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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From October 1979 to August 1991, 231 patients underwent renal artery balloon angioplasty at The Ohio State University Hospitals. Atherosclerotic renal vascular disease was present in 171 of these patients. From this cohort, 138 patients undergoing their first angioplasty had renal artery pressure gradients performed before and after renal artery angioplasty. The demographics of this group included age 66.9 +/- 10 years (+/- SD), male 51%, white 94%, black 6%, diabetes mellitus 28%, systolic blood pressure 157 +/- 26 mm Hg, diastolic blood pressure 86 +/- 13 mm Hg, standard daily doses of antihypertensive medications 4.2 +/- 3, and serum creatinine 2.6 +/- 2.3 mg/dL. Plasma renin activity was measured in 25 patients and was shown to be elevated in 16. The renal artery stenoses were main renal artery 75%, orificial 22%, distal renal artery 1.4%, and combinations of the above 2.2%. Solitary kidneys were present in six patients (4.3%). Bilateral renal artery stenosis was present in 45% of patients and bilateral angioplasties were performed in one third of these patients. The preangioplasty systolic blood pressure gradient was 109 +/- 50 mm Hg (range, 20 to 230 mm Hg) and the postangioplasty renal artery pressure gradient was 12 +/- 16 mm Hg (range, 0 to 78 mm Hg) (P < 0.001). There were no complications related to measurement of the pressure gradients. The magnitude of the renal artery pressure gradients did not correlate with blood pressure level, number of antihypertensive medications, or serum creatinine level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal artery pressure gradients in patients with angiographic evidence of atherosclerotic renal artery stenosis. 794 30

Renal artery stenotic disease is the most common form of surgically correctable hypertension. Occlusive lesions of the renal artery are categorized as: arteriosclerotic, fibrodysplastic (intimal fibroplasia, medial fibrodysplasia, perimedial dysplasia) and developmental. The incidence of stroke, heart disease and renal failure has been reduced with contemporary drug management of hypertensive vascular disease, but similar salutary outcomes have not accompanied the medical treatment of renin-mediated renovascular hypertension. Selection of patients for operation implies documentation that a renal artery stenosis is of functional importance. Advances in the surgical management of renovascular hypertension have evolved over the past 50 years, such that carefully performed reconstructions benefit 85-95% of properly selected patients.
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PMID:The evolution of surgery for renovascular occlusive disease. 804 46

The renin-angiotensin system traditionally has been conceived as a neuroendocrine system functioning in the circulation. Recent research has confirmed the existence of autocrine/paracrine tissue renin-angiotensin systems present and functioning at multiple sites, including cardiac, vascular, and renal tissues, which contain the majority of angiotensin-converting enzyme in the body. It appears that the circulating renin-angiotensin system is activated acutely to maintain homeostasis and is then turned off at cardiovascular compensation, while the tissue renin-angiotensin systems exert long-term actions that affect cardiovascular function and structure, which may play a pathophysiological role in congestive heart failure, hypertension, and vascular disease and influence the response to therapy with angiotensin-converting enzyme-inhibiting agents.
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PMID:Tissue renin-angiotensin system in myocardial hypertrophy and failure. 838 20

Hypertension is an important cardiovascular risk factor. High blood pressure per se is not a disease but a hemodynamic alteration associated with vascular disease. Two classes of drugs are especially effective in lowering blood pressure and preventing cardiovascular complications, angiotensin converting enzyme (ACE) inhibitors and calcium antagonists. The hemodynamic effects of ACE inhibitors and calcium antagonists are complementary. While ACE inhibitors inhibit the renin-angiotensin system and reduce sympathetic outflow, calcium antagonists dilate large conduit and resistance arteries. Certain calcium antagonists, such as verapamil, lower heart rate. In the blood vessel wall, the local vascular effects of ACE inhibitors and calcium antagonists are also complementary. While ACE inhibitors inhibit activation of angiotensin I into angiotensin II and prevent the breakdown of bradykinin (which stimulates nitric oxide and prostacyclin formation), calcium antagonists inhibit the effects of vasoconstrictor hormones such as angiotensin II at the level of vascular smooth muscle by reducing calcium inflow and facilitating the vasodilator effects of nitric oxide. Calcium antagonists reduce smooth muscle cell proliferation and atherosclerosis. In hypertensive animals, verapamil and trandolapril normalize endothelial dysfunction. In large angiographic trials, nifedipine and nicardipine reduced the development of new atherosclerotic plaques. After myocardial infarction, verapamil reduces mortality and cardiac events in patients without heart failure. In contrast, ACE inhibitors are effective after myocardial infarction in patients with impaired left ventricular function. Urinary albumin excretion rate decreases during ACE inhibitor therapy or with a calcium antagonist such as verapamil; combination of the two drugs has an additive effect. In resistance arteries, hypertension is associated with an increased media/lumen ratio. ACE inhibitors, but not beta-blockers, markedly improve these structural changes. In summary, ACE inhibitors and calcium antagonists have a complementary profile, both in their hemodynamic and local vascular action. Hence, combination therapy with these two classes of drugs appears particularly useful in patients with hypertension, not only to lower blood pressure, but hopefully to achieve improved cardiovascular protection.
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PMID:Vascular protective effects of ACE inhibitors and calcium antagonists: theoretical basis for a combination therapy in hypertension and other cardiovascular diseases. 856 68

