansion, suggesting a vasopressin release. Endogenous ANP has a pathophysiologic critical central nervous system participation in this response. role in augmenting the prolactin release in stress either by ANPis also produced within neurons that have cell bodies in the inhibiting release of prolactin-inhibiting factors or, alterna- rostral hypothalamus and axons that extend to the median tively, by enhancing release of prolactin-releasing factors. eminence and neural lobe. In addition to its natriuretic effect, Endogenous ANP appears to inhibit resting, without altering the peptide can inhibit the release ofcorticotropin (ACTH) and stress-induced inhibition of growth hormone release by stim- prolactin, anterior pituitary hormones that are released during ulating somatostatin release and/or inhibiting growth hor- stress. To determine the physiologic sinfca of ANP in the mone-releasing hormone release or by both actions. control ofbasal and stress-induced release ofanterior pituitary hormones, highly specific antiserum against the peptide (AB- Atrial natriuretic peptide (ANP) produced and released from ANP) was microinjected into the third cerebral ventricle of atrial myocytes induces natriuresis, diuresis, and lowering of conscious freely moving male rats to Immunoneutralize hypo- blood pressure (1, 2). In addition, it decreases water and salt thalamic ANP. In the initial experiment, the antiserum or intake (3-6). All of these actions tend to promote a decrease control normal rabbit serum (NRS) was injected into the third in body fluid volume and they appear to be homeostatic cerebral ventride to determine the effect of the antiserum on responses to increased extracellular fluid volume. Further- basal release of pituitary hormones. The antiserum had no more, the peptide suppresses vasopressin release from the effect on the concentrations of plasma ACTH, prolactin, or neural lobe (7), which can cause renal water loss and inhibits thyroid-stimulating hormone for 3 hr after the injection; release corticotropin (ACTH) (8) and prolactin (9) from the however, plasma growth hormone concentration, although anterior lobe of the pituitary gland. The decreased ACTH unchanged for 2 hr, was markedly elevated at 3 hr. These release would reduce the secretion of aldosterone from the results indicate that although ANP appears to have no effect on adrenal glomerulosa, which is further reduced by direct the basal release ofthe other hormones, it has a physiologically action of ANP (10), leading to additional renal sodium loss. significant inhibitory effect on growth hormone release. The The decreased prolactin release could further augment na- delay of the effect is probably related to the time required for triuresis since prolactin has a direct salt-retaining action on the antiserum to diffuse to the site of action of the peptide, the kidney (11). presumably at some distance from the ventricle. Since this Stress increases ACTH and prolactin and inhibits the effect was demonstrable after 3 in the stress release of growth hormone (GH) and thyroid-stimulating only hr, experi- hormone (TSH) in the rat (12) and the actions ofANP to alter ment, the antiserum or NRS was microinjected into the third the release of these hormones suggest that it may influence ventricle 3 hr prior to application of ether stress. The rapid the hypothalamic pituitary response to stress. These effects elevation of plasma ACTH in NRS-injected rats was markedly of ANP may be mediated via a hypothalamic ANP neuronal augmented by AB-ANP. Ether also induced a rapid increase in system with cell bodies that extend from the anteroventral plasna prolactin in the NRS-injected animals, as expected. third ventricle region to the paraventricular nucleus and have Contrary to the ACTH response, the maximal increase in axons that project to the median eminence and neural lobe of plasma prolactin after ether was attenuated in animals prein- the pituitary (13, 14). In the median eminence the peptide jected with AB-ANP. In the NRS-inJected animals, there was could enter hypophyseal portal veins and be delivered to the a significant decline in plasma growth hormone after the anterior pituitary to affect its function. Alternatively, the application of ether that was significantly accentuated by ANP neurons might alter the release of hypothalamic releas- AB-ANP, but this was probably the result of the her initial ing and inhibiting hormones via a hypothalamic action that levels of plasma growth hormone in the ANP-AB group fol- would, in turn, alter release of anterior pituitary hormones. lowed by its disappearance with a half-time similar to that of The physiologic significance of the actions of ANP on the NRS-injected group. The decline in plasma thyroid- anterior pituitary hormone release is unknown. Conse- stimulating hormone after ether stress was unaltered in the in the we evaluated the effects of animals injected with AB-ANP. The results of these immuno- quently, present study, neutralization studies suggest that endogenous ANP does not Abbreviations: ANP, atrial natriuretic peptide; ACTH, corticotropin; NRS, normal rabbit serum; TSH, thyroid-stimulating hormone; GH, The publication costs of this article were defrayed in part by page charge growth hormone; 3V, third cerebral ventricle; CRH, corticotropin- payment. This article must therefore be hereby marked "advertisement" releasing hormone. in accordance with 18 U.S.C. §1734 solely to indicate this fact. tTo whom reprint requests should be addressed. 11391 11392 Physiology: Franci et al. Proc. Nadl. Acad. Sci. USA 89 (1992) passive immunoneutralization of brain ANP by microinject- provided with the kits. Plasma ACTH was measured with a ing highly specific antiserum developed against the peptide method (20) using commercially available antiserum (IgG into the third cerebral ventricle (3V) and measuring the effect Corp., Nashville, TN) and human ACTH provided by the on plasma pituitary hormone concentrations in conscious, NIDDK pituitary hormone program. normal, and stressed male rats. Preliminary reports of this Statistics. The values of plasma hormones were compared work have been presented (15, 16). by an ANOVA followed by the Newman-Keul test. Signif- icance of differences between two means, as for the areas values, was determined MATERIALS AND METHODS under two curves ofplasma hormone by Student's t test. Male Harlan-Sprague-Dawley rats, 200-220 g, were housed in a constant light-dark cycle (lights on between the hours of RESULTS 0500 and 1900) and temperature (23-250C)-controlled room. Laboratory chow and water were freely available. One week Table 1 shows plasma concentrations ofGH, TSH, prolactin, before the experiments, a stainless steel guide cannula was and ACTH immediately before (time 0) and 15, 30, 60, 120, implanted into the 3V as described (17) under anesthesia and 180 min after 3V microinjection of NRS or AB-ANP in induced by 2.5% tribromoethanol [Aldrich; 1 mg/100 g (body unstressed rats. Hormone values in the NRS-injected animals weight), i.p.]. Animals that had regained preoperative weight were not altered except for a significant decline in plasma were submitted to an additional operation 24 hr before the TSH by 180 min. There were no significant differences in experiments during which a catheter was introduced into the hormone concentrations between the control group (3V mi- external jugular vein under tribromoethanol anesthesia (18). croinjection of NRS) and the group that received 3V micro- erimental Procedure. All experiments began between injection of AB-ANP, except that the plasma GH concentra- the hours of0830 0900 when a heparinized blood sample (0.6 tions, although unaltered earlier, were significantly higher ml) was collected from the jugular catheter immediately 180 min after microinjection of AB-ANP than NRS. before 3V microinjection of normal rabbit serum (NRS) or There was a significant elevation of plasma ACTH con- antiserum against ANP (AB-ANP). Additional blood samples centration 2 min after the onset of ether stress and a peak at (0.6 ml) were collected from unstressed animals 15, 30, 60, 5 min in the animals previously injected with NRS (Fig. 1). 120, and 180 min after the microinjections. After removal of The levels declined precipitously at 15 min and were no each blood sample,
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