Constrictor actions of acetylcholine, 5‐hydroxytryptamine and histamine on bovine coronary artery inner and outer muscle

Garland, C J; Keatinge, W. R.

doi:10.1113/jphysiol.1982.sp014236

Cited by 34 publications

(19 citation statements)

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“…Our work is consistent with the work of Garland and Keatinge (14). In bovine carotid arterial strips, they suggested that the inner and outer muscle layers of arterial strips were equally sensitive to high concentrations of histamine but that there was a difference in the constrictor response of outer and inner muscle layers to acetylcholine.…”

Section: Discussionsupporting

confidence: 82%

“…Results from functional studies suggest differential expression of the myosin isoforms in the luminal and adluminal regions of the arterial media. In bovine carotid arteries, Garland and Keatinge (14) found differences in the acetylcholine-mediated constrictor responses of the adluminal and luminal arterial muscle layers. Additionally, SMCs within the inner tunica media of the artery have been shown to proliferate in experimental models of arteriosclerosis, but SMCs within the deeper layers of the tunica media only rarely proliferate (16,31,35).…”

mentioning

confidence: 99%

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Shortening velocity and myosin heavy- and light-chain isoform mRNA in rabbit arterial smooth muscle cells

Sherwood

Eddinger

2002

American Journal of Physiology-Cell Physiology

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Sherwood, Jennifer J., and Thomas J. Eddinger. Shortening velocity and myosin heavy-and light-chain isoform mRNA in rabbit arterial smooth muscle cells. Am J Physiol Cell Physiol 282: C1093-C1102, 2002. First published January 2, 2002 10.1152/ajpcell.00307.2001.-In smooth muscle cells (SMCs) isolated from rabbit carotid, femoral, and saphenous arteries, relative myosin isoform mRNA levels were measured in RT-PCR to test for correlations between myosin isoform expression and unloaded shortening velocity. Unloaded shortening velocity and percent smooth muscle myosin heavy chain 2 (SM2) and myosin light chain 17b (MLC17b) mRNA levels were not significantly different in single SMCs isolated from the luminal and adluminal regions of the carotid media. Saphenous artery SMCs shortened significantly faster (P Ͻ 0.05) than femoral SMCs and had more SM2 mRNA (P Ͻ 0.05) than carotid SMCs and less MLC17b mRNA (P Ͻ 0.001) and higher tissue levels of SMB mRNA (P Ͻ 0.05) than carotid and femoral SMCs. No correlations were found between percent SM2 and percent MLC17b mRNA levels and unloaded shortening velocity in SMCs from these arteries. We have previously shown that myosin heavy chain (MHC) SM1/SM2 and SMA/SMB and MLC17a/MLC17b isoform mRNA levels correlate with protein expression for these isoforms in rabbit smooth muscle tissues. Thus we interpret these results to suggest that 1) SMC myosin isoform expression and unloaded shortening velocity do not vary with distance from the lumen of the carotid artery but do vary in arteries located longitudinally within the arterial tree, 2) MHC SM1/SM2 and/or MLC17a/MLC17b isoform expression does not correlate with unloaded shortening velocity, and 3) intracellular expression of the MHC SM1/SM2 and MLC17a/MLC17b isoforms is not coregulated. SM1; SM2; MLC 17a; MLC17b; SMA; SMB; unloaded shortening velocity; arterial smooth muscle MUSCLE CONTRACTION requires the interaction of myosin with actin. Muscle myosin is a member of a large family of motor proteins with a similar molecular structure, composed of two myosin heavy chains (MHCs) and two pairs of myosin light chains (MLCs). Smooth muscle (SM) expresses several different MHC and MLC isoforms. The alternate association of these SM MHC and MLC isoforms results in different myosin molecules that may have distinct contractile or structural roles. In striated muscle, myosin isoforms have been assigned unique contractile roles, but the physiological significance has not yet been clearly defined for the SM myosin isoforms.SM MHC isoforms result from the alternative splicing of a single gene. Alternative splicing near the 3Ј end of the MHC pre-mRNA results in expression of either one of two proteins, SM1 (204 kDa) or SM2 (200 kDa), differing only at their carboxy termini (1, 10). In studies performed in chemically permeabilized tissue strips, SM1 expression has been correlated with an increase in unloaded shortening velocity (21), an increase in calcium sensitivity, and also a decrease in shortening velocity (3). However, studies on purified...

