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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arterial compliance describes a change in the volume of arteries following a change in blood pressure. The physical basis of the compliance concept and experimental procedures in animals both indicate that the relation between arterial compliance and blood pressure pattern is often unclear. Compliance is pressure-dependent because of the biphasic elastin and collagen composition of arteries and, hence, decreases when blood pressure increases. Compliance also determines the pulsatile amplitude of the pressure wave by regulating the buffering function of an artery's face to the cardiac pump and, accordingly, its reduction induces a selective increase in systolic level. The questions are whether these theoretical and experimental phenomena can be extrapolated to human hypertension and whether they can be assessed from indirect measurement of arterial compliance by means of a time-domain analysis of arterial pressure and flow waves via various models of the arterial tree. Whatever the method and site of measurement, arterial compliance was found to be decreased in different forms of hypertension. This low compliance can be considered to have a causal role in elderly patients with isolated systolic hypertension. In contrast, in patients with systolo-diastolic hypertension physiologic and pharmacologic arguments exist against the fact that low arterial compliance may be the pure consequence of mean blood pressure elevation. Moreover, it is suggested that aging acts in concurrence with pressure elevation to decrease arterial compliance, and that in certain hypertensive patients additional factors, perhaps atherosclerotic in nature, contribute to impair the elastic properties of arteries.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Use of arterial compliance for evaluation of hypertension. 200 4

One of the well-known consequences of established hypertension is an increase in connective tissue proteins in the walls of the large arterial blood vessels. Using renal clip and Dahl salt-sensitive rat models of systemic hypertension, we investigated the effect of developing hypertension on elastin production and accumulation in rat aorta. In both models of hypertension, increased accumulation of arterial elastin appeared coincidentally with, and was proportional to, elevation of blood pressure. In spite of large increases in absolute amounts of elastin, the proportion of elastin present in the vessel wall remained essentially constant from the earliest stage of the response. These changes in elastin synthesis and accumulation took place in the absence of evidence of cell proliferation. Treatment of Dahl rats with colchicine during development of hypertension affected blood pressure rise only marginally but abolished the vascular hypertrophic response. Our results suggest that the response of elastin production to increased blood pressure is rapid and sensitive, and that the stimulus for increased synthesis is an increase in wall stress. The striking effect of colchicine may indicate a role of elements of the cytoskeleton in the perception of stress by the vascular smooth muscle cells or in the transduction of that stress into increased production of connective tissue proteins.
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PMID:Response of aortic elastin synthesis and accumulation to developing hypertension and the inhibitory effect of colchicine on this response. 201 56

In chronic models of hypertension such as the spontaneously hypertensive rat (SHR), thickening of the media of large arteries occurs mainly through smooth muscle cell (SMC) hypertrophy accompanied by DNA replication resulting in large polyploid cells. In resistance vessels of SHR, medial hypertrophy occurs through a hyperplastic response. It has been suggested that this hyperplasia is due to mitogens such as platelet-derived growth factor (PDGF), while the hypertrophied polyploid cells occur from stimulation by angiotensin II from within the vessel wall. Angiotensin II activates many of the same cellular pathways as PDGF, including stimulation of phospholipase C, mobilization of intracellular calcium and activation of Na+/H+ exchange. Both induce transient increases in the proto-oncogenes c-fos and c-myc. However, a possible explanation for the difference in SMC response may be involvement of an intracellular pathway stimulated by PDGF (but not by angiotensin II), such as stimulation of JE (a cytokine-like molecule), which may activate transcriptional events necessary for mitogenesis. In atherosclerosis vascular hypertrophy occurs in the form of focal intimal thickening and results from hyperplasia of diploid SMC and their greatly increased production of extracellular matrix, (particularly collagen) and the accumulation of intra- and extracellular lipid. The SMC involved in atherogenesis are phenotypically modified compared with the SMC of undiseased regions, and amongst other features have a lower volume fraction of myofilaments (Vvmyo). Associated with modulation to a low Vvmyo are increases in SMC expression of mRNA for collagens type I (alpha 1 and alpha 2) and type III (alpha 1), elastin, fibronectin, as well as massive increases in collagen protein (26- to 45-fold), glycosaminoglycans (5-fold), and lipid accumulation (7-fold).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular biology of vascular hypertrophy. 203 94

