Nω-Nitro-L-Arginine Blocks the Second Phase But Not the First Phase of the Endothelium-Dependent Relaxations Induced by Substance P in Isolated Rings of Pig Carotid Artery

Fiscus, Ronald R.; Gross, David R.; Hao, Huiqing; Wang, Xian; Arden, W. A.; Maley, Richard H.; Salley, Robert K.

doi:10.1097/00005344-199204002-00030

Cited by 22 publications

(4 citation statements)

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“…NO seems to be an important mediator of the SP‐induced relaxation in human omental vessels since the nitric oxide synthase inhibitor L‐NMMA diminished the relaxation. This is consistent with findings in some other vessels such as mouse pial arterioles (Rosenblum et al , 1993), dog superficial temporal arteries (Enokibori et al , 1994), pig and rabbit carotid arteries (Fiscus et al , 1992; Gross et al , 1994), dog cerebral arteries (Onoue et al , 1988) and human pial arteries (Petersson et al , 1995). In the present study the cyclo‐oxygenase inhibitor indomethacin did not affect the relaxation induced by SP, indicating that prostanoid synthesis is not involved in the relaxing mechanism triggered by SP, which contrasts to the findings in the human umbilical artery, where prostanoids, but not NO, mediate the SP‐induced relaxation (Bodelsson & Stjernquist, 1994).…”

Section: Discussionsupporting

confidence: 91%

Endothelium‐dependent relaxation by substance P in human isolated omental arteries and veins: relative contribution of prostanoids, nitric oxide and hyperpolarization

Wallerstedt

Bodelsson

1997

British J Pharmacology

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1 The objective of the present study was to investigate human omental arteries and veins with respect to: (i) the contractile eect of the thromboxane A 2 analogue U46619, (ii) endothelium-dependency and mediators of the relaxing eect of substance P (SP) and acetylcholine (ACh). 2 Changes in isometric tension in response to administration of U46619, SP and ACh were measured in human isolated omental arteries and veins with and without endothelium. To investigate the mechanism of action of SP, the SP-induced relaxation was measured in the presence of indomethacin (cyclo- 3 U46619 contracted both the artery and the vein segments. Endothelium removal did not alter the contraction. 4 ACh caused neither contraction nor relaxation in artery and vein segments precontracted with U46619. 5 In both artery and vein segments precontracted with U46619, SP produced endothelium-dependent relaxation. The relaxation was unaected by indomethacin, but was incompletely reduced by L-NMMA and KCl respectively. The L-NMMA-resistent relaxation was abolished in the presence of KCl. 6 TEA inhibited the SP-induced relaxation in artery and vein segments both in the presence and absence of L-NMMA and indomethacin, while glibenclamide and clotrimazole had no eect. 7 In conclusion, the SP-induced relaxation in human omental arteries and veins seems to be mediated via NO and endothelium-dependent hyperpolarization. K ATP and I KCa are probably not involved in the hyperpolarization, but activation of BK Ca may contribute to the hyperpolarization. Prostanoid synthesis and the cytochrome P450-system are probably not involved in the SP-induced relaxation in this area.

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Section: Discussionsupporting

confidence: 91%

Endothelium‐dependent relaxation by substance P in human isolated omental arteries and veins: relative contribution of prostanoids, nitric oxide and hyperpolarization

Wallerstedt

Bodelsson

1997

British J Pharmacology

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“…Endothelial cells may also respond to heightened activation of NK1 receptors by releasing inflammatory agents, including IL‐1β, prostacylins [ 23] and nitric oxide [ 24]. This reinforced local circuit provides a mechanistic explanation for a positive feedback pathway within the submucosa.…”

Section: Discussionmentioning

confidence: 99%

Increased expression of substance P receptor‐encoding mRNA in bladder biopsies from patients with interstitial cystitis

Marchand¹,

Sant

Kream³

1998

British Journal of Urology

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Increased levels of NK1 receptor-encoding mRNA within the bladder vascular endothelium suggests the up-regulation of NK1 receptor as a putative factor in the pathogenesis of pain related to IC. Increased responsiveness to SP released from the perivascular sensory terminals may result in a local cascade of neurogenic inflammatory responses which trigger the pathophysiological changes, including pain, characteristic of IC.

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“…calcitonin generelated peptide (CGRP) and substance P [16,17]. CGRP and substance P are recognized as major participants (i.e.…”

Section: Identification Of Edrf As No and The Discovery Of Other Actimentioning

confidence: 99%

Involvement of Cyclic GMP and Protein Kinase G in the Regulation of Apoptosis and Survival in Neural Cells

2002

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Our current understanding of nitric oxide (NO), cyclic GMP (cGMP) and protein kinase G (PKG) signaling pathways in the nervous systems has its origins in the early studies conducted on vascular tissues during the late 1970s and early to mid-1980s. The pioneering research into the NO/cGMP/PKG pathway in blood vessels conducted by the laboratories of Drs. Ferid Murad, Louis Ignarro and Robert Furchgott ultimately led to the awarding of the 1998 Nobel Prize in Physiology or Medicine to these three scientists. On the basis of further pioneering studies by Drs. John Garthwaite, Solomon Snyder, Steven Vincent and many other neuroscientists during the late 1980s and throughout the 1990s, it became recognized that NO serves as a neurotransmitter/neuromodulator in the central and peripheral nervous systems and that certain neural cells possess a cGMP signaling pathway similar to that in vascular smooth muscle cells. Although NO (at high concentrations) is toxic and thought to participate in neuronal cell death during stroke and neurodegenerative diseases (e.g. amyotrophic lateral sclerosis, Alzheimer’s disease, HIV dementia and Parkinson’s disease), recent evidence suggests that NO at low physiological concentrations can act as an antiapoptotic/prosurvival factor in certain neural cells (e.g. PC12 cells, motor neurons and neurons of dorsal root ganglia, hippocampus and sympathetic nerves). The antiapoptotic effects of NO are mediated, in part, by cGMP and a downstream target protein, PKG. Other cGMP-elevating factors (e.g. atrial and brain natriuretic peptides) and direct PKG activator (e.g. 8-bromo-cGMP) also have antiapoptotic effects which have been quantified by the new capillary electrophoresis with laser-induced fluorescence detector technology. Inhibition of soluble guanylyl cyclase and lowering of basal cGMP levels cause apoptosis in unstressed neural cells (NG108-15 and N1E-115 cells). The cGMP/PKG pathway appears to play an essential role in preventing activation of a proapoptotic pathway, thus promoting neural cell survival.

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Nω-Nitro-L-Arginine Blocks the Second Phase But Not the First Phase of the Endothelium-Dependent Relaxations Induced by Substance P in Isolated Rings of Pig Carotid Artery

Cited by 22 publications

References 0 publications

Endothelium‐dependent relaxation by substance P in human isolated omental arteries and veins: relative contribution of prostanoids, nitric oxide and hyperpolarization

Endothelium‐dependent relaxation by substance P in human isolated omental arteries and veins: relative contribution of prostanoids, nitric oxide and hyperpolarization

Increased expression of substance P receptor‐encoding mRNA in bladder biopsies from patients with interstitial cystitis

Involvement of Cyclic GMP and Protein Kinase G in the Regulation of Apoptosis and Survival in Neural Cells

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