CCK as a modulator of cardiovascular function

Lovick, T.A.

doi:10.1016/j.jchemneu.2009.06.007

Cited by 21 publications

(11 citation statements)

References 109 publications

(141 reference statements)

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“…These findings indicate that CCK has a variety of effects as a novel cardiovascular hormone. Previous studies have shown that CCK regulates blood pressure [22-24] and increases cardiac contractility [25]. Moreover, clinical studies have reported that plasma CCK levels are linked to cardiovascular mortality; thus, CCK concentrations may be useful as valuable biomarkers in elderly females with symptoms of cardiac disease, as shown in a previous study [26].…”

Section: Introductionmentioning

confidence: 69%

Cholecystokinin Expression in the Development of Postinfarction Heart Failure

Dong

Wang

Zhang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Cholecystokinin (CCK) is expressed in cardiomyocytes and may also play an important role in cardiovascular regulation. Clinical studies have shown that plasma CCK levels are an independent marker of cardiovascular mortality in cardiac disease. However, whether the development of postinfarction heart failure is associated with changes in CCK expression is unknown. Methods: To investigate CCK expression patterns and the association between CCK expression and heart functional parameters, we randomized male Sprague-Dawley rats into myocardial infarction (MI) or sham operation (SO) groups. CCK expression levels were assessed by western blotting, immunohistochemistry, real-time polymerase chain reaction (PCR), and enzyme-linked immunosorbent assay (ELISA) at different time points (2, 4 or 6 weeks) after surgery. Brain natriuretic peptide (BNP) concentrations were determined using Western blotting and ELISA, myocardial morphology was assessed by microscopy. Results: Plasma CCK and BNP levels were significantly increased in all the MI groups compared with the corresponding SO groups. However, the degree to which myocardial CCK mRNA and protein expression levels were increased the MI groups compared with the SO groups was greater in the 4- and 6-week groups than in the 2-week group. Furthermore, plasma CCK levels were positively correlated with BNP concentrations and left ventricular end-systolic diameter (LVDs) and significantly negatively correlated with the ejection fraction (EF) and shortening fraction (SF) in model animals. Conclusions: Heart failure progression after infarction is associated with upregulated CCK levels; thus, CCK may be useful as a novel marker of heart failure.

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Section: Introductionmentioning

confidence: 69%

Cholecystokinin Expression in the Development of Postinfarction Heart Failure

Dong

Wang

Zhang

et al. 2017

Cell Physiol Biochem

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“…We do not have evidence defining the role of the SFO in mediating CCK function, however, given the fact that CCK exerts a variety of physiological functions, a number of possibilities exist. These include potential CCK actions in the SFO to modulate cardiovascular function that occur in parallel to the meal termination process (42). CCK causes splanchnic vasodilatation that is followed by depressor and bradycardic effects (70).…”

Section: Discussionmentioning

confidence: 99%

The subfornical organ: a novel site of action of cholecystokinin

Ahmed

Dai

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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The subfornical organ (SFO) is an important sensory circumventricular organ implicated in the regulation of fluid homeostasis and energy balance. We investigated whether the SFO is activated by the hormone cholecystokinin (CCK). CCK₁ and CCK₂ receptors were identified in the SFO by RT-PCR. Dissociated SFO neurons that responded to CCK (40/77), were mostly depolarized (9.2 ± 0.9 mV, 30/77), but some were hyperpolarized (-7.3 ± 1.1 mV, 10/77). We next examined the responses of SFO neurons in vivo to CCK (16 μg/kg ip), in the presence and absence of CCK₁ or CCK₂ receptor antagonists (devazepide; 600 μg/kg and L-365,260; 100 μg/kg, respectively), using the functional activation markers c-Fos and phosphorylated extracellular signal-related kinase (p-ERK). The nucleus of the solitary tract (NTS) served as a control for CCK-induced activity. There was a significant increase in c-Fos expression in the NTS (259.2 ± 20.8 neurons) compared with vehicle (47.5 ± 2.5). Similarly, in the SFO, c-Fos was expressed in 40.5 ± 10.6 neurons in CCK-treated compared with 6.6 ± 2.7 in vehicle-treated rats (P < 0.01). Devazepide significantly reduced the effects of CCK in the NTS but not in SFO. L-365,260 blocked the effects of CCK in both brain regions. CCK increased the number of p-ERK neurons in NTS (27.0 ± 4.0) as well as SFO (18.0 ± 4.0), compared with vehicle (8.0 ± 2.6 and 4.3 ± 0.6, respectively; P < 0.05). Both devazepide and L-365,260 reduced CCK-induced p-ERK in NTS, but only L-365,260 reduced it in the SFO. In conclusion, the SFO represents a novel brain region at which circulating CCK may act via CCK₂ receptors to influence central autonomic control.

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“…In adult BPH/2J mice we observed higher levels of mRNA for cholecystokinin (Cck), which is able to stimulate vasopressin and oxytocin release (28), receptor activity modifying protein 3 (Ramp3), which is correlated with stress-induced hypertension (26), RAR-related orphan receptor alpha (Rora), a transcription factor that provides neuroprotection by increas- Fig. 1.…”

Section: Discussionmentioning

confidence: 99%

Global identification of the genes and pathways differentially expressed in hypothalamus in early and established neurogenic hypertension

Marques

Campain

Davern³

et al. 2011

Physiological Genomics

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The hypothalamus has an important etiological role in the onset and maintenance of hypertension and stress responses in the Schlager high blood pressure (BP) (BPH/2J) mouse, a genetic model of neurogenic hypertension. Using Affymetrix GeneChip Mouse Gene 1.0 ST Arrays we identified 1,019 hypothalamic genes whose expression differed between 6 wk old BPH/2J and normal BP (BPN/3J) strains, and 466 for 26 wk old mice. Of these, 459 were in 21 mouse BP quantitative trait loci. We validated 46 genes by qPCR. Gene changes that would increase sympathetic outflow at both ages were: Dynll1 encoding dynein light chain LC8-type 1, which physically destabilizes neuronal nitric oxide synthase, decreasing neuronal nitric oxide, and Hcrt encoding hypocretin and Npsr1 encoding neuropeptide S receptor 1, each involved in sympathetic response to stress. At both ages we identified genes for inflammation, such as CC-chemokine ligand 19 (Ccl19), and oxidative stress. Via reactive oxygen species generation, these could contribute to oxidative damage. Other genes identified could be responding to such perturbations. Atp2b1, the major gene from genome-wide association studies of BP variation, was underexpressed in the early phase. Comparison of profiles of young and adult BPH/2J mice, after adjusting for maturation genes, pointed to the proopiomelanocortin-α gene (Pomc) and neuropeptide Y gene (Npy), among others, as potentially causative. The present study has identified a diversity of genes and possible mechanisms involved in hypertension etiology and maintenance in the hypothalamus of BPH/2J mice, highlighting both common and divergent processes in each phase of the condition.

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CCK as a modulator of cardiovascular function

Cited by 21 publications

References 109 publications

Cholecystokinin Expression in the Development of Postinfarction Heart Failure

Cholecystokinin Expression in the Development of Postinfarction Heart Failure

The subfornical organ: a novel site of action of cholecystokinin

Global identification of the genes and pathways differentially expressed in hypothalamus in early and established neurogenic hypertension

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