The degradation of elastin during various pathological processes such as emphysema or arteriosclerosis was demonstrated by several investigators. In the present work, we adapted an ELISA technique for the determination of elastin peptide (EP) levels in human sera and plasma, in healthy and arteriosclerotic subjects. This test makes use of human aorta elastin hydrolyzed by a chemical procedure (kappa-elastin) instead of EP produced by pancreatic or leukocyte elastase. Polyclonal antibodies to this antigen were obtained in rabbits. The indirect ELISA procedure is sensitive, specific and reproducible. No correlation could be demonstrated between EP level and anti-EP antibody concentration of IgG or IgM types determined in the same serum samples. These antibodies did not interfere with EP determinations. EP concentration did not change with age in control subjects. In obliterative arteriosclerosis of the legs and in type IIb hyperlipoproteinemia, EP levels showed a marked increase, while in hypertension, ischemic heart disease and diabetes mellitus, the increase was moderate. In stroke, only slight changes were observed. In type IV hyperlipoproteinemia, EP levels were lower than in controls.
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PMID:Determination of elastin peptides in normal and arteriosclerotic human sera by ELISA. 213 61

Although indapamide has been used for many years as a first-line treatment of hypertension, it is only recently that some of its activities on the changes of the cardiovascular system, brought on by age and high blood pressure, have been studied. Indapamide appears to reduce blood pressure by a combined diuretic and direct vascular activity reducing vascular reactivity and total peripheral resistance. In addition, it has discrete effects on a number of interrelated systems that may protect the cardiovascular system. Indapamide reduces intracellular calcium levels, maintains magnesium ions, but reduces phosphate ions that may be involved in arterial rigidity. Circulating catecholamines remain unchanged but there is a reduction in normetanephrine, suggesting a reduction in sympathetic tone. It stimulates prostacyclin synthesis, increases levels of circulating prostacyclin, reduces platelet aggregation and stimulates the vasodilation elicited by endothelium-derived relaxing factor in the presence of bradykinin. In addition, it inhibits the formation of the vasoconstrictor prostanoid, thromboxane A2. The free radical scavenging activity of indapamide could also protect the vascular smooth muscle from the reperfusion injury of cerebral and myocardial ischemia. Indapamide induces a reduction in cerebral ischemia after carotid ligation. Unlike some other antihypertensives, it does not upset the high-density/low-density lipoprotein-cholesterol balance, reducing the possible risk of atherosclerosis. Moreover, the combination of binding to elastin and reduction in uptake of calcium and phosphate into the smooth muscle could be a mechanism for reducing arterial rigidity seen in the elderly and hypertensive patient. In hypertensive patients, these properties induce an improvement in arterial compliance, and in the long term a reduction in left ventricular hypertrophy. These pharmacologic and clinical results, together with a good antihypertensive efficacy and acceptability, suggest that indapamide may be a preferential agent in the long-term cardiovascular protection of the hypertensive patient.
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PMID:Cardiovascular protective properties of indapamide. 218 50

Hypertensive patients are at an increased risk of developing cerebrovascular and cardiovascular disease. Treatment has resulted in a substantial reduction in cerebrovascular deaths but not in cardiovascular mortality. As the number of deaths from myocardial infarction exceeds the sum of all other hypertension-related mortalities, these results are disappointing. The hypothesis that metabolic side effects of many antihypertensive drugs offset the potential benefit of decreasing blood pressure is of particular interest. In established hypertension there is an increase in total peripheral resistance. Long-term therapy with diuretics decreases vascular resistance. This is also evident with dihydropyridine calcium antagonists, vasodilators, angiotensin-converting enzyme inhibitors and alpha blockers. In patients with hypertension, an increased wall to lumen ratio occurs in resistance vessels where mechanisms such as smooth muscle hypertrophy and increased amounts of elastin and collagen are present. In small resistance vessels, long-term antihypertensive therapy has a positive effect, but the effect in large arteries is variable.
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PMID:Cardiovascular effects of antihypertensive drugs--involvement in the therapeutic choice. 218 51

We created an animal model to understand better the pathogenesis and underlying mechanism of progressive central pulmonary venous (PV) obstruction, a condition not amenable to current therapy. Twenty piglets underwent banding of their PVs, 18 had a sham operation, and 12 were nonoperated controls. After 1, 3, and 6 weeks hemodynamic data were obtained and correlated with ventricular weights, PV and pulmonary artery (PA) distensibilities (at 1 week), morphometric structural and ultrastructural analyses, and biochemical assessment of elastin determined gravimetrically (and by desmosine level at 1 week), collagen, and elastase activity. At 1 week, PV banding was associated with increased PV compliance (p less than 0.05). At 3 weeks, an increased PA pressure (Ppa) (p less than 0.05) was observed, unaccompanied by a rise in PV pressure (Pcw). In the PV, however, there was breakdown of the internal elastic lamina with apparent migration of smooth muscle cells from media to subendothelium. At 6 weeks, a rise in Pcw (p less than 0.01), a further rise in Ppa (p less than 0.01), and right ventricular hypertrophy (p less than 0.005) were observed. We also observed mild PV intimal thickening (p less than 0.01), complete degradation of elastic laminae (p less than 0.05), and an increase in collagen assessed morphometrically (p less than 0.01). The banding procedure resulted in an overall increase in PV elastin synthesis and in the proportion of elastin determined gravimetrically (p less than 0.05 for both) but not by desmosine level, suggesting the possibility of poor cross-linking of elastin, which might account for the early increased distensibility of the PV. However, our assay could not detect an increase in elastase activity associated with either the increased distensibility or the ultrastructural changes of elastin degradation. The increased Ppa was not associated with significant PA biochemical or structural changes. We speculate that in response to distal venous obstruction, early remodeling of the PVs increases distensibility, protecting the lung from venous congestion and blunting a rise in Pcw. PA hypertension precedes the rise in Pcw, likely because of reflex vasoconstriction. The subsequent modest rise in Pcw is already associated with extensive fibrosis of the PV, suggesting a reason for unsuccessful current therapy and a need for consideration of earlier assessment and intervention.
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PMID:Alterations in elastin and collagen related to the mechanism of progressive pulmonary venous obstruction in a piglet model. A hemodynamic, ultrastructural, and biochemical study. 229 12

