The hypotensive effect of centrally administered neutrotensin in rats

Rioux, Francis; Quirion, Rémi; St‐Pierre, Serge; Regoli, Doménico; Jolicoeur, F.B.; Bélanger, F.; Barbeau, A.

doi:10.1016/0014-2999(81)90469-6

Cited by 70 publications

(14 citation statements)

References 19 publications

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“…14 In our experiments with conscious animals, neurotensin always gave a pressor response, whereas, in the studies where neurotensin was depressor, 20 -2I animals were pentobarbitone anesthetized and so sympathetic activity was reduced. 23 In the anesthetized rats, it is possible that neurotensin does not appear pressor since the activity of the sympathetic nervous system is so reduced.…”

Section: Discussionmentioning

confidence: 99%

Central pressor action of neurotensin in conscious rats.

Sumners¹,

Phillips²,

Richards³

1982

Hypertension

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SUMMARY The effects of neurotensin upon blood pressure in conscious rats were examined after intracerebroventricular (i.v.t.) or intravenous (i.v.) administration of this peptide. Whereas i.v. injected neurotensin (0.1-2.0 /u.g/kg) was depressor, i.v.t. injected neurotensin (1 fig and above) was pressor. Peripheral depressor responses could not be repeated in the same animal due to tachyphylaxis, but central pressor responses were repeatable without reduction in magnitude, showing that the two effects were separate entities. Thyrotropin-releasing hormone (TRH), which is reported to be a potent neurotensin antagonist, completely abolished the neurotensin depressor response, and attenuated the central pressor action. TRH did not alter the central pressor effect of another peptide, angiotensin II (All). The potent AH receptor antagonist saralasin, while abolishing the central pressor effect of AH, was completely without effect upon the neurotensin-induced pressor response. These results indicate that i.v.t. injected neurotensin and AH stimulate a rise in blood pressure via different receptors. The alpha-adrenergic antagonists phentolamine, prazosin, or yohimbine (injected i.v.t.) were able to abolish or attenuate the pressor response due to i.v.t.-injected neurotensin, suggesting involvement of the sympathetic nervous system in this response. These results are discussed in relation to the central pressor actions of other neuropeptides. (Hypertension 4: 888-893, 1982) KEY WORDS • blood pressure • neurotensin • angiotensin II thyrotropin releasing hormone * alpha adrenergic antagonists N EUROTENSIN is a basic tridecapeptide that was first isolated from bovine hypothalami. 1 This peptide is now known to be widespread in the central nervous system (CNS), 2 -3 and peripherally. -3 Neurotensin has fulfilled many of the criteria for being recognized as a CNS neurotransmitter, 3 and has many actions in the CNS. Such actions include its pronounced hypothermic effect after intracranial administration, and its marked enhancement of pentobarbital sleeping time. 4 Peripherally, neurotensin modulates glucoregulatory systems, leading to hyperglycemia or hyperglucagonemia. 5 In the blood it is a very potent hypotensive agent. ' The findings that other neurbactive peptides such as angiotensin II (All), substance P, enkephalin, and bradykinin are pressor agents when administered centrally to conscious rats, 6 " 9 and that bradykinin causes hypotension after peripheral administration, 10 led us investigate the effects of centrally administered neurotensin upon arterial blood pressure. These experiments were performed with the following aims: 1) to compare the blood pressure actions of neurotensin with those of other neuropeptides; 2) to determine whether the peripheral depressor effect of neurotensin contains a central component; and 3) to understand the mechanisms involved in the central vascular actions of neurotensin.Methods In all experiments, the animals used were male 250 to 300 g Sprague-Dawley rats. Animals were anesthe...

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Section: Discussionmentioning

confidence: 99%

Central pressor action of neurotensin in conscious rats.

Sumners¹,

Phillips²,

Richards³

1982

Hypertension

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“…The drop in blood pressure is of rapid onset (30–60 s) and of short duration (1–4 min) (Rioux et al, 1981). Interestingly, the hypotensive effect of NT is not accompanied by any alteration in cardiac actions (Rosell et al, 1976; Rioux et al, 1981). …”

Section: Potential Side Effects Of Nt Agonistsmentioning

confidence: 99%

Diverse Roles of Neurotensin Agonists in the Central Nervous System

Boules¹,

Li²,

Smith³

et al. 2013

Front. Endocrinol.

113

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Neurotensin (NT) is a tridecapeptide that is found in the central nervous system (CNS) and the gastrointestinal tract. NT behaves as a neurotransmitter in the brain and as a hormone in the gut. Additionally, NT acts as a neuromodulator to several neurotransmitter systems including dopaminergic, sertonergic, GABAergic, glutamatergic, and cholinergic systems. Due to its association with such a wide variety of neurotransmitters, NT has been implicated in the pathophysiology of several CNS disorders such as schizophrenia, drug abuse, Parkinson’s disease (PD), pain, central control of blood pressure, eating disorders, as well as, cancer and inflammation. The present review will focus on the role that NT and its analogs play in schizophrenia, endocrine function, pain, psychostimulant abuse, and PD.

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“…It is implicated in the modulation of dopamine (DA) signaling [1–5] and exerts potent effects including hypothermia [6], hypotension [7], and analgesia [8], as well as antipsychotic-like effects [9]. However, NT is easily degraded by peptidases and cannot cross the blood-brain barrier.…”

Section: Introductionmentioning

confidence: 99%

The role of NTS2 in the development of tolerance to NT69L in mouse models for hypothermia and thermal analgesia

Smith

Boules

Williams

et al. 2011

Behavioural Brain Research

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NT69L is a neurotensin (NT)(8–13) analog that binds the two major NT receptors, NTS1 and NTS2, and elicits similar behavioral effects as endogenous NT. Tolerance develops rapidly to some, but not to all of NT69L's effects, and to date, little is known about the mechanisms responsible for this tolerance. The development of tolerance appears to be more prevalent in behavioral effects mediated by NTS1 than by those mediated by NTS2, including hypothermia and thermal analgesia. However, we hypothesize that both NTS1 and NTS2 have important roles in mediating the effects of NT69L. Here we investigate the role of NTS2 on NT69L-mediated hypothermia and thermal analgesia with the use of NTS2 knock-out mice. We show that tolerance develops to NT69L-mediated hypothermia and thermal analgesia following sub-chronic treatment in wild-type mice, and that NTS2 is necessary for the development of that tolerance. Additionally, we suggest potential means by which NTS2 influences these NT69L-mediated behaviors.

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The hypotensive effect of centrally administered neutrotensin in rats

Cited by 70 publications

References 19 publications

Central pressor action of neurotensin in conscious rats.

Central pressor action of neurotensin in conscious rats.

Diverse Roles of Neurotensin Agonists in the Central Nervous System

The role of NTS2 in the development of tolerance to NT69L in mouse models for hypothermia and thermal analgesia

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