Renal response to secretin

Viteri, Alfredo L.; Poppell, J. William; Lasater, John; Dyck, Walter P.

doi:10.1152/jappl.1975.38.4.661

Cited by 20 publications

(17 citation statements)

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“…Secretin was previous found to increase the nephron filtration rate, glomerular filtration rate, and reabsorption rate of water and bicarbonate. [12][13][14] These actions of secretin are therefore consistent with the presence of secretin receptor in the kidney as previously predicted. 15…”

Section: Secretin Receptor Expression In Peripheral Tissuessupporting

confidence: 90%

The Prenatal Expression of Secretin Receptor

Siu

Sham

Chow

2006

Annals of the New York Academy of Sciences

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Secretin is a classical gastrointestinal peptide while its neuroactive functions in the central nervous system have recently been consolidated. In the past, there was little information regarding the expression of secretin receptor in prenatal development. In this article, using mouse embryos and by in situ hybridization, secretin receptor transcripts were detected in several developing brain regions including the cerebellar primordium and choroid plexus. In the developing intestine, secretin receptor is present in the epithelial lining of the villi and the inner circular muscle. Interestingly, the transcripts for secretin receptor were also detected in the epicardium and myocardium of the developing heart as well as the glomerulus and collecting duct in the developing kidney. Taken together, our data suggest a potential pleiotrophic role of secretin during embryonic development.

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Section: Secretin Receptor Expression In Peripheral Tissuessupporting

confidence: 90%

The Prenatal Expression of Secretin Receptor

Siu

Sham

Chow

2006

Annals of the New York Academy of Sciences

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“…Moreover, inconsistent findings on the renal function of secretin have been reported. Early studies suggested a diuretic role for this peptide to increase renal excretion of water, bicarbonate, sodium, potassium, and calcium in normal humans and dogs (2,3,42,43), whereas another study demonstrated an antidiuretic action of secretin when administered intravenously to anesthetized hydrated rats (7). In the latter study, secretin was shown to act on the receptor on the renal medulla to decrease urine output through the activation of adenylate cyclase, and this effect is as potent as that of Vp in Brattleboro rats.…”

Section: Discussionmentioning

confidence: 99%

Phenotypes Developed in Secretin Receptor-Null Mice Indicated a Role for Secretin in Regulating Renal Water Reabsorption

Chu¹,

Chung²,

Lam³

et al. 2007

Molecular and Cellular Biology

119

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Aquaporin 2 (AQP2) is responsible for regulating the concentration of urine in the collecting tubules of the kidney under the control of vasopressin (Vp). Studies using Vp-deficient Brattleboro rats, however, indicated the existence of substantial Vp-independent mechanisms for membrane insertion, as well as transcriptional regulation, of this water channel. The Vp-independent mechanism(s) is clinically relevant to patients with X-linked nephrogenic diabetes insipidus (NDI) by therapeutically bypassing the dysfunctional Vp receptor. On the basis of studies with secretin receptor-null (SCTR ؊/؊ ) mice, we report here for the first time that mutation of the SCTR gene could lead to mild polydipsia and polyuria. Additionally, SCTR ؊/؊ mice were shown to have reduced renal expression of AQP2 and AQP4, as well as altered glomerular and tubular morphology, suggesting possible disturbances in the filtration and/or water reabsorption process in these animals. By using SCTR ؊/؊ mice as controls and comparing them with wild-type animals, we performed both in vivo and in vitro studies that demonstrated a role for secretin in stimulating (i) AQP2 translocation from intracellular vesicles to the plasma membrane in renal medullary tubules and (ii) expression of this water channel under hyperosmotic conditions. The present study therefore provides information for at least one of the Vp-independent mechanisms that modulate the process of renal water reabsorption. Future investigations in this direction should be important in developing therapeutic means for treating NDI patients.Secretin was originally isolated from upper intestinal mucosal extract, injection of which into the jugular vein of an anesthetized dog resulted in elevation of pancreatic and hepatic bile flow (4). The primary function of secretin in releasing bicarbonate, electrolytes, and water from pancreatic ductal epithelial cells is firmly established. Additionally, it can also stimulate electrolyte and water secretion in the epididymis, as well as bicarbonate-rich ductal bile secretion from cholangiocytes (1, 9). In cholangiocytes, a secretin-induced choleretic effect is associated with microtubule-dependent exocytotic insertion of cytoplasmic vesicles containing the water channel aquaporin 1 (AQP1) onto the apical plasma membrane (PM), leading to osmotic water movement (28). Interestingly, this type of regulated translocation of water channels has also been demonstrated in other cell types (5). For example, vasoactive intestinal polypeptide-induced translocation of AQP5 in Brunner's gland of the duodenum is associated with bicarbonate and mucin secretion, which is essential for mucosal protection (38), while Vp-and oxytocin-triggered translocation of AQP2 to and from the PM in renal collecting tubules (19, 36) is critical for renal water reabsorption. As there is considerable evidence indicating the involvement of Vp-independent mechanisms in the regulation of renal water reabsorption (19,21,25,44) and some of these mechanisms are associated with cyclic-AMP (cAMP...

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“…In stomach, secretin stimulates gastric pepsin secretion and suppresses gastric emptying, which facilitates digestion of proteins in duodenum ( Vagne and Andre, 1971 ; Sanders et al, 1983 ). In the kidney, secretin plays a role in increasing urinary volume and bicarbonate excretion in normal human subjects, which helps to maintain body water homeostasis ( Baron et al, 1958 ; Viteri et al, 1975 ). In the rodent brain, secretin can act as a central nervous system peptide neurotransmitter ( Yang et al, 2004 ; Nishijima et al, 2006 ; Yamagata et al, 2008 ).…”

Section: Secretinmentioning

confidence: 99%

The Role of Gasotransmitters in Gut Peptide Actions

et al. 2021

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Although gasotransmitters nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H2S) receive a bad connotation; in low concentrations these play a major governing role in local and systemic blood flow, stomach acid release, smooth muscles relaxations, anti-inflammatory behavior, protective effect and more. Many of these physiological processes are upstream regulated by gut peptides, for instance gastrin, cholecystokinin, secretin, motilin, ghrelin, glucagon-like peptide 1 and 2. The relationship between gasotransmitters and gut hormones is poorly understood. In this review, we discuss the role of NO, CO and H2S on gut peptide release and functioning, and whether manipulation by gasotransmitter substrates or specific blockers leads to physiological alterations.

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Renal response to secretin

Cited by 20 publications

References 0 publications

The Prenatal Expression of Secretin Receptor

The Prenatal Expression of Secretin Receptor

Phenotypes Developed in Secretin Receptor-Null Mice Indicated a Role for Secretin in Regulating Renal Water Reabsorption

The Role of Gasotransmitters in Gut Peptide Actions

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