In young rats consuming 1% NaCl drinking solution, unilateral nephrectomy and bilateral adrenal enucleation caused a hypertension. Plasma corticosterone concentration in hypertensive rats was not significantly higher than that of normotensive control rats in early hypertensive or chronic hypertensive stage. At the end of experiment, each rat received an intravenous injection of 0.4 microCi/g of 3H-lysine and was sacrificed 2 hours after the injection. Incorporation of 3H-lysine into collagen or elastin of the mesenteric artery and heart in hypertensive rats was greater than that of normotensive rats. Administration of phenoxybenzamine hydrochloride lower the blood pressure of hypertensive rats and reduced the incorporation of 3H-lysine into collagen and elastin of the mesenteric artery and heart. From these findings, increased protein synthesis of collagen and elastin in hypertensive rats appears to play an important role for the maintenance of adrenal regeneration hypertension.
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PMID:[Adrenal regeneration hypertension--effects of vascular connective tissue protein and plasma corticosterone on hypertension in rats with adrenal regeneration hypertension]. 230 14

We evaluated the processes controlling the accumulation of collagen and elastin in main pulmonary arteries of rats during an episode of hypoxic pulmonary hypertension. Explant cultures of main pulmonary arteries were incubated with [3H]proline to measure collagen and protein synthesis and percent collagen synthesis. Elastin synthesis was measured by [14C]valine incorporation into insoluble elastin. Relative collagen synthesis increased twofold (from 1.1 +/- 0.2 x 10(3) to 2.0 +/- 1.0 x 10(3) disintegrations per minute [14C]hydroxyproline/vessel/hr/mg protein), relative collagen synthesis doubled (from 2% to 4-5% of total protein synthesis), and elastin synthesis increased ninefold (from 0.4 +/- 0.2 x 10(4) to 3.6 +/- 0.6 x 10(4) dpm [14C]valine/vessel/hr/mg protein) in early hypertension. The level of pro alpha l(I) collagen RNA paralleled the relative collagen synthetic rate during the study period. Within 7 days of recovery from hypoxia, collagen and elastin contents were normal. We conclude that collagen and elastin in main pulmonary arteries are synthesized rapidly during an episode of hypoxic pulmonary hypertension and that collagen and elastin are rapidly removed from the hypertensive vessel during normoxic recovery.
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PMID:Collagen and elastin metabolism in hypertensive pulmonary arteries of rats. 231 97

Elastin of the ascending aortic media of 10 cases with type A dissecting aneurysm, 14 hypertensive cases, and 30 control cases were prepared by the treatment of aortas with hot formic acid, and three-dimensional architecture was observed by scanning electron microscopy. In the control cases, elastin showed framework-like continuous structure consisting of elastic laminae, and interlaminar fibers that interconnected the laminae. In 6 of 10 cases of dissecting aneurysm, the interlaminar fibers were apparently irregular in arrangement and shape, and decreased in number, especially in the outer media. This architectural alteration resulted in a rarefaction of interconnection between the elastic laminae in the media, and possibly resulted in the local weakness against the dissecting force of the laminae. This medial weakness may be related to the mechanism of initiation and progression of dissecting aneurysm. The cystic medial necrosis (CMN) was found in 3 cases, but only 1 of them was accompanied by a mild decrease of the interlaminar fibers in the area outside of CMN, suggesting that the initiation of CMN did not directly relate to the decrease of the interlaminar fibers. The aortic media of hypertensives generally showed an increase of interlaminar fibers, but their focal decrease was encountered in the outer media of 3 cases. These findings suggest that the decrease of the interlaminar fibers of medial elastin seen in dissecting aneurysms were related to hypertension.
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PMID:Alterations of elastic architecture in human aortic dissecting aneurysm. 235 59


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