Vasoactive intestinal polypeptide relaxes isolated rat pulmonary artery rings through two distinct mechanisms

Zhang, Shuang; Liu, Yun; Guo, Shouli; Zhang, Jianing; Chu, Xiaojie; Jiang, Chun; Zhu, Daling

doi:10.1007/s12576-010-0107-x

Cited by 18 publications

(10 citation statements)

References 31 publications

(32 reference statements)

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“…23,56 In rats, pulmonary artery ring glibenclamide can abolish the vasodilation effect of VIP, 57 and VIP-elicited coronary vasodilation in rats involves activation of K ATP channels. 23,56 In rats, pulmonary artery ring glibenclamide can abolish the vasodilation effect of VIP, 57 and VIP-elicited coronary vasodilation in rats involves activation of K ATP channels.…”

Section: Discussionmentioning

confidence: 99%

“…Infusion of vasoactive intestinal polypeptide (VIP) induced a short-lasting dilation (30 minutes) and provoked migraine attacks in few patients. 23,56 In rats, pulmonary artery ring glibenclamide can abolish the vasodilation effect of VIP, 57 and VIP-elicited coronary vasodilation in rats involves activation of K ATP channels. 58 No pre-or clinical studies to date have investigated the effect of VIP on K ATP channels on VIP-induced dilation of cranial arteries.…”

Section: Discussionmentioning

confidence: 99%

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Levcromakalim, an Adenosine Triphosphate‐Sensitive Potassium Channel Opener, Dilates Extracerebral but not Cerebral Arteries

et al. 2019

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Background ATP‐sensitive potassium (KATP) channel opener levcromakalim induces migraine attacks in migraine patients. Underlying mechanisms responsible for headache and migraine induction after levcromakalim infusion are unknown. Objective To investigate the effect of levcromakalim on the cranial arteries and to explore the possible relationship between the middle meningeal artery (MMA) dilation and headache. Methods In a double‐blind, randomized, placebo‐controlled study, 20 healthy volunteers were scanned at the baseline and repeatedly after infusion of levcromakalim (n = 14) and placebo (n = 6). All participants received a subcutaneous injection of sumatriptan 6 mg before the last scanning. Results The MMA circumference was significantly larger after levcromakalim compared with placebo (P < .0001). The MMA dilation lasted over 5 hours during observational period. We found a significant association between headache and MMA dilation (P < .0001). The superficial temporal artery (STA) circumference was significantly larger after levcromakalim compared with placebo (P = .03) over the initial period (110 minutes). Over the entire observational period, there was no difference in circumference of the STA and the middle cerebral artery (MCA) between levcromakalim and placebo. Conclusion Levcromakalim dilated the MMA but not MCA. The MMA dilation was associated with headache. Future studies should investigate whether opening of KATP channels can activate and sensitize the perivascular nociceptors.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Levcromakalim, an Adenosine Triphosphate‐Sensitive Potassium Channel Opener, Dilates Extracerebral but not Cerebral Arteries

et al. 2019

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“…Because lesions of the superior cervical ganglion alone did not have this effect (Schmid et al, 1999), and because the loss of the PPG was common to all three groups, a role for the pterygopalatine ganglia is supported. If this is true, then the “fine tuning” may be mediated by VIP, a potent smooth muscle relaxant (Zhang et al, 2010) the loss of which would be common to all three groups. Perhaps acetylcholine and VIP innervate different subsets of NVSM.…”

Section: Discussionmentioning

confidence: 99%

Parasympathetic influences on emmetropization in chicks: Evidence for different mechanisms in form deprivation vs negative lens-induced myopia

