Effect of Mechanical Stimulation, Substance P and Vasoactive Intestinal Polypeptide on the Electrical and Mechanical Activities of Circular Smooth Muscles from Pig Coronary Arteries Contracted with Acetylcholine: Role of Endothelium

Bény, Jean‐Louis; Brunet, Pascale Claude; Huggel, H

doi:10.1159/000138202

Cited by 74 publications

(43 citation statements)

References 12 publications

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“…The hyperpolarization induced by ACh was transient and ceased within several minutes. Such hyperpolarization and sustained relaxation also occurred in the pig coronary artery (Beny et al, 1986) and in the rat aorta (Southerton et al, 1987). Furthermore, Komori & Suzuki (1987a) observed that although both ACh and oxotremorine cause release of EDRF and relax the precontracted rabbit saphenous artery, only ACh hyperpolarizes the membrane.…”

Section: Discussionmentioning

confidence: 92%

Factors inducing endothelium‐dependent relaxation in the guinea‐pig basilar artery as estimated from the actions of haemoglobin

Nishiye¹,

Nakao²,

Itoh³

et al. 1989

British J Pharmacology

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1 Factors inducing dilatation of guinea-pig basilar artery were investigated in intact and endothelium-denuded tissues by measurement of isometric tension and by electrophysiological methods. 2 The amplitudes of contractions induced by 9,1 1,epithio-1 1,12-methanothromboxane A2 (STA2) and by high K+ were enhanced by haemoglobin (oxyhaemoglobin, Hb) in a concentrationdependent fashion (above 1 pM). For the high K'-induced contraction, the initial tonic component was enhanced to a greater extent than the secondary phasic component. Mechanical responses evoked by STA2 and by high K' were greater in endothelium-denuded tissues, but Hb (below 10pM) had no effect on them.3 Hb (10pM) had no effect on the contractile proteins as estimated from the actions of Hb on Ca2+-induced contractions in skinned muscle tissues. Further, Hb had no effect on the release of Ca2+ from intracellular stores but it accelerated the Ca2 + accumulation into the sarcoplasmic reticulum as judged from the caffeine-or STA2-induced contraction generated in intact tissues. 4 Acetylcholine (ACh) relaxed tissues that were precontracted by STA2 but Hb prevented this relaxation, in a concentration-dependent fashion. The ACh-induced relaxation was sustained for over 10min in the absence of Hb, but following application of Hb, ACh caused only a transient relaxation. 5 STA2 (up to 100nM) did not modify the resting membrane potential of smooth muscle cells of the basilar artery. ACh (1O pM) caused transient hyperpolarization which was only slightly inhibited by Hb (10pM) whether or not STA2 was present. The hyperpolarization induced by ACh required the presence of endothelial cells. 6 A23187 (0.01-1 pM) relaxed tissues which were precontracted by STA2, in a concentrationdependent fashion but had no effect on the membrane potential. 7 These results suggest that in guinea-pig basilar artery, ACh induces relaxation of tissues that were precontracted by STA2 by causing release of both endothelium-derived relaxing (EDRF) and endothelial dependent hyperpolarizing factor (EDHF) (sustained and initial transient relaxation, respectively), but via different mechanisms. Hb inhibits the former and to a lesser extent, the latter.Since A23187 produced relaxation of pre-contracted tissue but caused no detectable change in the membrane potential, this agent may release EDRF but not EDHF.

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Section: Discussionmentioning

confidence: 92%

Factors inducing endothelium‐dependent relaxation in the guinea‐pig basilar artery as estimated from the actions of haemoglobin

Nishiye¹,

Nakao²,

Itoh³

et al. 1989

British J Pharmacology

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“…Some agents which induce endothelium-dependent vasorelaxation are known to induce simultaneously endothelium-dependent membrane hyperpolarization of smooth muscle cells, and there have also been reports discussing whether or not SP induces endothelium-dependent membrane hyperpolarization of smooth muscle cells. SP is known to induce hyperpolarization and relaxation of vascular smooth muscles, including the porcine coronary artery (Beny et al, 1986;Pacicca et al, 1992;Zhang et al, 1994), although in certain types of tissue, SP relaxes the arteries in the absence of any changes in the membrane potential (Bolton & Clapp, 1986). Chen & Suzuki (1989) reported that hyperpolarization is generated by an increase in K+ conductance of the membrane.…”

Section: Discussionmentioning

confidence: 99%

“…Today, endothelium-dependent relaxation is considered to be produced by, at least, three factors: PG12, EDRF and EDHF. Substance P (SP) induces an endothelium-dependent va-sorelaxation. There have been reports of SP-induced endothelium-dependent hyperpolarization of smooth muscle cells (Beny et al, 1986;Pacicca et al, 1992 (Di Virgilho et al, 1989) and 5% foetal bovine serum for 1.5 h at 370C (Aoki et al, 1994). After loading with fura-2, both vascular and valvular strips were incubated in normal PSS for at least 1 h before starting the measurement, in order to remove the dye in the extracellular space and for purposes of equilibration.…”

Section: Introductionmentioning

confidence: 99%

Mechanism of endothelium‐dependent relaxation induced by substance P in the coronary artery of the pig

