Thromboxane and vascular smooth muscle cell growth in genetically hypertensive rats.

Ishimitsu, Toshihiko; Uehara, Yoshio; Ishii, Masao; Ikeda, Toshio; Matsuoka, Hiroaki; Sugimoto, Tsuneaki

doi:10.1161/01.hyp.12.1.46

Cited by 59 publications

(15 citation statements)

References 26 publications

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“…15,16) It has been pointed out that the growth of cardiovascular cells is enhanced in SHR and that hypertrophy of cardiovascular tissues and organs develops before blood pressure elevation. [29][30][31][32] In the present study, the long-term therapy with CS prevented the increase in left ventricular mass and fibrosis of left ventricular tissue. This prevention of cardiac fibrosis, combined with inhibition of cardiac hypertrophy, may account for the observed preservation of myocardial contractility and distensibility.…”

Section: Discussionsupporting

confidence: 54%

Year-Long Antihypertensive Therapy With Candesartan Completely Prevents Development of Cardiovascular Organ Injuries in Spontaneously Hypertensive Rats

et al. 2010

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SummaryMost previous studies have examined the effects of antihypertensive drugs in hypertensive animals for only a few months, and little information has been provided as to the protective effects of lifetime antihypertensive medication against cardiovascular organ injury. In this study, spontaneously hypertensive rats (SHR) were treated for 1 year with an angiotensin-II receptor antagonist (ARB) and the development of hypertensive organ injury was evaluated. Male 15-week-old SHR (n = 9) were given 25 mg/L candesartan (CS) in their drinking water for 1 year. Twelve SHR and 9 normotensive Wistar-Kyoto rats (WKY) were given normal tap water. Tail-cuff blood pressure was almost normalized by CS throughout 1 year (at 12-months: WKY 132 ± 3, SHR 229 ± 3, CS 137 ± 4 mmHg). After 1 year, cardiac ventricular weight (SHR +33%, CS -2% versus WKY) and aortic thickness (SHR +34%, CS +4% versus WKY) in the CStreated SHR rats were not different than those of WKY. Echocardiographic midwall fractional shortening (SHR -18%, CS -1% versus WKY) and left ventricular hydroxyproline content (SHR +47%, CS +11% versus WKY) were also improved by CS to the WKY level. With respect to kidney function, GFR (SHR -24%, CS +9% versus WKY) was preserved, proteinuria (SHR +312%, CS +12% versus WKY) was reduced, and the histological glomerular injury rate (SHR +186%, CS +6% versus WKY) was reduced by CS. These results suggest that long-term antihypertensive therapy with CS can completely prevent hypertensive cardiovascular and renal injuries in SHR. (Int Heart J 2010; 51: 359-364)

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Section: Discussionsupporting

confidence: 54%

Year-Long Antihypertensive Therapy With Candesartan Completely Prevents Development of Cardiovascular Organ Injuries in Spontaneously Hypertensive Rats

et al. 2010

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“…In addition to platelet activation, TxA2 or TP receptor is also known to promote cell migration and proliferation of vascular smooth muscle cells (VSMCs) (15)(16)(17)(18)(19)(20), an important process that is involved in a number of vascular diseases, such as postangioplasty restenosis and atherosclerosis (21). The proliferative response of VSMCs to vascular injury is markedly exaggerated in transgenic mice with vascular overexpression of the human TP␣ receptor, which can be inhibited by the TP-specific antagonist S18886 (6).…”

Section: Tp-specific Agonists [1s-[1␣2␣(z)3␤(1e3s*)4 ␣]]-7-[3-[3-mentioning

confidence: 99%

Thromboxane A2 Activates YAP/TAZ Protein to Induce Vascular Smooth Muscle Cell Proliferation and Migration

Liu

Zhou

et al. 2016

Journal of Biological Chemistry

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“…Prostacyclin was without effect, at concentrations up to 100 fiM, on the restimulation of growth in quiescent bovine aortic smooth muscle cells. 123 Ishimitsu et al 105 - 106 have shown that a stable thromboxane A 2 analogue, 9,ll-epithio-ll,12-methanothromboxane A 2 , dose-dependenth/ stimulates the incorporation of pHJthymidine into DNA of rat thoracic aortic smooth muscle cells, with a maximal effect at a concentration of 10 pM. This concentration also significantly prolonged the doubling time.…”

Section: Eicosanoidsmentioning

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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Thromboxane and vascular smooth muscle cell growth in genetically hypertensive rats.

Cited by 59 publications

References 26 publications

Year-Long Antihypertensive Therapy With Candesartan Completely Prevents Development of Cardiovascular Organ Injuries in Spontaneously Hypertensive Rats

Year-Long Antihypertensive Therapy With Candesartan Completely Prevents Development of Cardiovascular Organ Injuries in Spontaneously Hypertensive Rats

Thromboxane A2 Activates YAP/TAZ Protein to Induce Vascular Smooth Muscle Cell Proliferation and Migration

Pharmacology of smooth muscle cell replication.

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