Effect of long-term sympathectomy on the arterial wall in rabbits and rats

Fronek, K.; Bloor, Colin M.; Amiel, David; Chvapil, Miloš

doi:10.1016/0014-4800(78)90002-3

Cited by 52 publications

(32 citation statements)

References 22 publications

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“…Mechanisms that may potentially account for higher aortic PWV among people with SCI include (a) structural changes in the vessel as a result of long-term sympathectomy and increased collagen content in the vascular wall (40) or (b) functional changes in the endothelium caused by decreased regional blood flow. Decreased regional blood flow as a result of inactivity impedes endothelium function and subsequently inhibits NO production, which is a mediator of endothelium dilatation (38).…”

Section: Discussionmentioning

confidence: 99%

Pulse Wave Velocity for Assessment of Arterial Stiffness Among People With Spinal Cord Injury: A Pilot Study

Miyatani

Masani

et al. 2009

The Journal of Spinal Cord Medicine

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Background/Objective: The most significant complication and leading cause of death for people with spinal cord injury (SCI) is coronary artery disease (CAD). It has been confirmed that aortic pulse wave velocity (PWV) is an emerging CAD predictor among able-bodied individuals. No prior study has described PWV values among people with SCI. The objective of this study was to compare aortic (the common carotid to femoral artery) PWV, arm (the brachial to radial artery) PWV, and leg (the femoral to posterior tibial artery) PWV in people with SCI (SCI group) to able-bodied controls (non-SCI group). Methods: Participants included 12 men with SCI and 9 non-SCI controls matched for age, sex, height, and weight. Participants with a history of CAD or current metabolic syndrome were excluded. Aortic, arm, and leg PWV was measured using the echo Doppler method. Results: Aortic PWV (mean 6 SD) in the SCI group (1,274 6 369 cm/s) was significantly higher (P , 0.05) than in the non-SCI group (948 6 110 cm/s). There were no significant between-group differences in mean arm PWV (SCI: 1,152 6 193 cm/s, non-SCI: 1,237 6 193 cm/s) or mean leg PWV (SCI: 1,096 6 173 cm/s, non-SCI: 994 6 178 cm/s) values. Conclusions: Aortic PWV was higher among the SCI group compared with the non-SCI group. The higher mean aortic PWV values among the SCI group compared with the non-SCI group indicated a higher risk of CAD among people with SCI in the absence of metabolic syndrome.

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Section: Discussionmentioning

confidence: 99%

Pulse Wave Velocity for Assessment of Arterial Stiffness Among People With Spinal Cord Injury: A Pilot Study

Miyatani

Masani

et al. 2009

The Journal of Spinal Cord Medicine

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“…For example, increased sympathetic innervation (Head, 1991) or exogenous elevation of plasma catecholamines (Stewart et al, 1992) has been associated with vascular smooth muscle hypertrophy in vivo. In addition, sympathetic denervation of blood vessels through mechanical (Bevan, 1975), chemical (Fronek et al, 1978), or immunological (Lee et al, 1987) methods results in decreases in DNA synthesis and cell number. The addition of catecholamines to vascular smooth muscle cell cultures increases DNA (Nakaki et al, 1990) and protein synthesis (Chen et al, 1995;Hu et al, 1999), as well as cell growth (Blase and Boissel, 1993).…”

Section: Discussionmentioning

confidence: 99%

Relationship between α₁-Adrenergic Receptor-Induced Contraction and Extracellular Signal-Regulated Kinase Activation in the Bovine Inferior Alveolar Artery

Hague

Gonzalez-Cabrera

Jeffries

et al. 2002

J Pharmacol Exp Ther

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The endogenous adrenergic agonists norepinephrine (NE) and epinephrine regulate vascular tone by stimulating ␣ 1 -adrenergic receptors (ARs) on smooth muscle cells to cause contraction. In addition, ␣ 1 -ARs also couple to growth factor pathways, through stimulation of mitogen-activated protein kinases (MAPKs). MAPKs are a family of serine-threonine kinases that include extracellular signal-regulated kinase (ERK) and a variety of other kinases that are able to activate transcription factors when stimulated. We examined ␣ 1 -AR stimulation of contraction and ERK activation in the bovine inferior alveolar artery (BIAA), using in vitro contraction studies and Western blotting. Using antagonists selective for individual adrenergic receptor types, we found that only ␣ 1 -ARs were coupled to ERK activation and contraction. NE stimulated contraction (EC 50 ϭ 11 M) and ERK activation (EC 50 ϭ 21 M) with similar potency. Using ␣ 1 -AR subtype-selective antagonists, we identified the ␣ 1 -AR subtypes coupled to each response. Affinity values for ␣ 1 -AR subtype-selective antagonists were consistent with ␣ 1A -AR-mediated contraction. In contrast, simultaneous treatment with concentrations of these antagonists selective for each ␣ 1 -AR subtype (␣ 1A -, ␣ 1B -, and ␣ 1D -AR) was required to inhibit ERK activation, suggesting that all three ␣ 1 -ARs activate ERK in BIAA. Transmural electrical stimulation of BIAA segments resulted in activation of ERK, which was inhibited by the ␣ 1 -ARselective antagonist BE 2254 (2-[[␤-(4-hydroxyphenyl)ethyl]aminomethyl]-1-tetralone). These data suggest that in an intact artery, NE released from sympathetic nerves stimulates ␣ 1 -ARs to cause contraction and ERK activation, and that redundancy among subtypes exists for ␣ 1 -AR activation of ERK.The sympathetic nervous system controls peripheral vascular resistance by release of norepinephrine (NE) and epinephrine, which stimulate ␣ 1 -adrenergic receptors (ARs) on vascular smooth muscle cells. Molecular cloning and radioligand binding studies using selective antagonists have identified three distinct ␣ 1 -AR subtypes (␣ 1A -, ␣ 1B -, and ␣ 1D -AR).

