The vasodilator effect of thiamylal in dog mesenteric artery: contribution of intracellular action

1991 ◽  
Vol 69 (8) ◽  
pp. 1163-1167 ◽  
Author(s):  
Kumi Nakamura ◽  
Yoshio Hatano ◽  
Makoto Nishiwada ◽  
Kenjiro Mori
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Mesenteric Artery ◽  
Mesenteric Arteries ◽  
Skinned Fibers ◽  
Vasodilator Effect ◽  
Free Media ◽  
Dog Mesenteric Artery ◽  
Intracellular Action ◽  
Intracellular Mechanisms

The effects of thiamylal on contractions induced by various mechanisms were investigated in mesenteric arteries isolated from dogs. Thiamylal (10−4 to 10−3 M) significantly inhibited contractions induced by KCl (20 mM) in normal media, and those induced by norepinephrine (10−5 M) in normal and Ca2+-free media. Caffeine-induced contraction was significantly inhibited by thiamylal in the concentrations greater than 3 × 10−5 M in intact fibers and 10−5 M in chemically skinned fibers. Chemically skinned fibers that were precontracted with Ca2+ were relaxed by thiamylal in concentrations lower than those required to relax intact fibers that were precontracted with KCl (20 mM); the ED50 was 1.52 × 10−5 M in skinned fibers and 5.50 × 10−4 M in intact fibers. These results suggest that intracellular mechanisms are involved in thiamylal-induced vasodilatation of dog mesenteric artery.Key words: barbiturates, thiamylal, mesenteric artery, vascular smooth muscle.

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.

Heterogeneous distribution of endothelium-dependent relaxations resistant to NG-nitro-L-arginine in rats

1992 ◽  
Vol 263 (4) ◽  
pp. H1090-H1094 ◽  
Author(s):  
T. Nagao ◽  
S. Illiano ◽  
P. M. Vanhoutte
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Calcium Ionophore ◽  
Renal Arteries ◽  
Mesenteric Arteries ◽  
K Channel ◽  
Ionophore A23187 ◽  
Dependent Manner ◽  
Arterial Tree ◽  
Heterogeneous Distribution

Endothelium-dependent relaxations that are resistant to inhibitors of nitric oxide synthase probably are mediated by endothelium-dependent hyperpolarization of the vascular smooth muscle. Experiments were performed to examine the distribution of this type of relaxation along the arterial tree of the rat by measuring changes in isometric force. Acetylcholine induced concentration- and endothelium-dependent relaxations in aortas and in pulmonary, common iliac, femoral, mesenteric, and renal arteries contracted with phenylephrine. In the presence of NG-nitro-L-arginine, the cumulative administration of acetylcholine induced relaxations only in the femoral, mesenteric, and renal arteries. The calcium ionophore A23187 relaxed mesenteric arteries contracted with phenylephrine in a concentration- and endothelium-dependent manner. The concentration-relaxation curve to A23187 was shifted to the right in the presence of NG-nitro-L-arginine. The maximal relaxations induced by lemakalim, a K+ channel opener, were smaller in those arteries that did not exhibit NG-nitro-L-arginine-resistant relaxations. These results suggest that NG-nitro-L-arginine-resistant relaxations are more frequently observed in smaller arteries. The arteries that exhibit NG-nitro-L-arginine-resistant relaxations may be more sensitive to an endothelium-derived substance that causes hyperpolarization of vascular smooth muscle cells.

scholarly journals Effects of 2-nicotinamidoethyl nitrate on smooth muscle cells of the dog mesenteric artery and trachea

1983 ◽  
Vol 33 ◽  
pp. 216
Author(s):  
Toshiro Inoue ◽  
Kazuo Takeda ◽  
Shiro Ishikawa ◽  
Yushi Ito ◽  
Hirosi Kuriyama
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mesenteric Artery ◽  
Muscle Cells ◽  
Dog Mesenteric Artery

Effect of stretch on passive tension and contractility of isolated vascular smooth muscle

1962 ◽  
Vol 202 (5) ◽  
pp. 835-840 ◽  
Author(s):  
Harvey V. Sparks ◽  
David F. Bohr
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Standard Stimulus ◽  
Contractile Element ◽  
Passive Tension ◽  
Optimal Length ◽  
Length Variable

