Opioids in Pain and Cardiovascular Responses: Overview of Common Features

Carr, Daniel B.; Verrier, Richard L.

doi:10.1111/j.1540-8167.1991.tb01367.x

Cited by 8 publications

(2 citation statements)

References 94 publications

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“…This is suggested because other endorphin systems have typically been shown to remain quiescent without influence on a biological system until they are activated by a particular stress or pathology (Carr and Verrier, 1991;Kapusta and Obih, 1995). Although transgenic NOP Ϫ/Ϫ mice now provide an alternative approach in which to explore these possibilities, it was the purpose of these investigations to first determine whether or not the cardiovascular and renal excretory responses to central N/OFQ are unequivocally absent in transgenic NOP Ϫ/Ϫ mice compared with responses observed in conscious littermate NOP ϩ/ϩ mice and nontransgenic C57BL/6 mice, a genetic background strain similar to the C57BL/6 mice onto which NOP Ϫ/Ϫ mice were backcrossed.…”

Section: Discussionmentioning

confidence: 99%

Nociceptin/Orphanin FQ (N/OFQ)-Evoked Bradycardia, Hypotension, and Diuresis Are Absent in N/OFQ Peptide (NOP) Receptor Knockout Mice

Burmeister¹,

Ansonoff²,

Pintar³

et al. 2008

J Pharmacol Exp Ther

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Intracerebroventricular administration of the opioid-like peptide nociceptin/orphanin FQ (N/OFQ) produces bradycardia, hypotension, and diuresis in mice. We hypothesized that these responses are solely caused by selective activation of central N/OFQ peptide (NOP) receptors. To test this premise, we first examined whether i.c.v. N/OFQ produced dose-dependent diuretic and cardiovascular depressor responses in commercially available C57BL/6 mice. Next, using doses established in these studies, we examined the renal excretory and cardiovascular responses to i.c.v. N/OFQ in conscious transgenic NOP receptor knockout mice (NOP Ϫ/Ϫ ). In metabolic studies, i.c.v. N/OFQ, but not saline vehicle, dose-dependently increased urine output (V) in NOP ϩ/ϩ ; this response was significant at 3 nmol (N/OFQ, V ϭ 0.39 Ϯ 0.10 ml/2 h; saline, 0.08 Ϯ 0.05 ml/2 h). The N/OFQ-evoked diuresis was absent in littermate NOP Ϫ/Ϫ (N/OFQ, V ϭ 0.06 Ϯ 0.06 ml/2 h; saline, 0.03 Ϯ 0.03 ml/2 h).There were no significant changes in urinary sodium or potassium excretion or free water clearance in either group. In telemetry studies, i.c.v. N/OFQ dose dependently lowered heart rate (HR) and mean arterial pressure (MAP). At 3 nmol N/OFQ, both HR and MAP were reduced in NOP ϩ/ϩ (peak ⌬HR ϭ Ϫ217 Ϯ 31 bpm; peak ⌬MAP ϭ Ϫ47 Ϯ 7 mm Hg) compared with saline (peak ⌬HR ϭ Ϫ14 Ϯ 5 bpm; peak ⌬MAP ϭ 2 Ϯ 3 mm Hg). These N/OFQ-evoked bradycardic and hypotensive responses were absent in NOP Ϫ/Ϫ (peak ⌬HR ϭ Ϫ13 Ϯ 17 bpm; peak ⌬MAP ϭ Ϫ2 Ϯ 4 mm Hg, respectively). Basal 24-h cardiovascular and renal excretory function were not different between NOP Ϫ/Ϫ and NOP ϩ/ϩ mice. These results establish that the bradycardia, hypotension and diuresis produced by centrally administered N/OFQ are mediated by selective activation of NOP receptors.Nociceptin/orphanin FQ (N/OFQ) is an endogenous neuropeptide that selectively binds to and activates an opioidlike receptor called the N/OFQ peptide (NOP) receptor (previously called opioid receptor-like 1) (Meunier et al., 1995;Reinscheid et al., 1995). Although the N/OFQ-NOP system belongs to the opioid receptor family, classic opioid receptor agonists do not display appreciable binding affinity to the NOP receptor and vice versa (Lachowicz et al., 1995;Mollereau et al., 1999). Moreover, the N/OFQ-NOP system has pharmacological and physiological actions that are distinct from classic opioid receptor systems.We and other investigators have established that the central administration of N/OFQ produces novel changes in cardiovascular and renal excretory function. In conscious rats (Kapusta et al

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Section: Discussionmentioning

confidence: 99%

Nociceptin/Orphanin FQ (N/OFQ)-Evoked Bradycardia, Hypotension, and Diuresis Are Absent in N/OFQ Peptide (NOP) Receptor Knockout Mice

Burmeister¹,

Ansonoff²,

Pintar³

et al. 2008

J Pharmacol Exp Ther

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“…Chronic stress increases the risk of developing T2DM, CVD, and mental health disorders [12]. The HPA axis and the SNS are hyperactivated in T2DM and have been linked with the development of CVD [13,14]. Studies have reported that T2DM-related disorders begin during prediabetes, which is a condition that precedes T2DM [15].…”

Section: Introductionmentioning

confidence: 99%

The Role of Pro-Opiomelanocortin Derivatives in the Development of Type 2 Diabetes-Associated Myocardial Infarction: Possible Links with Prediabetes

Gumede,

Khathi

2024

Biomedicines

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Myocardial infarction is a major contributor to CVD-related mortality. T2DM is a risk factor for MI. Stress activates the HPA axis, SNS, and endogenous OPS. These POMC derivatives increase the blood glucose and cardiovascular response by inhibiting the PI3K/AkT insulin signaling pathway and increasing cardiac contraction. Opioids regulate the effect of the HPA axis and SNS and they are cardioprotective. The chronic activation of the stress response may lead to insulin resistance, cardiac dysfunction, and MI. Stress and T2DM, therefore, increase the risk of MI. T2DM is preceded by prediabetes. Studies have shown that prediabetes is associated with an increased risk of MI because of inflammation, hyperlipidemia, endothelial dysfunction, and hypertension. The HPA axis is reported to be dysregulated in prediabetes. However, the SNS and the OPS have not been explored during prediabetes. The effect of prediabetes on POMC derivatives has yet to be fully explored and understood. The impact of stress and prediabetes on the cardiovascular response needs to be investigated. This study sought to review the potential impact of prediabetes on the POMC derivatives and pathways that could lead to MI.

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Stress and endogenous opioids: Behavioral and circulatory interactions

McCubbin

1993

Biological Psychology

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Opioids in Pain and Cardiovascular Responses: Overview of Common Features

Cited by 8 publications

References 94 publications

Nociceptin/Orphanin FQ (N/OFQ)-Evoked Bradycardia, Hypotension, and Diuresis Are Absent in N/OFQ Peptide (NOP) Receptor Knockout Mice

Nociceptin/Orphanin FQ (N/OFQ)-Evoked Bradycardia, Hypotension, and Diuresis Are Absent in N/OFQ Peptide (NOP) Receptor Knockout Mice

The Role of Pro-Opiomelanocortin Derivatives in the Development of Type 2 Diabetes-Associated Myocardial Infarction: Possible Links with Prediabetes

Stress and endogenous opioids: Behavioral and circulatory interactions

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