PDGF-A expression correlates with blood pressure and remodeling in 1K1C hypertensive rat arteries

Dobrian, Anca D.; Wade, Suzanne S.; Prewitt, Russell L.

doi:10.1152/ajpheart.1999.276.6.h2159

Cited by 19 publications

(25 citation statements)

References 40 publications

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“…As is the case for hypertrophy itself, PDGF-A expression can be attributed to elevated pressure or stimulation of the VSMCs by hormonal factors including ANG II. Previous work from this laboratory showed that PDGF-A expression and vascular wall hypertrophy both correlate with blood pressure in the 1K1C hypertensive rat (6). Decreasing blood pressure by different antihypertensive agents in the SHR also produced a decrease in PDGF-A expression and aortic hypertrophy, both of which correlated with the change in blood pressure (29).…”

Section: Discussionmentioning

confidence: 75%

“…Previous studies in our laboratory demonstrated that PDGF-A chain but not -B chain was elevated in the aortic wall in 1K1C hypertension (6). There are significant differences between the proliferative effects of the dimeric chains on VSMCs; PDGF-BB and -AB promote DNA synthesis (25), whereas PDGF-AA is a weak mitogen (19).…”

Section: Discussionmentioning

confidence: 92%

“…Recently, we have shown that vascular hypertrophy following chronic infusion of ANG II was entirely prevented when the blood pressure was kept from rising by the simultaneous administration of minoxidil (34). Pressure, like ANG II, is also a hypertrophic stimulus (20,30) and is correlated with PDGF-A chain expression (6).…”

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confidence: 99%

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AT₁ receptor inhibition does not reduce arterial wall hypertrophy or PDGF-A expression in renal hypertension

Parker

Dobrian

Wade

et al. 2000

American Journal of Physiology-Heart and Circulatory Physiology

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. AT 1 receptor inhibition does not reduce arterial wall hypertrophy or PDGF-A expression in renal hypertension. Am. J. Physiol. Heart Circ. Physiol. 278: H613-H622, 2000.-To separate the role of ANG II from pressure in hypertrophy of the vascular wall in one-kidney, one-clip (1K1C) hypertension, experimental and shamoperated rats were given the AT 1 -receptor antagonist losartan (20 mg · kg Ϫ1 · day Ϫ1 ) or tap water for 14 days. Mean arterial pressure was elevated in both experimental groups compared with controls. Rats were anesthetized with pentobarbital sodium, and the thoracic aorta and carotid, small mesenteric, and external spermatic arteries were harvested and embedded in paraffin. Tissue sections were used for morphological analysis, immunohistochemistry for 5-bromo-2Ј-deoxyuridine (BrdU) and platelet-derived growth factor (PDGF)-AA, stereological measurements, and in situ hybridization with a 35 S-labeled riboprobe for PDGF-A mRNA. Elevated cross-sectional areas of thoracic, carotid, and small mesenteric artery in 1K1C rats were not reduced by losartan. The internal diameter of the external spermatic artery and microvascular density of the cremaster muscle were reduced in 1K1C rats. The number of BrdU-positive nuclei per cross section did not differ between 1K1C and control arteries. PDGF-A mRNA was elevated in the arterial walls of 1K1C rats compared with controls and was hardly changed by losartan. PDGF-A protein stained strongly in the media of 1K1C arteries and was not inhibited by losartan; it appeared in the adventitia of all aortas and carotid arteries. These observations demonstrate that effects of ANG II mediated through the AT 1 receptor are not necessary for hypertrophy of the vascular wall during 1K1C hypertension or expression of PDGF-A.one-kidney, one-clip hypertension; losartan; arterial pressure; angiotensin; platelet-derived growth factor DURING THE COURSE of hypertension, individual arteries adapt to mechanical and hormonal stresses through alterations in medial thickness and/or internal and external diameters, depending on the size and function of the particular blood vessel. The larger arteries increase wall cross-sectional area with the development of outward hypertrophy (30, 45). The smaller arterioles undergo a decrease in lumen size without an increase in wall area and/or rarefaction, the reduction in number of functional vessels (16,31,38). Lumen reduction in the absence of hypertrophy is termed ''inward, eutrophic remodeling.'' Both ANG II and pressure have been implicated as stimuli for the vascular changes associated with hypertension (4,9,18,30,45). ANG II is a hypertrophic (18) as well as hyperplastic stimulus (47) of vascular smooth muscle cells (VSMCs) and has been shown to induce platelet-derived growth factor (PDGF)-A chain expression (28). Recently, we have shown that vascular hypertrophy following chronic infusion of ANG II was entirely prevented when the blood pressure was kept from rising by the simultaneous administration of minoxidil (34). Pressure, like ANG II,...

