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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report our experience in the treatment of 47 cases of renal hypertension patients with renovascular hypertension or hypertensive reno-parenchymal disease surgical therapy is essential and non-surgical therapy has its limitations. The necessity for an operation can be based on the determination of bilateral renal vein plasma renin values. Blood should be drawn from both renal veins in patients in an upright position. Surgical treatment usually produces excellent results in patients in whom renin activity on the side of the lesion is more than normal and more than 2 times that on the uninvolved side. It is advisable to perform an operation within 4 years of the onset of renal hypertension. Complete surgical cure of renal hypertension is accomplished more frequently in patients with fibromuscular dysplasia than in those atherosclerosis. The therapeutic effect of an operation in correcting hypertension is virtually the same, regardless of whether the arterial stenotic lesions are in the main renal artery or in the intrarenal arterial branches. We have found nephrectomy or dacron bypass graft to be the surgical procedure of choice in renovascular hypertension cases.
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PMID:Therapeutic experience in renal hypertension: response treatment in 47 cases. 123 71

The involvement of the circulating and local renin-angiotensin system in atherosclerotic process has been hypothesized on the basis of experimental data showing presence and specific actions of the components of this system in the vascular wall. In particular, angiotensin II may participate in well known events in atherogenesis as the control of smooth muscle cell growth and proliferation. Recent studies have shown an effect of angiotensin converting enzyme (ACE) inhibition on the development of atherosclerosis in animal models. Captopril and cilazapril prevent myointimal proliferation after vascular injury in rat. Captopril reduces aortic cholesterol content and percentage intimal aortic surface covered by lesions in Watanabe heritable hyperlipidemic rabbits. Captopril also significantly reduces the progression of carotid and coronary lesions in monkeys fed a high cholesterol diet. In addition, a role for converting enzyme inhibitors in reducing aortic and microvascular growth either in hypertensive or normotensive rats has been demonstrated. It is possible that ACE-inhibitors prevent angiotensin II-induced vascular proliferation and thereby suppress the development of atherosclerosis in animals. It is also conceivable that the blood pressure effects of ACE-inhibitors could play a role in the antiatherosclerotic effect shown by these drugs, even though this explanation cannot be addressed by studies dealing with normotensive animals. Then, other mechanisms could be involved, including hypothesized effects of blockade of the renin-angiotensin system on sympathetic nervous system activity, regulation of vascular growth factors and insulin sensitivity. The clinical significance of these experimental findings is unknown.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:ACE-inhibitors and atherosclerosis. 132 85

Arterial hypertension is a major risk factor for atherosclerosis. The mechanisms involved include elevation of blood pressure, increased velocity of the sphygmic wave and increased blood flow turbulence. These hemodynamic features however do not fully explain the link between hypertension and atherosclerosis. An important role is also played by humoral factors including catecholamines, the renin-angiotensin-aldosterone system, serotonin, endothelin, platelets and endothelium-derived growth factors. Furthermore in the last few years great relevance has been attributed to hyperinsulinemia (accompanied by hypercholesterolemia and hypertriglyceridemia) that is frequently found in hypertensive subjects. Several recent reports on the antiatherogenic effect of some antihypertensive agents that could slow down the progression of atherosclerotic lesions in hypertensive subjects are promising.
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PMID:[Hypertension and arteriosclerosis]. 136 25

Transgenic experimentation has become a crucial part of hypertension and atherosclerosis research, and is growing more important in several other areas of cardiovascular disease. It has recently made a particular contribution to understanding the role of the renin-angiotensin system in controlling hypertension. The study of blood pressure regulation, cardiac hypertrophy, atherogenesis and thrombosis are also benefiting from the transgenic approach.
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PMID:Transgenic animal models of cardiovascular disease. 136 20