Helically cut strips of the wall of small branches of dog superior mesenteric artery were stretched in a stepwise fashion. Tension developed in response to stretch or to a standard stimulus (epinephrine or electricity) was recorded isometrically. The elastic diagram of the vessel is comparable to that reported by other investigators. Contraction in response to a standard stimulus increased with stretch, as much as 100% for a 10% increase in length. The increase in response continued until the strip reached a certain optimal length (variable from strip to strip), after which the response decreased with further stretch. When the strip was released in a stepwise fashion hysteresis was observed. Possible relationships of tension and length at the level of the contractile element are discussed together with ways in which the information presented here may relate to myogenic autoregulation.

Evidence against the role of α1-adrenoceptor reserve in buffering the inhibitory effect of nifedipine on the contractility of canine vascular smooth muscle

1990 ◽  
Vol 68 (10) ◽  
pp. 1346-1350 ◽  
Author(s):  
Yong-Yuan Guan ◽  
Chiu-Yin Kwan ◽  
Edwin E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Saphenous Vein ◽  
Mesenteric Artery ◽  
Inhibitory Effect ◽  
Contractile Responses ◽  
Intracellular Ca ◽  
Adrenoceptor Agonists ◽  
The Difference ◽  
Muscle Calcium

The relationship between the postsynaptic α1-adrenoceptor reserve and the sensitivity of vasoconstriction induced by α-adrenoceptor agonists to the dihydropyridine Ca2+ entry blocker nifedipine was investigated in isolated muscle strips of dog mesenteric artery (DMA) and saphenous vein (DSV). The amplitudes of the contractile responses of DMA induced by phenylephrine were the same as those in DSV in the presence and in the absence of extracellular Ca2+. The use of 3 × 10−9 M phenoxybenzamine to irreversibly block the α1-adrenoceptors revealed a marked difference in the size of the α1-adrenoceptor reserve between DMA (40%) and DSV (7%). In spite of a larger receptor reserve, the contractile responses induced by phenylephrine in DMA were more sensitive to nifedipine compared with those in DSV. These results suggest that the postsynaptic α1-adrenoceptor reserve in vascular smooth muscle, at least in DMA and DSV, does not play an important role in buffering the inhibitory effect of nifedipine on the contractile response to a full agonist of α1-adrenoceptors. Other factors, such as the difference in the membrane depolarizing effect, the ability to utilize intracellular Ca2+ for contraction, and the possible existence of α1-adrenoceptor subtypes, may contribute to the different inhibitory effects of nifedipine on these blood vessels.Key words: adrenoceptors, nifedipine, smooth muscle, calcium, saphenous vein, mesenteric artery.

Inhibition of Ca2+-activated K+ channels by tyrosine phosphatase inhibitors in rat mesenteric artery

2000 ◽  
Vol 78 (9) ◽  
pp. 745-750 ◽  
Author(s):  
Hisashi Yokoshiki ◽  
Takashi Seki ◽  
Masanori Sunagawa ◽  
Nicholas Sperelakis
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Mesenteric Artery ◽  
Single Channel ◽  
Tyrosine Phosphatase ◽  
Phosphatase Inhibitors ◽  
Rat Mesenteric Artery ◽  
Dependent Signal ◽  
Single Channel Currents ◽  
Channel Currents

To investigate the possible regulation of large-conductance Ca2+-activated K+ channels (BKCa) by tyrosine phosphatases (Tyr-PPs), single-channel currents of myocytes from rat mesenteric artery were recorded in open cell-attached patches. Two structurally different Tyr-PP inhibitors, sodium orthovanadate (Na3VO4) and dephostatin, were used. The channels (236 pS) evoked at +40 mV and pCa 6, were significantly inhibited by 1 mM Na3VO4 (-81 ± 3%, n = 10; P < 0.005). Similarly, 100 µM dephostatin strongly inhibited the BKCa channels (-80 ± 7%, n = 7 ; P < 0.05). Therefore, BKCa channels in vascular smooth muscle cells may be regulated by tyrosine phosphatase-dependent signal transduction pathways, whose inhibition could attenuate the channel activity.Key words: Ca2+-activated K+ channel, vascular smooth muscle, tyrosine phosphatase, vanadate, dephostatin.

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