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Section: Discussionmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 92%

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AT₁ receptor inhibition does not reduce arterial wall hypertrophy or PDGF-A expression in renal hypertension

Parker

Dobrian

Wade

et al. 2000

American Journal of Physiology-Heart and Circulatory Physiology

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“…Lysate was purified from insoluble material by centrifugation at 14,000 g for 10 min, and protein concentrations were determined through the use of a commercially available protein assay (Bio-Rad). Equal protein levels were then loaded onto 10% SDS-polyacrylamide gels under nonreducing conditions (10). After electrophoresis, proteins were transferred to Immun-Blot polyvinylidene difluoride membranes (Bio-Rad) and were blocked with 5% milk in Tris-buffered saline containing 0.1% Tween 20 for 1 h at room temperature.…”

Section: Methodsmentioning

confidence: 99%

Shear stress inhibits smooth muscle cell migration via nitric oxide-mediated downregulation of matrix metalloproteinase-2 activity

Garanich¹,

Pahakis²,

Tarbell³

2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…Thin sections of the paraffin-embedded tissue were stained for 1 min with toluidine blue and analyzed as described previously (10).…”

Section: Vascular Hypertrophy and Kidney Sclerosismentioning

confidence: 99%

Effect of salt on hypertension and oxidative stress in a rat model of diet-induced obesity

Dobrian

Schriver

Lynch

et al. 2003

American Journal of Physiology-Renal Physiology

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. Effect of salt on hypertension and oxidative stress in a rat model of diet-induced obesity. Am J Physiol Renal Physiol 285: F619-F628, 2003. First published June 10, 2003 10.1152 10. /ajprenal.00388. 2002 diet is known to induce or aggravate hypertension in animal models of hypertension and in humans. When Sprague-Dawley rats (n ϭ 60) are fed a moderately high-fat diet (32% kcal fat, 0.8% NaCl) for 10 wk, about one-half develop obesity [obesity prone (OP)] and mild hypertension, whereas the other half [obesity resistant (OR)] maintain body weight equivalent to a low-fat control (C) and are normotensive. The aim of this study was to test the effect of high-NaCl diets (2 and 4% NaCl) on the development of hypertension and obesity, oxidative stress, and renal function. Both 2 and 4% NaCl induced an early increase in systolic blood pressure of OP but not OR or C rats. High-salt intake induced an increase in the size and reduction in number of adipocytes, concomitant to a twofold increase in circulating leptin in OP rats. Aortic superoxide generation indicated a 2.8-fold increase in the OP high-salt vs. normalsalt groups, whereas urine isoprostanes were not significantly increased. Also, hydroxynonenal protein adducts in the kidney were highly increased in OP rats on 2 and 4% NaCl, indicating oxidative stress in the renal tissue. Urine albumin was increased threefold in the OP on 2% NaCl and fourfold in the same group on 4% NaCl vs. 0.8% NaCl. Kidney histology indicated a higher degree of glomerulosclerosis in OP rats on high-salt diets. In summary, high-salt diet accelerated the development but did not increase the severity of hypertension; high salt increased oxidative stress in the vasculature and kidney and induced kidney glomerulosclerosis and microalbuminuria. Also, the OP rats on high salt displayed adipocyte hypertrophy and increased leptin production.glomerulosclerosis; kidney; leptin; sodium dietary OBESITY IS A complex, multifactorial disease that is associated with essential hypertension in ϳ78% of men and ϳ65% of women, as indicated by the data from the Framingham Heart Study (25). Another important contributor to hypertension in humans is the excessive consumption of dietary salt, and epidemiological studies have demonstrated a significant but weak relation between salt intake and hypertension (32, 33). Some, but not all, interventional studies have shown that salt restriction may lower blood pressure (BP) (19,33). Some recent studies report correlation among hypertension, salt sensitivity, and insulin resistance in obese humans (38), whereas others fail to observe a significant relationship (8). Animal models of obesity, hypertension, and insulin resistance display differences with respect to salt sensitivity. In Zucker rats, there is a clear correlation between salt intake and the severity of hypertension (4, 47), whereas in chronic hyperinsulinemic Sprague-Dawley (SD) rats, hypertension is not salt sensitive, albeit a shift in pressure-natriuresis relationship was reported (2). One important cont...

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PDGF-A expression correlates with blood pressure and remodeling in 1K1C hypertensive rat arteries

Cited by 19 publications

References 40 publications

AT₁ receptor inhibition does not reduce arterial wall hypertrophy or PDGF-A expression in renal hypertension

AT₁ receptor inhibition does not reduce arterial wall hypertrophy or PDGF-A expression in renal hypertension

Shear stress inhibits smooth muscle cell migration via nitric oxide-mediated downregulation of matrix metalloproteinase-2 activity

Effect of salt on hypertension and oxidative stress in a rat model of diet-induced obesity

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PDGF-A expression correlates with blood pressure and remodeling in 1K1C hypertensive rat arteries

Cited by 19 publications

References 40 publications

AT1 receptor inhibition does not reduce arterial wall hypertrophy or PDGF-A expression in renal hypertension

AT1 receptor inhibition does not reduce arterial wall hypertrophy or PDGF-A expression in renal hypertension

Shear stress inhibits smooth muscle cell migration via nitric oxide-mediated downregulation of matrix metalloproteinase-2 activity

Effect of salt on hypertension and oxidative stress in a rat model of diet-induced obesity

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AT₁ receptor inhibition does not reduce arterial wall hypertrophy or PDGF-A expression in renal hypertension

AT₁ receptor inhibition does not reduce arterial wall hypertrophy or PDGF-A expression in renal hypertension