scholarly journals Vasorelaxing Action of Vasonatrin Peptide is Associated with Activation of Large-Conductance Ca2+-activated Potassium Channels in Vascular Smooth Muscle Cells

2010 ◽  
pp. 187-194
Author(s):  
J Yu ◽  
M Zhu ◽  
Z Fu ◽  
X Zhu ◽  
Y Zhao ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Patch Clamp ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Radial Artery ◽  
Vascular Smooth Muscle Cells ◽  
Guanylyl Cyclase ◽  
Muscle Cells ◽  
Whole Cell ◽  
Rat Mesenteric Artery

The aim of this study was to test the hypothesis that vasorelaxing action of vasonatrin peptide (VNP) is due to activation of the large-conductance Ca2+-activated potassium channel (BKCa) via guanylyl cyclase (GC)-coupled natriuretic peptide receptors (NPRs) in vascular smooth muscle cells (VSMCs). Contraction experiments were performed using human radial artery, whereas BKCa current by patch clamp was recorded in cells from rat mesenteric artery. Contractility of rings cut from human radial artery was detected in vitro. As a result, VNP induced a dose-dependent vasorelaxation of human radial artery, which could be mimicked by 8-Br-cGMP, and suppressed by TEA, a blocker of BKCa, HS-142-1, a blocker of GC-coupled NPRs, or methylene blue (MB), a selective inhibitor of guanylyl cyclase. Sequentially, whole-cell K+ currents were recorded using patch clamp techniques. BKCa current of VSMCs isolated from rat mesentery artery was obtained by subtracting the whole cell currents after applications of 10-7 mol/l iberiotoxin (IBX) from before its applications. In accordance with the results of arterial tension detection, BKCa current was significantly magnified by VNP, which could also be mimicked by 8-Br-cGMP, whereas suppressed by HS-142-1, or MB. Taken together, VNP acts as a potent vasodilator, and NPRA/B-cGMP-BKCa is one possible signaling system involved in VNP induced relaxation.

Hydrogen sulfide-induced relaxation of resistance mesenteric artery beds of rats

2004 ◽  
Vol 287 (5) ◽  
pp. H2316-H2323 ◽  
Author(s):  
Youqin Cheng ◽  
Joseph Fomusi Ndisang ◽  
Guanghua Tang ◽  
Kun Cao ◽  
Rui Wang
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Mesenteric Artery ◽  
Muscle Cells ◽  
Mesenteric Arteries ◽  
Vascular Effects ◽  
Rat Mesenteric Artery

Hydrogen sulfide (H2S) has been shown recently to function as an important gasotransmitter. The present study investigated the vascular effects of H2S, both exogenously applied and endogenously generated, on resistance mesenteric arteries of rats and the underlying mechanisms. Both H2S and NaHS evoked concentration-dependent relaxation of in vitro perfused rat mesenteric artery beds (MAB). The sensitivity of MAB to H2S (EC50, 25.2 ± 3.6 μM) was about fivefold higher than that of rat aortic tissues. Removal of endothelium or coapplication of charybdotoxin and apamin to endothelium-intact MAB significantly reduced the vasorelaxation effects of H2S. The H2S-induced relaxation of MAB was partially mediated by ATP-sensitive K+ (KATP) channel activity in vascular smooth muscle cells. Pinacidil (EC50, 1.7 ± 0.1 μM, n = 6) mimicked, but glibenclamide (10 μM, n = 6) suppressed, the vasorelaxant effect of H2S. KATP channel currents in isolated mesenteric artery smooth muscle cells were significantly augmented by H2S. l-Cysteine, a substrate of cystathionine-γ-lyase (CSE), at 1 mM increased endogenous H2S production by sixfold in rat mesenteric artery tissues and decreased contractility of MAB. dl-Propargylglycine (a blocker of CSE) at 10 μM abolished l-cysteine-dependent increase in H2S production and relaxation of MAB. Our results demonstrated a tissue-specific relaxant response of resistance arteries to H2S. The stimulation of KATP channels in vascular smooth muscle cells and charybdotoxin/apamin-sensitive K+ channels in vascular endothelium by H2S represents important cellular mechanisms for H2S effect on MAB. Our study also demonstrated that endogenous CSE can generate sufficient H2S from exogenous l-cysteine to cause vasodilation. Future studies are merited to investigate direct contribution of endogenous H2S to regulation of vascular tone.

Stretch-activated single-channel and whole cell currents in vascular smooth muscle cells

1992 ◽  
Vol 262 (4) ◽  
pp. C1083-C1088 ◽  
Author(s):  
M. J. Davis ◽  
J. A. Donovitz ◽  
J. D. Hood
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Single Channel ◽  
Muscle Cells ◽  
Cation Channel ◽  
Nonselective Cation Channel ◽  
Whole Cell ◽  
Cell Stretch

Mechanosensitive ion channels may play a key role in transducing vascular smooth muscle (VSM) stretch into active force development. To test this hypothesis, we recorded single-channel and macroscopic currents during mechanical stimulation of enzymatically dispersed vascular smooth muscle cells. Patch pipette suction activated a nonselective cation channel that was permeable to K+, Na+, and Ca2+. Whole cell stretch was accomplished using two patch-type micropipettes attached to the cell ends with suction. Stretch elicited a sustained depolarization with a magnitude similar to that observed in pressurized arteries. Under whole cell voltage clamp, stretch activated an inward current with a reversal potential near -15 mV. In another series of experiments, whole cell stretch failed to modify the current-voltage relationship for voltage-gated calcium currents. Thus, in VSM, both single-channel and whole cell data are consistent with activation of a nonselective cation channel by stretch. This mechanism may, in part, account for pressure-induced activation of intact blood vessels.

scholarly journals Myosin in cultured vascular smooth muscle cells: immunofluorescence and immunochemical studies of alterations in antigenic expression.

1984 ◽  
Vol 99 (5) ◽  
pp. 1582-1589 ◽  
Author(s):  
D M Larson ◽  
K Fujiwara ◽  
R W Alexander ◽  
M A Gimbrone
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Immunofluorescent Staining ◽  
Sds Page ◽  
Rat Mesenteric Artery ◽  
Antigenic Expression

Vascular smooth muscle cells (VSMC) in the rat mesenteric artery show specific immunofluorescent staining with antisera against purified human uterine myosin (ASMM) but not human platelet myosin (APM). However, in primary cultures produced by enzymatic dissociation of this vessel, VSMC stain specifically with both ASMM and APM within 5 h after plating and throughout growth to confluence (4-10 d). In confluent cultures, APM staining remains bright while ASMM staining is reduced in intensity in most cells. In contrast, cellular myosin content, determined by quantitative SDS PAGE, is comparable in confluent and growing cultures. Immunoprecipitation of high salt extracts of cultured VSMC with ASMM and APM yields myosins with the same mobilities on SDS PAGE. When serial, exhaustive precipitations are performed with one antiserum, followed by reprecipitation with the other, myosin in subconfluent and confluent VSMC cultures is exhaustively precipitated by either antiserum, thus indicating complete immunological cross-reactivity. These results might be explained by synthesis of a new myosin isoform reactive with both ASMM and APM. However, the development of APM staining in cultured VSMC did not require protein synthesis. Therefore, it is more likely that the changes in immunofluorescent staining observed in vitro reflect conformational alterations, perhaps related to cytoskeletal rearrangements. These changes in myosin antigenic expression may be relevant to the problem of VSMC phenotypic modulation both in vitro and in vivo.

Sign in / Sign up

Export Citation Format

Share Document