Calcitonin gene-related peptide (CGRP) and its role in hypertension

Smillie, Sarah-Jane; Brain, Susan D.

doi:10.1016/j.npep.2010.12.002

Cited by 105 publications

(81 citation statements)

References 132 publications

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“…Numerous studies have shown that CGRP is one of the most potent microvascular vasodilators (Brain et al 2004;Gherardini et al 2009;Huang et al 2011;Smillie et al 2011). Owing to this property, CGRP has long been considered to be involved in the inflammation response; however, earlier studies have demonstrated that ablation of certain sensory fibers could result in a marked increase in the severity of inflammation (Szallasi et al 1996).…”

Section: Discussionmentioning

confidence: 99%

Calcitonin Gene-Related Peptide Ameliorates Hyperoxia-Induced Lung Injury in Neonatal Rats

Dang

Yang

Wang

et al. 2012

Tohoku J. Exp. Med.

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Therapies with prolonged exposure to high-concentration oxygen are common in the treatment of critical pulmonary and cardiac conditions in newborns. However, prolonged exposure to hyperoxia could result in lung damages and developmental disorders manifested as acute lung injury and bronchopulmonary dysplasia, respectively. Calcitonin gene-related peptide (CGRP) has been shown to have a broad regulatory effect on the respiratory system. In this study, we explored the protective effects of CGRP on the hyperoxia-induced lung damage. Newborn Sprague-Dawley rats were randomly divided into three groups: normoxia, hyperoxia, and hyperoxia with CGRP. Hyperoxia groups were exposed to 95% oxygen for 14 days and treated once every other day with saline or CGRP. Hyperoxia exposure reduced the survival rate to 73%, when compared with the 93% survival rate observed in the normoxia group. The survival rate was improved to 84% with CGRP treatment. Treatment with CGRP under hyperoxia significantly alleviated the hyperoxia-induced lung histomorphological changes and the increases in leukocyte counts and total protein levels in bronchoalveolar lavage fluid that reflect the pulmonary microvasular damages. CGRP treatment also restored the decreased activity of superoxide dismutase, while it decreased the increased level of malondialdehyde in the lung tissues. Importantly, CGRP treatment significantly decreased the magnitude of the hyperoxia-mediated increase in the expression levels of tumor necrosis factor-α mRNA and transforming growth factor-β 1 protein. In conclusion, the hyperoxia-induced acute lung injury is associated with both oxidative stress and inflammatory responses, and CGRP may ameliorate the hyperoxia-induced lung injury by down-regulating these processes.

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Section: Discussionmentioning

confidence: 99%

Calcitonin Gene-Related Peptide Ameliorates Hyperoxia-Induced Lung Injury in Neonatal Rats

Dang

Yang

Wang

et al. 2012

Tohoku J. Exp. Med.

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“…In subtotal nephrectomy (SN) and salt-induced hypertension, CGRP plays a compensatory role to attenuate the BP increase in the absence of an increase in the neuronal synthesis and release of this peptide (12,13). Therefore, the purpose of this study was to determine whether or not the mechanism of this anti-hypertensive activity is through enhanced sensitivity of the vasculature to the dilator actions of this neuropeptide.…”

Section: Discussionmentioning

confidence: 99%

Nicousamide normalizes renovascular hypertension in two-kidney one-clip hypertensive rats

Zhang

et al. 2012

Biomedical Reports

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Abstract. Nicousamide, a coumarin-aspirin compound, was proven to have a renal protective effect on diabetic and hypertensive nephropathy. The present study aimed to investigate the anti-hypertensive effect of nicousamide and its action mechanisms. The two-kidney one-clip (2K1C) hypertensive animal model was introduced in this study. Subsequent to treatment with nicousamide for three weeks, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were measured, and the plasma concentration of angiotensin II (Ang II), nitric oxide (NO), endothelin-1 (ET-1), nitric oxide synthase (NOS) and calcitonin gene-related peptide (CGRP) was examined. Results showed that nicousamide markedly decreased SBP as well as DBP on renovascular hypertensive rats (P<0.05). Nicousamide also reduced the Ang II and ET-1 concentration (P<0.05) in the plasma of hypertensive rats while increasing the plasma NO level (P<0.05). Nicousamide treatment did not show a marked effect on the NOS and CGRP concentrations in animal plasma (P>0.05).

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“…The vasodilator action of CGRP in mammals including humans is well documented (for reviews, see Brain and Grant, 2004;Smillie and Brain, 2011). CGRP-induced vasodilation is mediated in part through a nitric oxide (NO)-dependent mechanism or by production of prostaglandins.…”

Section: Ventilatory and Cardiovascular Actions Of Peripherally Adminmentioning

confidence: 99%

“…In mammals, CGRP and its receptors are widely distributed throughout the peripheral and central nervous systems (CNS). In the periphery, CGRP is a vasodilator, a hypotensive peptide and produces positive chronotropic and inotropic effects in the heart (Ando et al, 1990;Brain and Grant, 2004;Smillie and Brain, 2011). CGRP also affects gastrointestinal functions (Martinez and Tache, 2006).…”

Section: Introductionmentioning

confidence: 99%

Central ventilatory and cardiovascular actions of calcitonin gene-related peptide in unanesthetized trout

Mével

Lancien

Mimassi

et al. 2012

Journal of Experimental Biology

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SUMMARYCalcitonin gene-related peptide (CGRP) and its receptors are widely distributed in the tissues of teleost fish, including the brain, but little is known about the ventilatory and cardiovascular effects of the peptide in these vertebrates. The present study was undertaken to compare the central and peripheral actions of graded doses (5-50pmol) of trout CGRP on ventilatory and cardiovascular variables in unanesthetized rainbow trout. Compared with vehicle, intracerebroventricular injection of CGRP significantly elevated the ventilation frequency (f V ) and the ventilation amplitude (V AMP ) and, consequently, the total ventilation (V TOT ). The maximum hyperventilatory effect of CGRP (V TOT : +300%), observed at a dose of 50pmol, was mostly due to its stimulatory action on V AMP (+200%) rather than f V (+30%). In addition, CGRP produced a significant and dose-dependent increase in mean dorsal aortic blood pressure (P DA ) (50pmol: +40%) but the increase in heart rate (f H ) was not significant. Intra-arterial injections of CGRP were without effect on the ventilatory variables but significantly and dose-dependently elevated P DA (50pmol: +36%) without changing f H . At the highest dose tested, this hypertensive phase was preceded by a rapid and transient hypotensive response. In conclusion, our study suggests that endogenous CGRP within the brain of the trout may act as a potent neurotransmitter and/or neuromodulator in the regulation of cardio-ventilatory functions. In the periphery, endogenous CGRP may act as a local and/or circulating hormone preferentially involved in vasoregulatory mechanisms.

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Calcitonin gene-related peptide (CGRP) and its role in hypertension

Cited by 105 publications

References 132 publications

Calcitonin Gene-Related Peptide Ameliorates Hyperoxia-Induced Lung Injury in Neonatal Rats

Calcitonin Gene-Related Peptide Ameliorates Hyperoxia-Induced Lung Injury in Neonatal Rats

Nicousamide normalizes renovascular hypertension in two-kidney one-clip hypertensive rats

Central ventilatory and cardiovascular actions of calcitonin gene-related peptide in unanesthetized trout

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