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Secretin and Body Fluid Homeostasis Jessica Y.S

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Secretin and Body Fluid Homeostasis Jessica Y.S CORE Metadata, citation and similar papers at core.ac.uk Provided by Elsevier - Publisher Connector mini review http://www.kidney-international.org & 2011 International Society of Nephrology Secretin and body fluid homeostasis Jessica Y.S. Chu1, Carrie Y.Y. Cheng1, Vien H.Y. Lee1, YS Chan2 and Billy K.C. Chow1 1School of Biological Sciences, The University of Hong Kong, Hong Kong, China and 2Department of Physiology and Research Centre of Heart, Brain, Hormone and Healthy Aging, The University of Hong Kong, Hong Kong, China Body fluid homeostasis is critical for the survival of living The progression of life forms from the paleozoic oceans to organisms and hence is tightly controlled. From initial studies rivers and to different terrestrial eco-niches required the on the effects of secretin (SCT) on renal water reabsorption in coevolution of osmoregulatory mechanisms that defend body the 1940s and recent investigations of its role in cardiovascular cells from the changes in the osmotic pressure imposed by and neuroendocrine functions, it has now become the surrounding fluids. In terrestrial mammals, sophisticated increasingly clear that this peptide is an integral component physiological, behavioral, and cardiovascular responses of the homeostatic processes that maintain body fluid evolved so as to ensure the constancy of milieu interieur. balance. This review, containing some of our recent findings The physiological approach comprises adjustments in the of centrally expressed SCT on water intake, focuses on renal handling of water and electrolytes, which is primarily the actions of SCT in influencing the physiological, regulated by the antidiuretic hormone, vasopressin (Vp). The neuroendocrine, and cardiovascular processes that behavioral approach consists of the regulation of water subserve body fluid homeostasis. and salt intake, which is mainly modulated by the dipsogen, Kidney International (2011) 79, 280–287; doi:10.1038/ki.2010.397; angiotensin II (ANGII). The cardiovascular approach published online 13 October 2010 controls the volume and pressure of body fluid using KEYWORDS: aquaporin; secretin; vasopressin; water drinking behavior both the renin–ANG system and Vp. These osmoregulatory responses arose from stimuli that activated groups of specialized nerve cells which are capable of transducing changes in plasma osmolality into electrical signals to maintain fluid and electrolyte balance in our body. In recent years, it has become evident that secretin (SCT), the oldest known peptide hormone1 controlling pancreatic secretion of bicarbonate ion, is actually expressed in those osmoregulatory neurons and could regulate multiple processes, including neuroendocrine, behavioral, and cardio- vascular responses, that underlie body fluid homeostasis. This review will center on the influence of SCT in these processes at various tissues. SECRETIN SCT is a 27-residue peptide hormone with an amidated carboxyl terminus. The peptide was discovered by Bayliss and Starling in 19021 and has subsequently been isolated/cloned from porcine,2 chicken,3 cow,4 human,5 dog,6 rat,7 rabbit,8 guinea pig,9 ovine,10 and mouse.11 The best known action of SCT is its stimulatory effects on the exocrine secretion of pancreas, whereas the physiology of this peptide is complex exerting pleiotropic activities in many tissues.12 When reviewing its function, SCT is depicted as a peptide that controls directional fluxes of water and electrolytes across the plasma membrane. It was found to exhibit nanomolar potency in stimulating channel-mediated ClÀ efflux in the Correspondence: Billy K.C. Chow, School of Biological Sciences, 13 The University of Hong Kong, Pokfulam, Hong Kong, China. lung, and evoke the translocation of aquaporin-1 (AQP1) E-mail: [email protected] from intracellular compartments to the apical membrane for Received 18 March 2010; revised 28 July 2010; accepted 4 August 2010; the transepithelial movement of water into the ductal bile 14 published online 13 October 2010 lumen. 280 Kidney International (2011) 79, 280–287 JYS Chu et al.: Secretin and water homeostasis mini review RENAL EFFECTS OF SCT the conclusion that SCT is a diuretic peptide.15–17 These In the early 1930s, it became apparent that SCT could observations contrast with the findings by Charlton et al.,18 modulate renal functions.15 Unfortunately, these investigations who showed an anti-diuretic function of SCT, with an effective bunged up, in part, because of the conflicting reports showing dose 50 at about 0.70 nmol/kg. Therefore, it is until the recent diuretic and antidiuretic effects of SCT. A number of studies usage of the SCT receptor (SCTR)-deficient mouse model19 monitoring the effects of SCT on renal water handling led to that a role of SCT in the kidney was finally confirmed. a Collecting tubules Bowman’s capsule Thick ascending limb of loop of Henle PT Proximal tubules (PT) Loop of Henle GTP-Gas Basolateral b SCTR H2O AC AQP4 AQP3 cAMP ? PKA CREB