A novel action of the newly described prolactin-releasing peptides: cardiovascular regulation

Samson, Willis K.; Resch, Zachary T.; Murphy, Tonya C.

doi:10.1016/s0006-8993(99)02451-8

Cited by 96 publications

(65 citation statements)

References 23 publications

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“…These results, together with our previous finding that both A2 and A1 cell groups were activated according to the running speed increase (25), suggest that PrRP and norepinephrine may be involved in not only ACTH release induced above the LT but also other responses, such as the cardiovascular response (23,34), associated with below-LT running. It is of interest that PrRP neurons in the DMH are highly activated by below-LT running, also suggesting that the PrRP neurons respond to stimuli other than running stress induced above the LT.…”

Section: Discussionsupporting

confidence: 75%

Possible inhibitory role of prolactin-releasing peptide for ACTH release associated with running stress

Ohiwa¹,

Chang²,

Saito³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Exercise around the lactate threshold induces a stress response, defined as "running stress." We have previously demonstrated that running stress is associated with activation of certain regions of the brain, e.g., the paraventricular hypothalamic nucleus (PVN) and supraoptic nucleus, that are hypothesized to play an integral role in regulating stress-related responses, including ACTH release during running. Thus we investigated the role of prolactin-releasing peptide (PrRP), found in the ventrolateral medulla and the nucleus of the solitary tract, which is known to project to the PVN during running-induced ACTH release. Accumulation of c-Fos in PrRP neurons correlated with running speeds, reaching maximal levels under running stress. Intracerebroventricular injection of neutralizing anti-PrRP antibodies led to increased plasma ACTH level and blood lactate accumulation during running stress, but not during restraint stress. Exogenous intracerebroventricular administration of low doses of PrRP had the opposite effects. Therefore, our results suggest that, during running stress, PrRP-containing neurons are activated in an exercise intensity-dependent manner, and likewise the produced endogenous PrRP attenuates ACTH release and blood lactate accumulation during running stress. Here we provide a novel perspective on understanding of PrRP in the endocrine-metabolic response associated with running stress. running; norepinephrine; hypothalamic paraventricular nucleus; lactate threshold; rat EXERCISE AT AROUND LACTATE threshold (LT) produces a variety of beneficial physiological and psychological effects on our body (22,40). The LT is a work rate at which the steady state of blood lactate accumulation breaks down (44) and the plasma ACTH level begins to increase during graded running (7,17,29). Because it is well known that the ACTH release is a stress maker (27), moderate running can generate one kind of stress, termed running stress, if it persists above the LT. To date, little is known about its regulatory mechanism; however, it is important in understanding the mechanisms behind the variety of physiological effects caused by exercise around the LT.To examine the regulating mechanism underlying running stress, we established the rat treadmill running model and used it to identify anatomic activation of the parvocellular part of the hypothalamic paraventricular nucleus (pPVN) and the supraoptic nucleus (SON) during running stress (32, 39). The next step in our studies will be to identify the nuclei or neuropeptides that regulate ACTH release during running stress via pPVN and SON activation. The ventrolateral medulla (VLM) and the nucleus of the solitary tract (NTS) that project to the paraventricular nucleus (PVN) are known to play a crucial role in multiple stresses (4,37,43). Furthermore, recently we identified that the A2 noradrenergic cell group in the NTS and the A1 noradrenergic cell group in the VLM were activated in running stress (24,25).Prolactin releasing peptide (PrRP) was recently isolated as the endoge...

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Section: Discussionsupporting

confidence: 75%

Possible inhibitory role of prolactin-releasing peptide for ACTH release associated with running stress

Ohiwa¹,

Chang²,

Saito³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…10 Although GPR10 and PrRP have not been extensively studied, physiological studies in mice have indicated a clear effect of PrRPs on blood pressure and appetite via hypothalamic processes. 11 Thus far, however, the documented characterization of GPR10 in humans is limited to our study. 10 One of the primary mechanisms through which physical activity affects blood pressure regulation is through modulation of sympathetic nervous function.…”