Primarily hypervolaemic, high output forms of hypertension, with features indicating or strongly suggesting fluid overload as the cause of elevated cardiac output, resulting from renal disease with reduced glomerular filtration rate causing sodium retention, renal tubular causes of sodium retention, greatly excessive sodium intake and low renin hypertension, can be treated by reduction of sodium intake and potentiation of its excretion by diuretic therapy, removal of the cause (e.g. aldosteronoma), and calcium antagonists. Excessive vasoconstriction resulting from noradrenaline (norepinephrine) in neurogenic hypertension, phaeochromocytoma, orthostatic hypertension and alpha-adrenergic drug administration; angiotensin excess due to renal ischaemia brought about by aortic coarctation, renal arterial and arteriolar stenosis, intraluminal obstruction, external renal compression, renin-producing tumours, intrinsic kidney diseases and excessive renin substrate; and vascular structural disorders such as atherosclerosis, arteriolitides and fibrosis with or without calcification of major arteries may also induce hypertension. Secondary hypertension of uncertain mechanism may occur in hyperparathyroidism, hyper-or hypothyroidism, or acromegaly. All are best treated by appropriate correction of the endocrine excess or deficiency. It may also occur in pregnancy, where the mechanism may involve prostaglandin-thromboxane imbalance or calcium deficiency; calcium deficiency with some evidence of benefit from calcium supplements; and the recumbent hypertension paradoxically associated with autonomic failure. Excellent responses to specific correction of the underlying cause or pathogenetic mechanism is usual in young individuals but less frequent in older patients.
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PMID:Secondary hypertension. An overview of its causes and management. 137 54

Factors that can influence cardiovascular growth are becoming increasingly important for our understanding of such complex diseases as cardiac hypertrophy, coronary artery disease, atherosclerosis, and hypertension. Several proto-oncogenes were found to be involved in the regulation of abnormal cell growth in cardiovascular disease. It is also evident that some peptide hormones, which are well known to be involved in blood pressure control, may play a role as growth modulators. Angiotensin II is one such peptide. It elevates blood pressure through its direct vasoconstrictor, sympathomimetic, and (through release of aldosterone) sodium-retaining activity but also appears to have mitogenic actions. Interestingly, all components of the renin-angiotensin system were found locally in cardiovascular tissues. The question remains whether angiotensin can act directly as a growth factor or whether it does so indirectly by influencing or modulating cell growth factors. A better understanding of the renin-angiotensin system as a direct or indirect mediator for cardiovascular hypertrophy would offer new and interesting insights into the pathophysiology of hypertension and possibly novel options for the treatment of cardiovascular disease.
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PMID:The molecular basis of cardiovascular hypertrophy: the role of the renin-angiotensin system. 138 95

The renin-angiotensin system (RAS) plays a major role in the control of blood pressure and cardiovascular homeostasis and is involved in the pathogenesis of a number of cardiovascular disorders. The efficacy of angiotensin-converting enzyme (ACE) inhibitors in the treatment of hypertension and congestive heart failure has led to the widespread clinical use of ACE inhibitors in primary or secondary prevention of heart disease. The demonstration of the expression of the components of the RAS in several extrarenal tissues, as well as local generation of angiotensin II, has confirmed the existence of a tissue RAS that may serve organ-specific functions and act independently from the plasma RAS. The concept of paracrine/autocrine functions of the local RAS has changed our understanding of the functions of the RAS and suggests that tissue ACE inhibition may be of greater importance than inhibition of circulating ACE in the treatment of congestive heart failure and other cardiovascular disorders. Whereas the circulating endocrine RAS appears to be responsible for mediation of acute effects, the tissue RAS seems to be involved in more chronic situations, such as secondary structural changes of the cardiovascular system, and therefore could contribute to the pathogenesis of hypertension as well as other cardiovascular disorders, such as cardiac hypertrophy, coronary artery disease, and atherosclerosis. Several experimental and clinical findings suggest that reversal of cardiovascular structural changes secondary to cardiovascular disease and enhancement of renal sodium excretion by ACE inhibitors are important long-term antihypertensive actions possibly mediated by inhibition of the tissue RAS.
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PMID:Effects of angiotensin-converting enzyme inhibitors on tissue renin-angiotensin systems. 141 88