Kuroiwa

Aoki

Kobayashi

et al. 1995

British J Pharmacology

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1Using front-surface fluorometry of fura-2-loaded porcine coronary arterial strips with the endothelium intact, we investigated the mechanisms of vasorelaxation induced by substance P (SP). Fura-2 fluorescence signals which indicated the cytosolic Ca2+-concentration ([Ca2+],), were observed to arise exclusively from the smooth muscle cells in these strips. 2 During the contractions induced by U46619 (100 nM), a thromboxane A2 analogue, an SP-induced endothelium-dependent, biphasic vasorelaxation was observed, which consisted of an initial rapid relaxation phase followed by a sustained phase, with a transient decrease in [Ca21],. Pretreatment with indomethacin (Ind) had no effect on the SP-induced relaxation; however, pretreatment with NG-nitro-Larginine (L-NOARG) partially, but significantly inhibited the decrease in both the [Ca2+]i and tension induced by SP; in addition, the sustained phase of SP-induced relaxation was almost completely abolished. Thus, part of the relaxation was considered to be mediated by L-NOARG-sensitive relaxing factor (endothelium-derived relaxing factor : EDRF). 3 During the 40 mm K+-depolarization-induced contraction which may eliminate the effects of endothelium-derived hyperpolarizing factor (EDHF), the vasorelaxation induced by SP was completely inhibited by L-NOARG. 6 We thus conclude that: (1) SP-induced vasorelaxation is mediated by an L-NOARG-sensitive factor (EDRF) and an L-NOARG-resistant factor; and (2) the first, rapid, phase of the relaxation is mediated by both factors while the sustained phase seems to be mediated mainly by EDRF. The underlying mechanisms of L-NOARG-resistant relaxation have yet to be elucidated, but EDHF appears to be a potentially contributing factor.

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“…obtained post mortem contract to acetylcholine. 58 Furchgott and Zawadzki 165 have pointed out that retention of even only a few percent of the endothelial cells allows substantial expression of relaxation. Constriction of the human arteries in vitro to acetylcholine in the presence or absence of endothelium has now been confirmed by others, 168 as has the stability of responses in postmortem coronary tissue up to 8 hours after death.…”

Section: Glml Added In Perfusion Reservoir) Of Vasoconstrictor Respomentioning

confidence: 99%

Cholinergic constriction in the general circulation and its role in coronary artery spasm.

Kalsner

1989

Circulation Research

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The release of acetylchoUne from autonomic nerves in those tissues that receive a cholinergic innervation is widely believed to dilate blood vessels. Exogenously administered acetylchoUne hi vivo does dilate vascular beds and produce hypotension; however, this latter effect is indirect and probably the result of liberation of endothelium-derived relaxing factor (EDRF) from endothelial cells. Some blood vessels contain a substantial population of medial constrictor receptors for acetylchoUne, and the implications of this presence for vascular control systems has been largely ignored, although it needs to be considered. A survey of the evolution of vasomotor control systems indicates that acetylchoUne serves principally as an excitatory transmitter to blood vessels. NeuraUy mediated cholinergic constriction and not dilation is found in fish, amphibians, reptiles, and birds, with responses initiated by medial muscarinic receptors. AcetylchoUne constricts many vascular preparations from these lower animals, but some vessels relax, reflecting the emergence of an EDRF responsive to acetylchoUne. An examination of cholinergic responses in mammalian vessels reveals that cholinergic (neurogenic) dilation is limited to a very few vascular beds and to only a few species. Both experimental evidence and evolutionary considerations support the likelihood that cholinergic (neural) constriction operates in some vascular regions in mammals and, in particular, in the coronary circulation of some species, including humans. In fact, constriction, and not dilation, may be the dominant vascular response to activation of the cholinergic axis in most mammals, including humans. The complications and contradictions introduced by the simultaneous presence of both EDRF and a cholinergic constrictor innervation involving medial muscarinic receptors are discussed. A variety of evidence is also presented that implicates cholinergic constriction in at least some instances of coronary artery spasm and sudden death. Received March 3, 1988; accepted January 24, 1989. little to say about neurogenic acetylcholine, except to reiterate its traditional functional assignment to a few specialized vascular beds, such as the male genitalia, the nasal mucosa, and the submandibular salivary glands. 3 -s Even such specific attributions of function, however, have generated little research interest in cholinergic mechanisms per se but instead have focused attention on the role of vasoactive peptides in neurogenic dilation. 6In fact, vasodilation by endogenously liberated acetylcholine, in those few beds in which it is postulated to occur, is linked to such ambiguities and uncertainties, with hardly a single exception, as to suggest that even such a restricted and modest assignment may overstate its role. As will be discussed here, the purported cholinergic vasodilator innervation of skeletal muscle, 7 -9 presumed to be activated as part of the defense reaction in the cat and dog, is unverifiable in primates, 10 and its hypothesized role in dilation of thoro...

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Effect of Mechanical Stimulation, Substance P and Vasoactive Intestinal Polypeptide on the Electrical and Mechanical Activities of Circular Smooth Muscles from Pig Coronary Arteries Contracted with Acetylcholine: Role of Endothelium

Cited by 74 publications

References 12 publications

Factors inducing endothelium‐dependent relaxation in the guinea‐pig basilar artery as estimated from the actions of haemoglobin

Factors inducing endothelium‐dependent relaxation in the guinea‐pig basilar artery as estimated from the actions of haemoglobin

Mechanism of endothelium‐dependent relaxation induced by substance P in the coronary artery of the pig

Cholinergic constriction in the general circulation and its role in coronary artery spasm.

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