Neurotensin and antinatriuresis in the conscious rabbit

Bloom, Stephen R.; Peart, W. S.; Unwin, Robert J.

doi:10.1111/j.1476-5381.1983.tb10489.x

Cited by 13 publications

(5 citation statements)

References 19 publications

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“…These observations collectively suggest that N T could function as a circulating hormone. Hence, the renal effects of N T demonstrated in the present as well as previous studies (Bloom et al 1983;Unwin et a / . 1987) lend support to the speculation that N T may be a mediator of the influence of gastrointestinal tract on renal excretion of sodium and water.…”

Section: Discussionsupporting

confidence: 88%

Antidiuretic Effects of Neurotensin in Chloralose Anaesthetized Dogs

Kivlighn

Jandhyala

1990

Clin Exp Pharma Physio

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1. Effects of cerebroventricular and/or intravenous infusions of neurotensin (NT), an endogenous tridecapeptide, on haemodynamics and renal function were investigated in chloralose anaesthetized dogs. 2. Cerebroventricular infusions (i.c.v.) of NT (10-6 mol/L and 10-5 mol/L, 0.1 mL/min) for 30 min did not produce any significant alterations in the measured variables. In the vagotomized dogs, intravenous (i.v.) infusion of NT (10(-5) mol/L) at a rate of 0.1 mL/min for 30 min significantly lowered the arterial blood pressure and glomerular filtration rate; these effects were accompanied by pronounced reductions in the urine flow and urinary sodium excretion and marked increases in urine osmolality. 3. In the dogs with vagi intact, i.v. infusions of NT failed to produce any alterations in the blood pressure; however, renal effects of NT were essentially identical to those observed in the vagotomized dogs. 4. Infusions of NT (10(-6) mol/L) and/or NT-metabolites NT1-8 and NT8-13 (10(-5) mol/L) directly into the renal artery failed to produce any significant alterations in the urine flow. Antidiuretic effects of i.v. NT were not prevented by acute renal denervation, adrenalectomy, or pretreatment of the animals with naloxone. However, morphine pretreatment completely abolished the hypotensive and anti-diuretic effects of NT. 5. It is proposed that i.v. infusion of NT rapidly facilitates the secretion of an endogenous substance possessing potent antidiuretic properties and opiate mechanisms are involved in mediating such an effect. Although it appears unlikely, a role for vasopressin cannot be ruled out.

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Section: Discussionsupporting

confidence: 88%

Antidiuretic Effects of Neurotensin in Chloralose Anaesthetized Dogs

Kivlighn

Jandhyala

1990

Clin Exp Pharma Physio

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“…Neurotensin plasma levels rise promptly in response to feeding. In conscious rabbits, neurotensin produces a dose-related fall in renal sodium excretion (54). It has also been shown that neurotensin and vasoactive intestinal polypeptide (VIP) reduce blood pressure and natriuresis, followed by a dose-related fall in plasma ANP (6).…”

Section: Neurotensinmentioning

confidence: 99%

Neuroendocrine Control of Body Fluid Metabolism

Antunes‐Rodrigues

Castro

Elias

et al. 2004

Physiological Reviews

401

310

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Mammals control the volume and osmolality of their body fluids from stimuli that arise from both the intracellular and extracellular fluid compartments. These stimuli are sensed by two kinds of receptors: osmoreceptor-Na+ receptors and volume or pressure receptors. This information is conveyed to specific areas of the central nervous system responsible for an integrated response, which depends on the integrity of the anteroventral region of the third ventricle, e.g., organum vasculosum of the lamina terminalis, median preoptic nucleus, and subfornical organ. The hypothalamo-neurohypophysial system plays a fundamental role in the maintenance of body fluid homeostasis by secreting vasopressin and oxytocin in response to osmotic and nonosmotic stimuli. Since the discovery of the atrial natriuretic peptide (ANP), a large number of publications have demonstrated that this peptide provides a potent defense mechanism against volume overload in mammals, including humans. ANP is mostly localized in the heart, but ANP and its receptor are also found in hypothalamic and brain stem areas involved in body fluid volume and blood pressure regulation. Blood volume expansion acts not only directly on the heart, by stretch of atrial myocytes to increase the release of ANP, but also on the brain ANPergic neurons through afferent inputs from baroreceptors. Angiotensin II also plays an important role in the regulation of body fluids, being a potent inducer of thirst and, in general, antagonizes the actions of ANP. This review emphasizes the role played by brain ANP and its interaction with neurohypophysial hormones in the control of body fluid homeostasis.