During the ten year period from 1981 to 1991, percutaneous transluminal renal angioplasty (PTRA) was performed in 180 renal arteries in 137 patients, where the underlying renovascular disease was fibromuscular dysplasia (FMD) in 30 patients (22%) and arteriosclerotic vascular disease (AVD) in 107 (78%). A preinterventional work-up and a re-evaluation of the patients after one year was designed for the assessment of the clinical, functional and technical outcome. Successful technical dilatation was achieved in 97% of procedures with FMD patients and in 82% of procedures with AVD patients. A beneficial effect on the blood pressure and the renal function was registered in both groups. The overall cure and improvement rate for hypertension was 86% in the FMD group and 64% in the AVD group after one year's follow-up. A significant gain in the total renal function was registered in both groups, the average increase in glomerular filtration rate being 13% (P < 0.001) for the FMD group and 11% (P < 0.001) for the AVD group one year after PTRA. Renal function was improved or unchanged in 89% of FMD patients and 74% of AVD patients. The improvement in renal function was made by the revascularized kidney. Renal vein renin investigation predicted the clinical outcome with an excellent diagnostic accuracy as no renin negative patient became normotensive, and renin positive patients, who did not turn normotensive, were in almost 90% of the cases affected by technical failure or restenosis/contralateral stenosis. Thus, the sensitivity of renal vein renin investigation was 95% and the specificity 75%. The outcome for patients with hypertension and renal insufficiency was considerably poorer than for the whole group of patients, with only a 20% success rate for hypertension, but 50% in this group had increased or unchanged GFR after intervention. The angiographic one-year follow-up revealed a recurrence rate of 6.7% for FMD and 15.1% for AVD. For the entire series of patients, the incidence of major complications was 5.4%, including one indirect fatality, while the incidence of minor complications was 5%. In conclusion, PTRA will cure or improve blood pressure in most patients with renovascular hypertension, and it preserves and even improves renal function in these patients. Complications and recurrence are in fact not very common and PTRA appears be the best first approach in all but ostial lesions for treatment of renovascular hypertension.
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PMID:Treatment of renovascular hypertension: one year results of renal angioplasty. 858 55

Earlier studies in diabetic animal models or ex vivo from diabetics suggest a deficiency in prostacyclin (PGI2) production and an increase in an alternate arachidonic acid metabolite, 12-hydroxyeicosatetraenoic acid (12-HETE), which stimulates angiogenesis, mitogenesis, and inhibits renin secretion. We studied the urinary excretion rate of 6-keto-PGF1 alpha (a stable metabolite of PGI2) and 12-HETE in controls and 42 noninsulin-dependent diabetes mellitus (NIDDM) patients with normal renal function and those with micro- or macroalbuminuria/hyporeninemic hypoaldosteronism (HH). The 2 eicosanoids were measured in urine using previously described high pressure liquid chromatography and RIA methods. Normal subjects and patients with NIDDM and microalbuminuria were infused with low dose calcium infusions that stimulate prostacyclin production in normal subjects. The PGI2 excretion rate of NIDDM patients with normal renal function was not different from that of controls (143 +/- 17 vs. 118 +/- 34 ng/g creatinine), but was reduced in those with microalbuminuria (75 +/- 10) and in macroalbuminuria patients (48 +/- 7; P < 0.01). In contrast, 12-HETE was increased in diabetics with normal renal function as well as in those with micro- or macroalbuminuria patients (69 +/- 18 vs. 250 +/- 62 vs. 226 +/- 60 and 404 +/- 131 ng/g creatinine; P < 0.01). Calcium did not stimulate PGI2, but increased 12-HETE in diabetics with microalbuminuria in contrast to levels in normal subjects. HH patients excreted less PGI2 (as previously reported), but had increased 12-HETE. HETE/PGI2 ratios further demonstrated these changes in the various groups. In a nondiabetic hypertensive microalbuminuria group, 12-HETE excretion was normal (73 +/- 28 ng/g creatinine). We conclude that the lipoxygenase product 12-HETE is increased early in the diabetic process, whereas PGI2 production is progressively impaired in NIDDM. These changes may play a role in the vascular disease of diabetes and partially explain the HH syndrome.
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PMID:A 12-lipoxygenase product, 12-hydroxyeicosatetraenoic acid, is increased in diabetics with incipient and early renal disease. 862 61