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Section: Discussionsupporting

confidence: 82%

mentioning

confidence: 99%

Shortening velocity and myosin heavy- and light-chain isoform mRNA in rabbit arterial smooth muscle cells

Sherwood

Eddinger

2002

American Journal of Physiology-Cell Physiology

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“…2, the isolated pig and cattle coronary arteries were contracted by histamine. These results were similar to previous reports in pigs (12,13) and cattle (3,14). In pig coronary arteries, removal of the endothelium increased the maximal response and pD2 value of the histamine-induced contraction ( Fig.…”

Section: Discussionsupporting

confidence: 82%

Vasomotor effect of histamine on pig and cattle coronary artery in vitro.

Obi¹,

Matsumoto

Nishio

1991

Jpn.J.Pharmacol

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ABSTRACT-Vasomotor effects of histamine were examined in isolated coronary arteries from pigs and cattle. Histamine produced a concentration-dependent contraction in these arteries. These contractile responses were dose-dependently inhibited by diphenhydramine. The slopes of the Schild plots, however, were significantly lower than unity in both species. Cimetidine potentiated the histamine-induced contractions at relatively high doses of histamine (larger than 10-5 M) in pig coronary arteries, but did not show a significant effect in cattle arteries. After the removal of endothelium, the Schild plot of diphenhydramine against histamine gave a straight line with a pA2 value of 7.80 and slope of 1.00 in pigs, confirming the competitive nature of the antagonism. In cattle, the slope was significantly lower than unity; however, in the presence of cimetidine, it was not significantly different from unity. Dimaprit did not contract the cattle coronary arteries with endothelium, but contracted them after the removal of endothelium. These results suggest that histamine-induced vasoconstriction in pig and cattle coronary arteries is mainly dependent on the Hi-receptors in the smooth muscle cells, and that H1-and H2-receptors in the endothelial cells of pigs and H2-receptors in the smooth muscle cells of cattle modify the histamine-induced vasoconstrictions. Remarkable species differences have been reported concerning the responsiveness of coronary vessels to histamine in vitro. Coronary arteries from monkeys and dogs respond to histamine with relaxations (1, 2), while human, pig and cattle coronary arteries respond with contractions (3-6).It has been postulated that the species difference might depend on the ability of histamine to activate H1-and H2-receptors in vascular smooth muscle and H1-receptors in endothelium, which possibly mediate the release of prostaglandin 12 (7, 8) or endothelium-derived relaxing factors (1,9,10

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“…Bell 114 in his own study of uterine vessel innervation questioned whether smooth muscle cells other than those in the outermost layers are directly affected by transmitter released from nerves. In further support of the idea of transmural gradients of reactivity and response, it has been shown that the outer layers of aorta have a low sensitivity to EDRF 175 ; coupled with EDRF's short half-life, this suggests that the substance interacts primarily with vascular smooth muscle cells in the inner media, near the sites of its release. The possibility of electrogenic propagation of the EDRF-initiated signal across the vascular wall needs to be considered, but there is no evidence at present to support the likelihood of its occurrence.…”

mentioning

confidence: 90%

“…In a unique approach to the question, Garland and Keatinge 175 established that the outer muscle of cattle coronary arteries is highly responsive to the choline ester and constricts to it, but that the inner muscle is essentially insensitive. Importantly, the cholinergic innervation is distributed in the adventitia, and only in the outer 25% of the media.…”

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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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Constrictor actions of acetylcholine, 5‐hydroxytryptamine and histamine on bovine coronary artery inner and outer muscle

Cited by 34 publications

References 31 publications

Shortening velocity and myosin heavy- and light-chain isoform mRNA in rabbit arterial smooth muscle cells

Shortening velocity and myosin heavy- and light-chain isoform mRNA in rabbit arterial smooth muscle cells

Vasomotor effect of histamine on pig and cattle coronary artery in vitro.

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

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