Calcitonin gene-related peptide mediates nitroglycerin and sodium nitroprusside-induced vasodilation in feline cerebral arterioles.

Wei, Enoch P.; Moskowitz, Mark A.; Boccalini, Pia; Kontos, Hermes A.

doi:10.1161/01.res.70.6.1313

Cited by 219 publications

(139 citation statements)

References 32 publications

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“…Previous studies have suggested that nitroglycerin activates capsaicin sensitive sensory nerves to release CGRP (Wei et al, 1992;Hu et al, 1999;Zhou et al, 2001a;Du et al, 2004;Ghatta and O'Rourke, 2006). The present results showed that nitroglycerin caused a concentration-dependent relaxation and a depressor effect, concomitantly with an increase in the release of CGRP in isolated rat thoracic aorta and in the concentration of CGRP in plasma.…”

Section: Discussionsupporting

confidence: 72%

“…Previous studies have suggested that nitroglycerin can evoke the release of CGRP from capsaicin-sensitive sensory nerves (Wei et al, 1992;Hu et al, 1999;Zhou et al, 2001a;Du et al, 2004;Ghatta and O'Rourke, 2006). We and others have also shown that CGRP mediates the depressor effect and vasodilation produced by nitroglycerin via the cGMP pathway (Zhou et al, 2001a;Booth et al, 2000), and that the decreased depressor effect of nitroglycerin in tolerant states is also related to a decrease in CGRP release (Oroszi et al, 1999;Zhou et al, 2001b;Ghatta and O'Rourke, 2006).…”

Section: Introductionmentioning

confidence: 64%

“…The present results showed that nitroglycerin caused a concentration-dependent relaxation and a depressor effect, concomitantly with an increase in the release of CGRP in isolated rat thoracic aorta and in the concentration of CGRP in plasma. We and others have demonstrated that the vasodilator responses and depressor effect of nitroglycerin are attenuated or abolished by CGRP-(0-37), the CGRP receptor antagonist, or capsaicin, which selectively depletes CGRP in sensory nerves (Wei et al, 1992;Zhou et al, 2001a,c). It has been reported that methylene blue, an inhibitor of soluble guanylate cyclase, abolishes the increased release of CGRP produced by nitroglycerin (Zhou et al, 2001a).…”

Section: Discussionmentioning

confidence: 91%

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Decrease in endogenous CGRP release in nitroglycerin tolerance: Role of ALDH-2

Chen

Nie

Wang

et al. 2007

European Journal of Pharmacology

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In the present study, we tested whether the decreased release of calcitonin gene-related peptide (CGRP) observed in nitroglycerin tolerance is associated with the decrease in aldehyde dehydrogenase (ALDH-2) activity. We further investigated the possible involvement of reactive oxygen species in the decrease in ALDH-2 activity. Tolerance was induced by exposure of isolated rat thoracic aortas and human umbical vein endothelial cells (HUVEC) to nitroglycerin in vitro or by pretreatment with nitroglycerin for 8 days in vivo. Pretreatment with ALDH-2 inhibitors and nitroglycerin significantly attenuated vasodilator responses to nitroglycerin concomitantly with a decrease in the release of CGRP from the isolated thoracic aorta. Nitroglycerin produced a depressor effect concomitantly with an increase in plasma concentrations of CGRP, and the effect of nitroglycerin was attenuated after pretreatment with an inhibitor of ALDH-2 or nitroglycerin for 8 days. Exposure of HUVEC to nitroglycerin for 16 h increased reactive oxygen species production and decreased ALDH-2 activity as well as cGMP production in a time-and concentration-dependent manner. Pretreatment with an ALDH-2 inhibitor also significantly decreased the cGMP production. However, tolerance to nitroglycerin in HUVEC was restored in the presence of N-acetylcysteine or captopril. The present results suggest that nitrate tolerance is, at least partially, associated with a decrease in endogenous CGRP release via a decrease in ALDH-2 activity as a result of stimulation of reactive oxygen species production.