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“…It acts as a paracrine and endocrine modulator of digestive functions in the gut (Ferris, 1989). It is located in specific glandular cells, called the N cells, and may be released into the blood after food ingestion, thus influencing not only the digestive system (Mashford et al , 1978; Blackburn et al , 1980; Croci et al , 1995a), but presumably the cardiovascular system and renal functions too (Quirion et al , 1982; Bloom et al , 1983; Unwin et al , 1987; Kivlighn & Jandhyala, 1990; Nisato et al , 1994). NT has antidiuretic action after i.v.…”

Section: Introductionmentioning

confidence: 99%

Negative modulation of nitric oxide production by neurotensin as a putative mechanism of the diuretic action of SR 48692 in rats

Croci

Landi

Gully

et al. 1997

British J Pharmacology

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*Sano® Recherche, 195 route d'Espagne, 31036 Toulouse, and {32/34 rue Marbeuf, 75374 Paris, France 1 We investigated the e ect of the non-peptide neurotensin (NT) antagonist SR 48692 on renal function in rats and the involvement of nitric oxide (NO) in the diuretic action of this compound. 2 In fed animals, SR 48692 dose-dependently (0.5 to 12.5 mg kg 71 , p.o., 0.03 to 1 mg kg 71 , i.p. and 0.1 to 1 mg/rat, i.c.v.) increased urine output and urinary excretion of Na + , K + and Cl 7 and reduced urine osmolality. The diuretic activity was also evident in water-deprived, fasted animals and in fasted, waterloaded rats. 3 NT (0.1 mg/rat, i.c.v.) had no e ect on urine output in fed rats, but reduced the diuretic action of SR 48692 (1 mg/rat, i.c.v.). The opposite result was obtained in fasted, water-loaded animals: NT dosedependently (0.01 and 0.1 mg/rat, i.c.v.) inhibited diuresis and this e ect was signi®cantly inhibited by i.c.v. SR 48692. In this experimental condition, SR 48692 did not further increase the on-going diuresis. 4 The NO synthesis inhibitor N o -nitro-L-arginine methyl ester (L-NAME; 30 mg kg 71 , i.p.) alone had no e ect on urine output in fed rats but prevented the diuretic action of i.c.v. or i.p. SR 48692; Larginine (1 g kg 71 , i.p.) but not D-arginine (1 g kg 71 , i.p.) restored the SR 48692-dependent increase in diuresis. L-NAME had no e ect on furosemide-stimulated diuresis. 5 Systemically administered L-NAME or i.c.v. NT in fasted, water-loaded rats signi®cantly reduced water diuresis but this e ect was no longer seen in animals given i.p. L-arginine. Rats receiving i.c.v. NT, whose diuresis was signi®cantly reduced, also excreted less nitrates and nitrites in urine. 6 Increased diuresis after central or systemic administration of SR 48692 to fed rats was paralleled by increased urinary excretion of nitrates and nitrites, this being consistent with peripheral enhancement of NO production after NT-receptor blockade by SR 48692. The increase in diuresis after furosemide also involved an increase of nitrates and nitrites in urine, but this e ect was about half that attained with an equipotent diuretic dose of SR 48692. 7 In fed rats, the NO donor isosorbide-dinitrate, reduced systolic blood pressure (unlike SR 48692 which did not a ect blood pressure) but also dose-dependently (1 and 5 mg kg 71 , i.p.) stimulated urine output. 8 The overall e ects of SR 48692 strongly support a link between the actions of endogenous NT, AVP and peripheral NO production in the modulation of renal excretion of water, Na + , K + and Cl 7 .

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Neurotensin and antinatriuresis in the conscious rabbit

Cited by 13 publications

References 19 publications

Antidiuretic Effects of Neurotensin in Chloralose Anaesthetized Dogs

Antidiuretic Effects of Neurotensin in Chloralose Anaesthetized Dogs

Neuroendocrine Control of Body Fluid Metabolism

Negative modulation of nitric oxide production by neurotensin as a putative mechanism of the diuretic action of SR 48692 in rats

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