The arteries of the small intestine in systemic hypertension

Short, David; Thomson, Allan D.

doi:10.1002/path.1700780202

Cited by 63 publications

(27 citation statements)

References 9 publications

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“…The possibility of vascular remodeling in hypertension is supported by the observation that wall-to-lumen ratio of intestinal arterioles is increased in humans with chronic hypertension, even without evidence of hypertrophy of the arteriolar wall. 16 Based on this rinding, it was proposed that, during prolonged hypertension, smooth muscle cells may become shorter and are no longer able to extend to their original length during relaxation, thus resulting in a reduction in maximal dilatation. 17 We are aware of no evidence to support the hypothesis that length of vascular smooth muscle decreases during chronic hypertension.…”

Section: Hypothesismentioning

confidence: 99%

Remodeling of cerebral arterioles in chronic hypertension.

1989

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Chronic hypertension impairs dilatation of cerebral arterioles. Impairment of dilatation generally has been attributed to hypertrophy of the vessel wall with encroachment on the vascular lumen. In this study, we tested the hypothesis that a reduction in external diameter may contribute to encroachment on the vascular lumen during chronic hypertension. We examined 10-12-month-old, anesthetized Wistar-Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP). External diameter, stress, and strain of pial arterioles were calculated from measurements of pial arteriolar pressure (servo null), diameter, and crosssectional area of the arteriolar wall. During maximal dilatation produced with ethylenediaminetetraacetic acid, cross-sectional area of the arteriolar wall was greater in SHRSP than in WKY rats (2,038±57 vs. 1,456±61 fim 2 , p<0.05). External, as well as internal, diameter was less in SHRSP than in WKY rats (101+3 and 88±3 /tm in SHRSP vs. 111±3 and 102±3 fim in WKY rats for external and internal diameter, respectively, p<0.05). Reduction in external diameter accounted for 76% of encroachment on the lumen in SHRSP, and hypertrophy per se accounted for only 24%. Distensibility of deactivated pial arterioles was increased in SHRSP. These findings suggest that reduction in external diameter plays an important role in impairment of maximal dilatation of cerebral arterioles in SHRSP, and reduction in vascular diameter in SHRSP cannot be accounted for by altered distensibility. We propose that, during chronic hypertension, cerebral arterioles undergo structural remodeling that results in a smaller external diameter and encroachment on the vascular lumen. Reduction in external diameter appears to account for most of the impairment of cerebral vasodilatation that occurs in chronic hypertension. (Hypertension 1989;13:968-972) C hronic hypertension impairs responses of cerebral blood vessels to a variety of dilator stimuli. Increases in cerebral blood flow during seizures and hypercapnia are less in hypertensive rats than normotensive rats.12 During maximal' dilatation, internal diameter of large cerebral arteries 3 -5 and cerebral arterioles 6 is smaller in spontaneously hypertensive rats (SHR) and strokeprone spontaneously hypertensive rats (SHRSP) than in normotensive Wistar-Kyoto (WKY) rats. This manuscript from the University of Iowa was sent to Carlos M. Ferrario, Guest Editor, for review by expert referees, for editorial decision, and for final disposition.Address for reprints: Gary L. Baumbach, MD, Department of Pathology, 120 Medical Laboratories, University of Iowa, Iowa City, IA 52242. Impairment of vasodilator capacity by chronic hypertension generally is attributed to hypertrophy of the vessel wall with encroachment on the lumen and reduction in internal diameter of the vessels. Hypertrophy during chronic hypertension has been demonstrated in cerebral arterioles.6 -8 It is not clear, however, whether the magnitude of hypertrophy is sufficient to account for the reduction in diameter of cereb...

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Section: Hypothesismentioning

confidence: 99%

Remodeling of cerebral arterioles in chronic hypertension.