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confidence: 89%

Association Between Physical Activity and Blood Pressure Is Modified by Variants in the G-Protein Coupled Receptor 10

et al. 2004

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Abstract-Hypertension is strongly related to cardiovascular disease and all-cause mortality. Exercise reduces blood pressure but the response varies between individuals. The mechanisms by which physical activity energy expenditure (PAEE) modifies blood pressure are not fully defined but include modulation of sympathetic tone. Novel polymorphisms in the G-protein coupled receptor (GPR10) have been linked with high blood pressure. GPR10 may mediate the relationship between PAEE and blood pressure via central nervous mechanisms. We examined whether two GPR10 polymorphisms (G-62A and C914T) modify the association between PAEE and blood pressure in the MRC Ely study (Nϭ687

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“…Intracerebroventricular (i.c.v.) administration of PrRP affects feeding behavior 11 , blood pressure 12 and neuroendocrine processes, such as corticotropin-releasing hormone (CRH) 13 and oxytocin 14 release.…”

mentioning

confidence: 99%

The prolactin-releasing peptide antagonizes the opioid system through its receptor GPR10

et al. 2005

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Prolactin-releasing peptide (PrRP) and its receptor G protein-coupled receptor 10 (GPR10) are expressed in brain areas involved in the processing of nociceptive signals. We investigated the role of this new neuropeptidergic system in GPR10-knockout mice. These mice had higher nociceptive thresholds and stronger stress-induced analgesia than wild-type mice, differences that were suppressed by naloxone treatment. In addition, potentiation of morphine-induced antinociception and reduction of morphine tolerance were observed in mutants. Intracerebroventricular administration of PrRP in wild-type mice promoted hyperalgesia and reversed morphine-induced antinociception. PrRP administration had no effect on GPR10-mutant mice, showing that its effects are mediated by GPR10. Anti-opioid effects of neuropeptide FF were found to require a functional PrRP-GPR10 system. Finally, GPR10 deficiency enhanced the acquisition of morphine-induced conditioned place preference and decreased the severity of naloxone-precipitated morphine withdrawal syndrome. Altogether, our data identify the PrRP-GPR10 system as a new and potent negative modulator of the opioid system.Opiate drugs, the prototype of which is morphine, are used largely for the treatment of severe pain. However, the prolonged use of opiate drugs induces a behavioral adaptation that results in the development of tolerance and dependence 1 . Although these adaptive mechanisms have been known for decades, the underlying pathophysiological pathways have not been fully clarified. It has been proposed that the opioid receptor signaling pathway is adaptively regulated at the cellular level, although more recently a growing contribution of the plasticity of neuronal networks involving opioidergic neurons has been recognized. In support of this latter hypothesis, a number of neuropeptides, including cholecystokinin (CCK) 2 , neuropeptide FF (NPFF) 3 and nociceptin (orphanin FQ) 4 , have been proposed as modulators of the opioid system. These various peptidergic pathways are collectively designated as an anti-opioid system. However, the action of individual peptides on the opioid pathway and on the processing of nociceptive signals is complex and some aspects remain controversial, particularly as the behavioral consequences can vary depending on the injection site of these peptides and the precise experimental setup 5,6 . Among these peptides, NPFF, which belongs to the RF-amide peptide family, was shown (among other actions) to regulate blood pressure 7 , prolactin release 8 and nociceptive signal processing 9 . Prolactin-releasing peptide (PrRP) has recently been identified as an additional member of the mammalian RF-amide peptide family, following its isolation as the natural agonist of the previously orphan GPR10 (ref. 10) (also known as hGR3 in human or UHR-1 in rat). Intracerebroventricular (i.c.v.) administration of PrRP affects feeding behavior 11 , blood pressure 12 and neuroendocrine processes, such as corticotropin-releasing hormone (CRH) 13 and oxytocin 14 release.In a...

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A novel action of the newly described prolactin-releasing peptides: cardiovascular regulation

Cited by 96 publications

References 23 publications

Possible inhibitory role of prolactin-releasing peptide for ACTH release associated with running stress

Possible inhibitory role of prolactin-releasing peptide for ACTH release associated with running stress

Association Between Physical Activity and Blood Pressure Is Modified by Variants in the G-Protein Coupled Receptor 10

The prolactin-releasing peptide antagonizes the opioid system through its receptor GPR10

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