Thus I would like to conclude by saying that an idiopathic form of obliterative renal arteriopathy account for the rare presentation of severe hypertension and progressive renal failure with or without overt hemolytic anemia and thrombocytopenia in children. It can be labelled as primary malignant nephrosclerosis (NScl) or atypical HUS, based on primary thrombotic angiopathy. This, essentially intimal changes, is seen in diverse conditions and appears to result from primary endothelial injury followed by intimal exudation, thrombosis, and repair by fibrosis. Persistent or recurrence of this process form the basis of progressive obliterative arteriopathy. The result is renal ischemia and renin-angiotensin mediated hypertension. Establishment of a vicious circle would further accelerate HT and lead to end stage renal failure. Early recognition and prompt therapeutic intervention might prove beneficial.
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PMID:Thrombotic microangiopathy with hypertension and acute renal failure in children (a typical hemolytic uremic syndrome). 869 75

Angiotensinogen (ANG) is present in the eye. However, the source has not been determined. We showed that ANG mRNA was present in several ocular tissues using RT-PCR with ANG-specific primers. One of 10 iris samples (10%), 1 of 10 ciliary body samples (10%), 3 of 10 choroid samples (30%) and 9 of 10 retina samples (90%) were positive for ANG. Our study provides the first direct evidence that the renin-angiotensin system (RAS) component ANG is synthesized locally in the eye, especially the retina and choroid portion. These are strategic locations for an ocular RAS to influence chorioretinal blood flow, raising the possibility that RAS alterations may be involved in chorioretinal vascular disease.
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PMID:Angiotensinogen mRNA is synthesized locally in rat ocular tissues. 928 6

Epidemiological and clinical studies have defined the lower incidence of atherosclerotic vascular disease in women than in age-matched men. After menopause the difference becomes less significant, what is due to estrogen deficiency. The mechanism of vascular protective effect of estrogen involves inhibition of smooth muscle cell proliferation, protection of endothelium function and improvement of lipid metabolism. One of the most important risk factor of atherosclerosis is hypertension. The prevalence of hypertension in elderly women is extremely high-up to 80%. Because of absence of the hormonal replacement therapy effect on blood pressure, there is an indication for antihypertensive therapy in postmenopausal women. Angiotensin-converting enzyme inhibitors are the class of drugs which can lower cardiovascular mortality due to hypertension and atherosclerosis in elderly women. They improve impaired insulin sensitivity and inhibit activation of renin-angiotensin system, both processes leading to the development of hypertension in postmenopausal women. Angiotensin-converting enzyme inhibitors also possess a direct anti-atherosclerotic properties, like inhibition of smooth muscle cell proliferation and migration, protection of endothelium function, reduced macrophages activation and foam cell accumulation, protection of LDL particles and improvement of fibrinolysis.
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PMID:[Treatment of hypertension in postmenopausal women]. 950 90

Authors deal in detail with the pathophysiology of the osmolal regulation. Besides hyperosmolality the secretion of antidiuretic hormone (ADH) in increased by hypovolemia and hypotension. Secretion of ADH is lowered in hypoosmolal states. All other mechanisms are preferebly volume regulating and they influence mainly retention and excretion of sodium. Authors discuss homeostatic effects of the renin-angiotensin-aldosteron system, effects of renal failure with prevailing glomerular or tubular function disorder, impact of diuretics, natriuretic peptides, digitalis-like hormone, urodilantin and influence of the other solutes. Disorders of the effective osmolality regulation are frequent in the cerebral affections that originate from trauma, vascular disease, inflammation or tumors. Hypoosmolality and hyponatremia are presented in two different conditions: Inappropriate Vasopressin Secretion Syndrome (IADHS) and Cerebral Salt Wasting Syndrome (CSWS). Quick differential diagnose is important because the treatment of both syndromes is essentially different. Typical cause of hypernatremia is central diabetes insipidus (DI). The group of available calculated renal function parameters is applied in the differential diagnosis of these syndromes. They are creatinin clearance, excretion fraction of water and sodium, electrolyte clearance and electrolyte free water clearance. Investigation of ADH and natriuretic peptide could be even misleading. Pathophysiologic consequence of the state given by inappropriate elevation of one hormone can be the elevation of the second one.
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PMID:[Disturbances of effective osmolality regulation in disorders of the central nervous system and possible methods of monitoring]. 974 51


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