ArticleThe Journal of physiology1998
Central role of heterocellular gap junctional communication in endothelium-dependent relaxations of rabbit arteries.
Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 280 citations in OpenAlex.
- Expression and function of Connexin 43 and Connexin 37 in the murine zona glomerulosa.Physiological reports · 2025Article
- Connexin 43 across the Vasculature: Gap Junctions and Beyond.Journal of vascular research · 2023Review
- Polarized Proteins in Endothelium and Their Contribution to Function.Journal of vascular research · 2021Review
- Uremic Toxins and Vascular Dysfunction.Toxins · 2020Review
- Connexin 43 gap junctions contribute to brain endothelial barrier hyperpermeability in familial cerebral cavernous malformations type III by modulating tight junction structure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Endothelium-Dependent Hyperpolarization (EDH) in Hypertension: The Role of Endothelial Ion Channels.International journal of molecular sciences · 2018Review
- Reactive oxygen species facilitate the EDH response in arterioles by potentiating intracellular endothelial Ca(2+) release.Free radical biology & medicine · 2016Article
- Contribution of K(+) channels to endothelium-derived hypolarization-induced renal vasodilation in rats in vivo and in vitro.Pflugers Archiv : European journal of physiology · 2016Article
- The role of epoxyeicosatrienoic acids in the cardiovascular system.British journal of clinical pharmacology · 2015Review
- Reduced activity of SKC a and Na-K ATPase underlies the accelerated impairment of EDH-type relaxations in mesenteric arteries of aging spontaneously hypertensive rats.Pharmacology research & perspectives · 2015Article
- The myoendothelial junction: connections that deliver the message.Physiology (Bethesda, Md.) · 2014Review
- Sex differences in endothelial function in porcine coronary arteries: a role for H2O2 and gap junctions?British journal of pharmacology · 2014Article
- Nitric oxide pretreatment enhances atheroma component highlighting in vivo with intercellular adhesion molecule-1-targeted echogenic liposomes.Ultrasound in medicine & biology · 2014Article
- Traumatic brain injury in vivo and in vitro contributes to cerebral vascular dysfunction through impaired gap junction communication between vascular smooth muscle cells.Journal of neurotrauma · 2014Article
- Endothelial control of vasodilation: integration of myoendothelial microdomain signalling and modulation by epoxyeicosatrienoic acids.Pflugers Archiv : European journal of physiology · 2014Review
- Regulation of cellular communication by signaling microdomains in the blood vessel wall.Pharmacological reviews · 2014Review
- Decoding dynamic Ca(2+) signaling in the vascular endothelium.Frontiers in physiology · 2014Article
- Specificity in the participation of connexin proteins in flow-induced endothelial gap junction communication.Pflugers Archiv : European journal of physiology · 2013Article
- Connexin43 hemichannel-mediated regulation of connexin43.PloS one · 2013Article
- Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The contribution of gap junctions to endothelium-dependent relaxation was investigated in isolated rabbit conduit artery preparations pre-constricted by 10 microM phenylephrine (PhE). 2. Acetylcholine (ACh) relaxed the thoracic aorta by approximately 60 % and the superior mesenteric artery (SMA) by approximately 90 %. A peptide possessing sequence homology with extracellular loop 2 of connexin 43 (Gap 27, 300 microM) inhibited relaxation by approximately 40 % in both artery types. Gap 27 also attenuated the endothelium-dependent component of the relaxation induced by ATP in thoracic aorta but did not modify force development in response to PhE. 3. NG-nitro-L-arginine methyl ester (L-NAME, 300 microM), an inhibitor of NO synthase, attenuated ACh-induced relaxation by approximately 90 % in the aorta but only by approximately 40 % in SMA (P < 0.05). Residual L-NAME-insensitive relaxations were almost abolished by 300 microM Gap 27 in aorta and inhibited in a concentration-dependent fashion in SMA (approximately 50 % at 100 microM and approximately 80 % at 10 mM). Gap 27 similarly attenuated the endothelium-dependent component of L-NAME-insensitive relaxations to ATP in aorta. 4. Responses to cyclopiazonic acid, which stimulates endothelium-dependent relaxation through a receptor-independent mechanism, were also attenuated by Gap 27, whereas this peptide exerted no effect on the NO-mediated relaxation induced by sodium nitroprusside in preparations denuded of endothelium. 5. ACh-induced relaxation of 'sandwich' mounts of aorta or SMA were unaffected by Gap 27 but completely abolished by L-NAME. 6. We conclude that direct heterocellular communication between the endothelium and smooth muscle contributes to endothelium-dependent relaxations evoked by both receptor-dependent and -independent mechanisms. The inhibitory effects of Gap 27 peptide do not involve homocellular communication within the vessel wall or modulation of NO release or action.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.