P Transcription CRE TATA 3′ IV AQP2 gene promoter AQP2 Nucleus H2O Apical AQP2 Principal cell Figure 1 | SCT and its receptor in the kidney. (a) Bright-field photomicrograph of mouse kidney sections labeled with rabbit anti-mouse SCTR antibody raised in our laboratory (1:250). The specificity of this antibody was tested using sections obtained from SCTRÀ/À mice.19 SCTR was shown to localize in almost every segment of the nephron. (b) Diagrammatic illustration of the functions of SCT in the renal collecting duct tubules. SCT might be capable of inducing water reabsorption in renal collecting duct principal cells by binding to SCTR, which is localized on the basolateral membranes of the cells.19 On binding to its receptor, SCT activates an AC-cAMP–PKA cascade, which could then lead to an increase in AQP2 expression, probably via the subsequent phosphorylation of CREB and the docking of this factor onto the CRE site of the AQP2 gene promoter. In addition, SCT also induces the trafficking of AQP2 from the IV to the apical membrane of the collecting duct. This could allow water influx into the principal cells via AQP2 and water outflux from the cells via AQP3 and AQP4, which are constitutively expressed on the basolateral membrane. It is therefore possible that SCT could enhance water reabsorption from the collecting tubules. AC, adenylyl cyclase; AQP, aquaporin; cAMP, cyclic adenosine monophosphate; CRE, cAMP responsive element; CREB, cAMP responsive element binding protein; GTP, guanosine triphosphate; IV, intracellular vesicles; PKA, protein kinase A; SCT, secretin; SCTR, SCT receptor. Kidney International (2011) 79, 280–287 281 mini review JYS Chu et al.: Secretin and water homeostasis SCTR is expressed throughout the kidney (Figure 1a). Its a serum concentration was found to increase significantly in hemodialysis patients20 and in patients with chronic 21 renal failure in comparison with controls, indicating SON that the peptide might be associated with clinical-patholo- gical status of the kidney. Morphologically, SCTR-deficient Rb-anti-SCT Ab Goat-anti-Vp Ab Overlay image mice showed no growth abnormality, but their kidney/body SCT weight ratio was significantly higher than their normal littermates.19 Besides, histological examination showed that the kidneys of SCTRÀ/À mice were abnormal, char- acterized by increased mesangial area, enlarged urinary space, PVN and frequent tubular dilation and hypertrophy in the collecting tubules of the medullary region.19 This suggested that SCTRÀ/À might have altered water absorption and filtration processes. Consistent to this notion, apart from the effects of SCT in increasing the renal blood flow,22 single-nephron glomerular filtration rate, and glomerular SON plasma flow,23 the peptide could probably induce renal water reabsorption in kidney tubules. In medullary tubules isolated þ / þ Rb-anti-SCTR Ab Goat-anti-Vp Ab Overlay image from the SCTR mice and normal Wistar rat, SCT was SCTR found to induce a dose-dependent increase in AQP2 expression on the plasma membrane and a dose-dependent decrease in AQP2 expression in the intracellular vesicles.19,24 This induced translocation of AQP2 was found to be PVN mediated via a cyclic adenosine monophosphate/protein kinase A-dependent pathway,24 and was found to be absent in À/À 19 the medullary tubules isolated from SCTR mice, hence b SCT SCTR indicating that SCT induces the movement of AQP2 on binding with its receptor (Figure 1b). This latest finding is in agreement with an early report from Charlton et al.,18 who showed a reduction of urine output via the stimulation of adenylate cyclase in the outer medulla of the kidney when SCT was injected intravenously. Apart from in vitro treatment of SCT to medullary tubules, the movement and the expression of AQP2 were also examined in vivo in dehydrated mice. It was found that SCTRÀ/À mice showed less movement of AQP2 to the plasma membrane than the SCTR þ / þ mice,19 suggesting that there was an altered AQP2 response during hyperosmolality. c As SCTRÀ/À mice showed normal transcript levels of Vp receptor in their kidney, and slightly higher serum Vp levels Figure 2 | Cellular distribution of SCT and SCTR in the central as well as hypothalamic Vp transcript levels (1.54-fold±0.19- osmoregulatory regions. (a) SCT and its receptor were colocalized with Vp in the hypothalamic SON and PVN. The fold; Po0.05; n ¼ 20) when compared with their wild-type antibodies employed were rabbit anti-SCT (1:250 dilution; Phoenix 19 littermates, these data collectively suggested that SCT has a Pharmaceuticals, Burlingame, CA), rabbit anti-SCTR (1:200 dilution; Vp-independent role in the expression and movement of Chu et al.19), goat anti-Vp (1:400 dilution; Santa Cruz AQP2s in the kidney, and hence were consistent with the Biotechnology, Santa Cruz, CA), Alexa Fluor 594 donkey anti-goat 18 IgG (1:500 dilution; Molecular Probes, Invitrogen, Carlsbad, CA), finding by Charlton et al., who reported that the and Alexa Fluor 488 chicken anti-rabbit IgG (1:500 dilution; antidiuretic effect of SCT was as potent as Vp in homozygous Molecular Probes.
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