1989

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“…However, contrary to the effects of ANG II, pressure elevations induce a reduction in the number of vessels rather than an increase (16,35,38). As a result of the effect of ANG II on blood pressure, it is often difficult to characterize its direct and indirect effects on the vascular changes associated with hypertension.…”

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confidence: 99%

“…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.''…”

mentioning

confidence: 99%

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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“…Thus increased expression of PDGF-A in the vascular wall has been shown in response to a variety of stimuli that suggest it could be important in hypertensive arterial remodeling. A non-renin-dependent model of experimental hypertension that exhibits arterial remodeling similar to that seen in human essential hypertension (1,35) is the one-kidney, oneclip (1K1C) hypertensive rat (13,30). We used this model to examine the correlation among blood pressure levels, arterial remodeling, and PDGF expression and secretion in the arterial wall of large-and small-sized arteries.…”

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confidence: 99%

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

Dobrian

Wade

Prewitt

1999

American Journal of Physiology-Heart and Circulatory Physiology

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Dobrian, Anca, Suzanne S. Wade, and Russell L. Prewitt. PDGF-A expression correlates with blood pressure and remodeling in 1K1C hypertensive rat arteries. Am. J. Physiol. 276 (Heart Circ. Physiol. 45): H2159-H2167, 1999.-We previously demonstrated remodeling of large and small arteries in angiotensin II-treated rats, paralleled by an increased expression of platelet-derived growth factor (PDGF)-A chain mRNA in large arteries. Both remodeling and PDGF-A expression were associated with elevation of blood pressure rather than a direct effect of angiotensin II. To further delineate the role of PDGF-A and elevated blood pressure, we assessed the level of PDGF-A and -B mRNA and protein in the wall of large as well as small arteries in the one-kidney, one-clip (1K1C) hypertensive rat, a non-renindependent model of hypertension. Fourteen days after renal artery stenosis, the thoracic aorta and both femoral arteries were collected from 1K1C rats (n ϭ 8) and uninephrectomized controls (n ϭ 8) and immediately processed for morphological measurement, immunohistochemistry, RT-PCR, and Western blotting. Systolic blood pressure was significantly elevated in hypertensive rats (202 Ϯ 26 mmHg) compared with control rats (122 Ϯ 7.9 mmHg) and was accompanied by arterial hypertrophy in both aorta and femoral arteries. The mRNA for PDGF-A chain was increased threefold in the thoracic aorta (P Ͻ 0.05) of 1K1C rats, whereas the message for PDGF-B was not significantly changed in hypertensive versus control animals. A higher staining of the intima-media was observed by using an anti-PDGF-A chain polyclonal antibody on paraffin-embedded sections. Western blot results indicated an ϳ2-fold increase in PDGF-A protein in aortic and femoral wall of the 1K1C rats. The results showed that both the mRNA and protein for PDGF-A chain are increased and well correlated with the blood pressure and wall area, suggesting a direct effect of elevated pressure on PDGF synthesis, which, in turn, may affect the onset and progression of vascular hypertrophy. hypertension; aorta; femoral artery; platelet-derived growth factors; hypertrophy HYPERTENSION IS ACCOMPANIED by vascular changes that vary according to the size and structure of each particular artery. These changes include the hypertrophy of large arteries (27, 41) and the inward eutrophic remodeling of arterioles (13, 28), whereas small arteries (internal diameter 150-250 µm) may undergo inward eutrophic or hypertrophic remodeling, depending on the type of hypertension (12, 16). The exact mechanisms and the factors affecting these vascular changes are only known in part. Lately, the involvement of growth factors in the processes of vascular growth and remodeling has been emphasized. Among them, plateletderived growth factor (PDGF) is of special interest for the autocrine regulation of protein synthesis (9) and growth (7) in smooth muscle cells. Large vessels from normotensive rats and humans constitutively express low levels of PDGF-A mRNA, mainly in the medial layer, whereas the PDGF-B chain mRNA is ...

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The arteries of the small intestine in systemic hypertension

Cited by 63 publications

References 9 publications

Remodeling of cerebral arterioles in chronic hypertension.

Remodeling of cerebral arterioles in chronic hypertension.

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

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

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The arteries of the small intestine in systemic hypertension

Cited by 63 publications

References 9 publications

Remodeling of cerebral arterioles in chronic hypertension.

Remodeling of cerebral arterioles in chronic hypertension.

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

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

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