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Section: Discussionsupporting

confidence: 72%

Section: Introductionmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 91%

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Decrease in endogenous CGRP release in nitroglycerin tolerance: Role of ALDH-2

Chen

Nie

Wang

et al. 2007

European Journal of Pharmacology

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“…In vivo experiments using a rat model of endotoxicosis have shown that the early hypotension and the loss of vascular responsiveness to noradrenaline occurring within the first 1 h of shock was dependent on NO production and apparently involved the activation of cNOS in either endothelial or neural cells (Wright et al, 1992;Szabo et al, 1993). Some studies have shown that NO appears to increase CGRP release from perivascular nerves in cerebral arteries (Wei et al, 1992), and microvessels in skin (Holzer & Jocic, 1994;Hughes & Brain, 1994;Kajekar et al, 1995) by observation of blood flow in response to a CGRP receptor blocker. On the other hand, several studies have indicated that CGRP does not account for vasodilatation in response to NO (Ralevic et al, 1992;Ayajiki et al, 1994;Faraci & Breese, 1994;Brian et al, 1995).…”

Section: Resultsmentioning

confidence: 99%

Rapid nitric oxide‐ and prostaglandin‐dependent release of calcitonin gene‐related peptide (CGRP) triggered by endotoxin in rat mesenteric arterial bed

Wang¹,

Wu²,

Tang³

et al. 1996

British J Pharmacology

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1 Our objective was to determine whether endotoxin (ETX) could directly trigger the release of calcitonin gene-related peptide (CGRP) from perivascular sensory nerves in the isolated mesenteric arterial bed (MAB) of the rat and to determine whether nitric oxide (NO) and prostaglandins (PGs) are involved. 2 ETX caused time-and concentration-dependent release of CGRP, and as much as a 17 fold increase in CGRP levels in the perfusate at 10-15 min after the administration of ETX (50 ,ug ml-'). 3 CGRP-like immunoreactivity in the perfusate was shown to co-elute with synthetic rat CGRP by reverse-phase h.p.l.c. 4 Pretreatment of MAB with capsaicin or ruthenium red inhibited ETX-induced CGRP release by 90% and 71%, respectively. ETX-evoked CGRP release was decreased by 84% during Ca2"-free perfusion.5 The release of CGRP evoked by ETX was enhanced by L-arginine by 43% and inhibited by Nwnitro-L-arginine (L-NOARG) and methylene blue by 37% and 38%, respectively. L-Arginine reversed the effect of L-NOARG. 6 Indomethacin and ibuprofen also inhibited the ETX-induced CGRP release by 34% and 44%, respectively. No additive inhibition could be found when L-NOARG and indomethacin were concomitantly incubated. 7 The data suggest that ETX triggers the release of CGRP from capsaicin-sensitive sensory nerves innervating blood vessels. The ETX-induced CGRP release is dependent on extracellular Ca2" influx and involves a ruthenium red-sensitive mechanism. Both NO and PGs appear to be involved in the ETXinduced release of CGRP in the rat mesenteric arterial bed.

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“…and is implicated in the pathogenesis of migraine by activating trigeminovascular fibers and causing release of CGRP [39,40]. NO is synthesized from L-arginine by NO synthase.…”

Section: Nitric Oxide Antagonismmentioning

confidence: 99%

Update on future headache treatments

Nagy

Rapoport

2013

Neurol Sci

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Headache disorders are common and heterogenous neurologic entities. The complexities of management are further encumbered by the relatively few effective choices for acute and preventive therapies available to the headache specialist to treat these diverse disorders. As advances have been made in uncovering headache pathophysiology, new therapies have surfaced and others are forthcoming. This article will highlight new lines of care in development. There are several novel delivery mechanisms of familiar medications which bypass the limitations of current delivery systems, including the sumatriptan iontophoretic patch Zecuity, the intranasal sumatriptan OptiNose system, the zolmitriptan Rapidfilm orally dissolvable film and the orally inhaled dihydroergotamine Levadex system. New lines of care based upon recently discovered therapeutic targets will also be discussed including calcitonin gene-related peptide (CGRP) receptor antagonists, serotonin receptor agonists, and sphenopalatine ganglion (SPG) intermittent stimulation. Finally, emerging targets for future therapeutics will be explored including transient receptor potential vanilloid (TRPV1) receptor modulators, nitric oxide (NO) antagonists, gap junction modulators, glutamate receptor antagonists, orexin receptor antagonists and prostanoid receptor antagonists. Therapies developing over the next several years will be welcome additions to the headache specialist's armamentarium.

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Calcitonin gene-related peptide mediates nitroglycerin and sodium nitroprusside-induced vasodilation in feline cerebral arterioles.

Cited by 219 publications

References 32 publications

Decrease in endogenous CGRP release in nitroglycerin tolerance: Role of ALDH-2

Decrease in endogenous CGRP release in nitroglycerin tolerance: Role of ALDH-2

Rapid nitric oxide‐ and prostaglandin‐dependent release of calcitonin gene‐related peptide (CGRP) triggered by endotoxin in rat mesenteric arterial bed

Update on future headache treatments

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