Circadian blood pressure (BP) variation were studied in patients with renovascular hypertension (RVH) and primary aldosteronism (PA). Ambulatory BP (ABP) was monitored every 5 min for 24 hrs in a ward setting in 23 patients with PA and 17 patients with RVH (13 patients with unilateral renal arterial stenosis and 4 with bilateral stenosis). In patients with RVH, ABP was monitored before and after treatment with a converting enzyme inhibitor or percutaneous transluminal angioplasty. Plasma renin activity (PRA) was high before percutaneous transluminal angioplasty in almost all patients with RVH and low in those with PA. Ordinary circadian BP variation, i.e. nocturnal fall and diurnal rise in BP, was confirmed in the patients with unilateral or bilateral renal artery stenosis. Percutaneous transluminal angioplasty successfully normalized both BP and PRA in those with RVH. Normal circadian BP variation was observed in those with RVH before the treatment with a converting enzyme inhibitor or percutaneous transluminal angioplasty as well as during treatment with the former and after treatment with the latter. Circadian BP variation in the patients with RVH was affected by the pathogenesis of renal artery stenosis alone, i.e, fibromuscular hyperplasia and atherosclerosis; with fibromuscular hyperplasia normal circadian BP variation was observed, while with atherosclerosis, nocturnal BP fall was restricted or eliminated. Circadian BP variation in those with PA before and after excision of adrenal adenoma was essentially similar to that in normal subjects and essential hypertensive patients. From these it seems that in patients with RVH or PA, circadian BP variation is not affected by hypertension per se or by pathogenesis of hypertension.
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PMID:Circadian blood pressure variation in patients with renovascular hypertension or primary aldosteronism. 142 21

Epidemiological data have revealed that the progestogen in oral contraceptives (OCs) is involved in hypertension, ischemic heart diseases, and stroke. Atherosclerotic lesions were implicated owing to the androgenic properties of progestogens. However, atherosclerosis did not develop despite reduced high density lipoprotein (HDL) and elevated low density lipoprotein (LDL), presumably because of the strong effect of ethinyl estradiol (EE) upon induction of hepatic LDL- and remnant-receptors. A series of findings indicate that vasospasms caused by the effect of progestogens are involved in arterial thromboses. In postmenopausal women, the addition of progestogens to the estrogen treatment may trigger ischemic diseases. Estrogens exert a vasodilatory effect and stabilize the vascular tonus through the responsiveness of the endothelium, neurotransmitter release, and direct blocking of calcium channels. Progestogens increase the sensitivity of arteries to vasoconstrictory compounds and reduce blood flow. In women treated with ovulation inhibitors, and EE-induced activation of the renin-angiotensin-aldosterone system was observed. Aldosterone acts vasodilatorily, while progestogens with high affinity to the aldosterone receptor may exert a strong vasoconstrictory effect. If vascular lesions are present, the vasoconstrictory action of progestogens may cause acute ischemic attacks. Therefore, the lowest effective dose of the progestogen has to be used for replacement therapy. In hysterectomized women, the extra administration of progestogens should be avoided and in women with arterial diseases they should be prescribed with discretion. Additional progestogens given for 14 days 3 months apart may suffice for the prevention of endometrial hyperplasia. Both the EE and progestogen doses in OCs should be reduced. Progestogen-dominant ovulation inhibitors should be restricted to cases with an additional indication.
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PMID:[Hormonal contraception and substitution therapy: the importance of progestogen for cardiovascular diseases]. 145

Endothelin is a newly discovered potent vasoconstrictive polypeptide released by endothelial cells in response to various stimuli, including vasoactive peptides such as angiotensin II, adrenaline and vasopressin, and thrombocyte products like transforming beta growth factor and thrombin. Endothelin is believed to exert its main effects locally, in a paracrine or autocrine way. In vascular tissue, endothelin induces longlasting contraction of smooth muscle cells, leading to decreased blood flow, especially in the coronary and renal circulation, together with an increase in systemic blood pressure. It acts also mitogenically in vascular smooth muscle cells. Endothelin stimulates release of aldosterone and catecholamines in non-vascular tissue, and inhibits release of renin. A physiological function of endothelin may be to modulate vascular tone, and increased levels of circulating endothelin are seen after the "cold pressor test". Moreover, plasma endothelin concentration is elevated during acute myocardial infarction, in acute renal failure, in patients with hypertension, and during cardiogenic chock. What role endothelin plays in the development of these conditions, and in other disorders such as vascular spasm and atherosclerosis is uncertain.
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PMID:[The endothelial cell as an endocrine organ--endothelin]. 155 33


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