Nickla

Schroedl

2012

Experimental Eye Research

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Ciliary ganglionectomy inhibits the development of myopia in chicks (Schmid et al., 1999), but has no effect on the compensatory responses to spectacle lenses (Schmid and Wildsoet, 1996). This study was done to assess the potential influence of the other parasympathetic input to the choroid, the pterygopalatine ganglia, on the choroidal and axial responses to retinal defocus, and to form deprivation. 4–5 week-old chicks had one of the following surgeries to one eye: (1) Section (X) of the autonomic part of cranial N VII (input to the pterygopalatine ganglia) (PPGX, n=16), (2) PPGX plus ciliary ganglionectomy (PPG/CGX, n=23) or (3) PPGX plus superior cervical ganglionectomy (PPG/SCGX, n=10). Experimental eyes were fitted with positive or negative lenses, or diffusers, several days after surgery. In one group of PPG/CGX, eyes did not wear any devices (n=8). Intact (no surgery) controls were done for all visual manipulations (lenses or diffusers). Sham surgeries were done for the PPG/CGX condition (n=4). Ocular dimensions were measured using A-scan ultrasonography prior to the surgery, 5 days later when visual devices were placed on the eyes, at the end of lens- or diffuser- wear, and in the case of diffusers, 4 days after diffuser removal to look at “recovery”. Refractive errors were measured using a Hartinger’s refractometer. IOP was measured in 7 PPG/CGX birds 7d after surgery. PPGX/CGX resulted in choroidal thickening (125 μm) and a decrease in IOP over one week post-surgery. It also prevented the development of myopia in response to form deprivation (X vs intact: 0.2 D vs −4.1 D; p<0.005), by preventing the increase in axial elongation (250 μm vs 670 μm/5d; p<0.005). In fact, growth rate slowed below normal (X vs fellow eyes: 250 μm vs 489 μm/5d; p=0.002). By contrast, there were no effects of this lesion on the development of myopia in response to negative lenses (X vs intact: −5.4 D vs −5.3 D). All three lesions inhibited the compensatory choroidal thickening in response to myopic defocus (ANOVA, p=0.0008), but had no effect on the thinning response to hyperopic defocus. These results argue for different underlying mechanisms for the growth responses to form deprivation versus negative lens wear. They also imply that choroidal thickening and thinning are not opposing elements of a single mechanism.

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“…Expression of VPAC2 in the lymphatic endothelium may suggest this cell layer as an intermediary in VIP actions. Indeed, in several vascular beds, vasodilatation caused by VIP has been suggested to be fully or partially mediated by endothelium‐derived NO (Hattori et al 1992; Jovanovic et al 1998; Grant et al 2006; Anaid et al 2007; Shahbazian et al 2007; Zhang et al 2010). In guinea pig mesenteric lymphatics, NO does not seem to be involved in VIP‐induced responses, as neither pump inhibition nor hyperpolarization was affected by the NOS inhibitor l ‐NNA.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of VIP‐induced inhibition of the lymphatic vessel pump

Weid

Rehal

Dyrda

et al. 2012

The Journal of Physiology

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Key points• Lymphatic pumping is characterized by the ability of collecting lymphatic vessels to contract in a phasic manner to propel lymph. This activity is critical for tissue fluid homeostasis and immune cell transport to lymph nodes.• Vasoactive intestinal peptide (VIP) is a neuro-immuno-modulator with anti-inflammatory properties released by peptidergic nerves and by inflammatory cells patrolling the interstitium and lymph.• Here we report that VIP is present in lymphatic vessels as well as in the lymph and that it potently inhibits lymphatic pumping and hyperpolarizes the lymphatic muscle via stimulation of VPAC2 VIP receptors, activation of protein kinase A and opening of ATP-sensitive K + channels.• These results suggest an important role for VIP in inhibiting lymphatic pumping. This process might become critical during inflammation, where it would lead to decreased lymph drainage, oedema formation and compromised immune cell trafficking.Abstract Lymphatic vessels serve as a route by which interstitial fluid, protein and other macromolecules are returned to the blood circulation and immune cells and antigens gain access to lymph nodes. Lymph flow is an active process promoted by rhythmical contraction-relaxation events occurring in the collecting lymphatic vessels. This lymphatic pumping is an intrinsic property of the lymphatic muscles in the vessel wall and consequent to action potentials. Compromised lymphatic pumping may affect lymph and immune cell transport, an action which could be particularly detrimental during inflammation. Importantly, many inflammatory mediators alter lymphatic pumping. Vasoactive intestinal peptide (VIP) is a neuro-and immuno-modulator thought to be released by nerve terminals and immune cells in close proximity to lymphatic vessels. We demonstrated the presence of the peptide in lymphatic vessels and in the lymph and examined the effects of VIP on mesenteric collecting lymphatic vessels of the guinea pig using pharmacological bioassays, intracellular microelectrode electrophysiology, immunofluorescence and quantitative real-time PCR. We showed that VIP alters lymphatic pumping by decreasing the frequency of lymphatic contractions and hyperpolarizing the lymphatic muscle membrane potential in a concentration-dependent manner. Our data further suggest that these channels. Inhibition of lymphatic pumping by VIP may compromise lymph drainage, oedema resolution and immune cell trafficking to the draining lymph nodes.

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Vasoactive intestinal polypeptide relaxes isolated rat pulmonary artery rings through two distinct mechanisms

Cited by 18 publications

References 31 publications

Levcromakalim, an Adenosine Triphosphate‐Sensitive Potassium Channel Opener, Dilates Extracerebral but not Cerebral Arteries

Levcromakalim, an Adenosine Triphosphate‐Sensitive Potassium Channel Opener, Dilates Extracerebral but not Cerebral Arteries

Parasympathetic influences on emmetropization in chicks: Evidence for different mechanisms in form deprivation vs negative lens-induced myopia

Mechanisms of VIP‐induced inhibition of the lymphatic vessel pump

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