Nitric oxide is an autocrine feedback inhibitor of vascular smooth muscle contraction

Yeh, Jennifer L.; Whitney, Eric; Lamb, Shannon; Brophy, Colleen M.

doi:10.1016/s0039-6060(96)80221-2

Cited by 21 publications

(13 citation statements)

References 15 publications

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“…A number of functional studies have failed to detect constitutive NOS enzymatic activity in vascular smooth muscle cells (Bredt & Snyder, 1990; Fleming et al , 1991; Nozaki et al , 1993). However, the marked facilitatory effects of NOS inhibitors on contractions in endothelium‐denuded strips of aorta and carotid artery suggest that some VSMCs do indeed possess a constitutive form of NOS (Charpie & Webb, 1993; Yeh et al , 1996). Additionally, the NO produced by this Ca 2+ ‐calmodulin dependent enzyme may serve as an autocrine inhibitor of contraction in vascular smooth muscle (Wood et al , 1990).…”

Section: Discussionmentioning

confidence: 99%

Internally applied endotoxin and the activation of BK channels in cerebral artery smooth muscle via a nitric oxide‐like pathway

Hoang

Mathers

1998

British J Pharmacology

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1 In this study the role of nitric oxide synthase (NOS) in the acute activation of large conductance, Ca 2+ -activated K + channels (BK channels) by internally applied E. coli lipopolysaccharide (LPS, endotoxin) was examined in vascular smooth muscle cells. 2 Cerebrovascular smooth muscle cells (CVSMCs) were enzymatically dispersed from the middle, posterior communicating and posterior cerebral arteries of adult Wistar rats and maintained at 48C for 2 ± 4 days before recording with standard patch-clamp techniques. 3 Acute application of LPS (100 mg ml 71 ) to inside-out patches of CVSMC membrane isolated in a cell-free environment rapidly and reversibly increased the open probability, P o of BK channels in these patches by 3.3+0.30 fold. 4 Acute application of the nitric oxide (NO) donor sodium nitroprusside (SNP, 100 mM) to inside-out patches of CVSMC membrane, studied in the presence of intact cells, also reversibly increased P o , by some 1.8+0.2 fold over control. 5 Kinetic analysis showed that both LPS and SNP increased P o by accelerating the rate of BK channel reopening, rather than by retarding the closure of open channels. 6 Neither LPS nor SNP altered the reversal potential or conductance of BK channels. 7 The NOS substrate L-arginine (1 mM) potentiated the acute activation of BK channels by LPS, while the synthetic enantiomer D-arginine (1 mM) inhibited the action of LPS on BK channels. 8 The acute activation of BK channels by LPS was suppressed by pre-incubation of cells with N o -nitro-L-arginine (50 mM) or N o -nitro-L-arginine methyl ester (1 mM), two competitive antagonists of nitric oxide synthases. N o -nitro-D-arginine (50 mM), a poor inhibitor of NOS in in vitro assays, had no e ect on BK channel activation by LPS. 9 These results indicate that excised, inside-out patches of CVSMC membrane exhibit a NOS-like activity which is acutely activated when LPS is present at the cytoplasmic membrane surface. Possible relationships between this novel mechanism and the properties of known isoforms of nitric oxide synthase are discussed.

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Section: Discussionmentioning

confidence: 99%

Internally applied endotoxin and the activation of BK channels in cerebral artery smooth muscle via a nitric oxide‐like pathway

Hoang

Mathers

1998

British J Pharmacology

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“…Removal of the endothelium has been previously confirmed with our preparation by the The vasomotor response of a vascular bed to a vasoabsence of relaxation to acetylcholine and by scanning electron miactive agonist reflects the interaction of neurogenic, croscopy [7]. The VSM was cut into transverse strips 2-3 mm wide.…”

Section: Introductionmentioning

confidence: 64%

Renal Artery Smooth Muscle Is Refractory to Contraction by Angiotensin II

et al. 1996

Journal of Surgical Research

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“…The interactions between NOS, nitric oxide (NO) and l ‐NMMA are also complicated. Calcium fluctuations induce NOS activity as a possible autocrine regulatory mechanism (Yeh et al 1996). Nitric oxide inhibits the neural release of ACh, with NOS inhibition resulting in increased ACh release (Hryhorenko et al 1994).…”

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confidence: 99%

Acetylcholine acutely modifies nitric oxide synthase function in the human coronary circulation

Miner

Al‐Hesayen

Nield

et al. 2010

Experimental Physiology

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Intracoronary infusions of acetylcholine (ACh) and the nitric oxide synthase (NOS) inhibitor NG -monomethyl-l-arginine (l-NMMA) are routinely used to assess endothelial function in the human coronary circulation. Currently, there are no studies that examine whether the response to one of these agents predicts the response to the other in a given individual. We sought to determine whether human coronary vasomotor responses to intracoronary ACh are predictive of the response to intracoronary l-NMMA. Following diagnostic coronary angiography, a coronary sinus catheter was placed. Sequential intracoronary infusions of ACh and l-NMMA were performed in 14 patients without severe coronary artery disease (CAD). In nine patients with severe CAD, only l-NMMA was infused. Quantitative coronary angiography was performed immediately following infusions to determine changes in coronary diameter. Coronary sinus oxygen saturation and the transcardiac oxygen saturation gradients were determined during infusions as an index of coronary blood flow (CBF). There were no significant differences in the prevalence of hypertension, diabetes, smoking or plasma creatinine or cholesterol levels between patients with and without severe CAD. In the 14 patients without severe CAD, ACh reduced coronary diameter on average by 8% (from 2.7 ± 0.8 to 2.5 ± 0.8 mm, P = 0.003) and reduced the transcardiac oxygen saturation gradient from 63 ± 8 to 42 ± 16% (P = 0.0001). N G -Monomethyl-l-arginine had no significant effect on coronary diameter (from 2.7 ± 0.8 to 2.7 ± 0.8 mm, n.s.) and did not alter the transcardiac oxygen saturation gradient (from 63 ± 8 to 63 ± 7%, n.s.). A positive rather than negative correlation was observed between the AChand l-NMMA-induced changes in coronary diameter (r = 0.752, P = 0.0002). In nine patients with severe CAD who did not receive ACh, l-NMMA had no effect on coronary diameter but produced an increased transcardiac oxygen saturation gradient consistent with reduced CBF (from 58 ± 5 to 62 ± 4%, P = 0.003). The CBF response to l-NMMA was significantly different between the two groups (P = 0.002). The failure of l-NMMA to reduce CBF following ACh infusion, in contrast to the results seen in the l-NMMA-only group, suggests that NOS had been rendered dysfunctional by the ACh infusion itself. The positive correlation in changes to coronary diameter between ACh and l-NMMA suggests that the degree of NOS dysfunction was directly correlated to the degree of preceding activation by ACh. Combined, these unexpected results suggest that ACh administration may acutely modify the function of NOS in the human coronary circulation.

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Nitric oxide is an autocrine feedback inhibitor of vascular smooth muscle contraction

Cited by 21 publications

References 15 publications

Internally applied endotoxin and the activation of BK channels in cerebral artery smooth muscle via a nitric oxide‐like pathway

Internally applied endotoxin and the activation of BK channels in cerebral artery smooth muscle via a nitric oxide‐like pathway

Renal Artery Smooth Muscle Is Refractory to Contraction by Angiotensin II

Acetylcholine acutely modifies nitric oxide synthase function in the human coronary circulation

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