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“…Chemical sympathectomy with 6-hydroxydopamine causes a reduction in the number of smooth muscle cells in rabbit aortic tunica media. 94 In rats sympathectomized by a combination of immunological and chemical means, there is a significant reduction in the number of medial smooth muscle cell layers in large and small mesenteric arteries, but not in the superior mesenteric artery.…”

Section: Catecholaminesmentioning

confidence: 99%

Pharmacology of smooth muscle cell replication.

1992

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The suggestion that smooth muscle cell proliferation contributes to hypertension, atherosclerosis, and restenosis after angioplasty has led to a growing interest in the use of drugs to inhibit this process. This review summarizes pharmacological studies of smooth muscle cell proliferation in vitro and in vivo and identifies specific mediators of proliferation that are implicated by drugs binding with high affinity to enzymes or receptors. (Hypertension 1992^0:713-736) KEY WORDS • atherosclerosis • growth substances • hypertension, essential • muscle, smooth, vascular T his review emphasizes agents that influence smooth muscle proliferation. Four overlapping categories of agents that could be discussed are growth factors, drugs with known pharmacological effects, endocrine hormones with growth regulatory properties, and intracellular mediators of replication. This review will concentrate on the last three categories. A great deal has already been written in other reviews about the growth factors, but the much longer list of possible targets discussed here has not been reviewed systematically. Moreover, a great deal is known about the pharmacology of some of the molecules in our review, so their therapeutic value in the treatment of conditions arising from smooth muscle replication is likely to be realized more quickly in a clinical sense than treatments based on the still very poorly understood pharmacology of growth factors. Pathology of Smooth Muscle ProliferationSmooth muscle proliferation has been implicated as playing a central role in atherosclerosis and hypertension.1 The evidence that smooth muscle cell proliferation occurs in these diseases is clear. As we will briefly review, however, evidence for a causal connection is not well established. Smooth Muscle Replication in HypertensionThe argument for a role of smooth muscle cell replication in hypertension is an outgrowth of the structural hypothesis of hypertension proposed by Folkow.2 Folkow explained that the ability of a resistance artery to restrict blood flow depends on the thickness of the vessel wall as well as on the size of the vessel lumen, the responsiveness of the wall to vasoactive stimuli, and the level of stimulation by vasoconstrictors. Folkow's idea is based on the simple physical fact that a thicker vessel wall will act as an amplifier, so that an equal vasoconstrictor stimulus will produce greater narrowing of the lumen in a hypotensive vessel than in a normotensive vessel. Studies of essential and secondary hypertension have confirmed that hypertensive vessel walls are thickened.3 Indeed, there is evidence that such structural changes precede any elevation in blood pressure,*-5 and, at least for the spontaneously hypertensive rat, wall thickening may depend on the increased sympathetic innervation that develops in the spontaneously hypertensive rat vessel wall within the first month of life. 5 -6 A correlation exists between the development of sympathetic innervation and the development of arterial medial hypertrophy in normotensive...

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Effect of long-term sympathectomy on the arterial wall in rabbits and rats

Cited by 52 publications

References 22 publications

Pulse Wave Velocity for Assessment of Arterial Stiffness Among People With Spinal Cord Injury: A Pilot Study

Pulse Wave Velocity for Assessment of Arterial Stiffness Among People With Spinal Cord Injury: A Pilot Study

Relationship between α₁-Adrenergic Receptor-Induced Contraction and Extracellular Signal-Regulated Kinase Activation in the Bovine Inferior Alveolar Artery

Pharmacology of smooth muscle cell replication.

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Effect of long-term sympathectomy on the arterial wall in rabbits and rats

Cited by 52 publications

References 22 publications

Pulse Wave Velocity for Assessment of Arterial Stiffness Among People With Spinal Cord Injury: A Pilot Study

Pulse Wave Velocity for Assessment of Arterial Stiffness Among People With Spinal Cord Injury: A Pilot Study

Relationship between α1-Adrenergic Receptor-Induced Contraction and Extracellular Signal-Regulated Kinase Activation in the Bovine Inferior Alveolar Artery

Pharmacology of smooth muscle cell replication.

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Relationship between α₁-Adrenergic Receptor-Induced Contraction and Extracellular Signal-Regulated Kinase Activation in the Bovine Inferior Alveolar Artery