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

The development and evolution of hypertensive vascular lesions affecting the arterial supply of (a) the kidney and (b) organs other than the kidney were studied in rats developing either malignant (MHY) or benign (BHY) hypertension 3, 6, 9 and 12 days after aortic ligation between the renal arteries. Vascular disease evolved into two distinct patterns which suggested acute renal damage to be the determinant for the development of either the malignant or benign form of hypertension. Three days after aortic ligation MHY and BHY animals showed widespread fibrinoid deposition in vascular territories above the aortic ligature. However, in MHYs these lesions were much more severe and, in the kidney, they were accompanied by the development of focal parenchymal atrophy, microinfarcts and hyalin droplet degeneration of cells of the Bowman capsule. The degree of renal damage correlated with elevations in blood urea nitrogen (BUN) and plasma creatinine; however, there was no correlation with rises in blood pressure, plasma renin activity (PRA), aldosterone or corticosterone which were similarly elevated in 3-day MHY and 3-day BHY animals. Between 6 and 12 days a marked clearance of fibrinoid took place in all organ beds of BHYs, but in the non-renal vasculature of MHY animals fibrinoid remained prominent and served as the central core for necrotising arterial lesions. In the kidney of MHYs some reduction in the fibrinoid content was observed, but the parenchymal damage perpetuating from the earlier stages had exacerbated leading to collagen deposition and a marked increase in the collagen concentration of the renal cortex. These features were accompanied by further elevations in PRA and corticosteroids and a progressive deterioration of renal function. By contrast, in 12-day BHY animals, despite sustained hypertension, PRA and corticosteroids were falling from their previously higher levels and normal renal function was maintained. These studies warrant inference that extensive parenchymal damage of the kidney due in part to severe arterial fibrinoid deposition is one of the initial events in the development of malignant hypertension.
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PMID:Acute arterial fibrinoid deposition and ischaemic parenchymal damage of the kidney. Pathogenic factors in the development of malignant hypertension. 636 44

Based on the retrospective analysis of 38 cases of renovascular hypertension treated by surgical intervention, the following indications are proposed for arterial reconstructive surgery: younger age of patient, short duration of hypertension, renin-mediated hypertension and extent and functional significance of the obstructing arterial lesion, favorable level of renal function in the affected side, and renal function threatened by advanced progressive vascular disease, surgically correctable lesion, and focal, unilateral renal arterial atherosclerosis without generalized atherosclerosis, good surgical risk, and hypertension not responding to medical treatment. Although the clinical use of the angiotensin I converting enzyme inhibitor and induction of percutaneous transluminal angioplasty can provide a new approach to non-surgical treatment for renovascular hypertension, the long-term use of antihypertensive drugs induces gradual decrease in renal function. Surgical treatment is best reserved for the patient on whom the available data meet the above criteria for vascular surgery.
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PMID:[Surgical treatment of renovascular hypertension with special reference to the indications for reconstructive surgery]. 637 7

Captopril 12.5 to 50 mg as a single dose was given to six patients with pulmonary hypertension secondary to collagen vascular disease. Total pulmonary resistance was decreased in four patients from 19% to 39%, but mean pulmonary artery pressure (63 +/- 15 mm Hg) was not decreased, probably because of the concurrent increase in cardiac output from 21% to 52% (2p less than 0.05). The systemic arterial pressure was slightly decreased due to the decrease in total systemic resistance. Control plasma renin activity ranged from 0.15 to 16 ng/ml/hr and was increased during captopril from 19% to 356%. These results, although preliminary, suggest that captopril may be beneficial in certain patients with pulmonary hypertension secondary to collagen vascular disease.
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PMID:Hemodynamic effects of captopril in pulmonary hypertension of collagen vascular disease. 675 Oct 58

The level of arterial blood pressure is set by complete interactions of several mechanisms which influence both blood flow in and resistance of the vascular system. An imbalance favouring elevation of vascular resistance or extracellular volume will result in hypertension. Such alterations may include increased activity of the sympathetic nervous system, of the renin-angiotensin system, or excessive secretion of mineralocorticoids. Of equal importance may be a reduced activity of blood pressure-lowering factors such as prostaglandins and the kallikrein-kinin system. This paper describes the possible significance of prostaglandins in the pathophysiology of hypertension and in degenerative vascular disease, based on their involvement in the control of vascular resistance, renal regulation of extracellular volume and platelet-vessel wall interactions. An abnormality in the biosyn-thesis of certain prostaglandin endoperoxide metabolites may lead to hypertension even without an increase in the activity of the classic blood-pressure-elevating systems. The contribution of prostaglandins for the development of hypertension and degenerative vascular disease may be based on an inherent abnormality of the prostaglandin system, as well as on the effects of major risk factors such as dietary intake of sodium and fat on prostaglandin synthesis. Specific blockade or stimulation of distinct biosynthetic pathways leading to antagonistically acting prostaglandins and nutritional manipulation of precursor fatty acids should lead to a better understanding of the pathomechanisms involved and may offer new strategies for therapy or prevention of these cardiovascular disorders.
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PMID:Arachidonic acid metabolites, hypertension and arteriosclerosis. 695 29

Systemic hemodynamics, intravascular volume, and plasma renin activity were determined in 135 lean, midly obese, or distinctly overweight subjects who were normotensive or had borderline or established essential hypertension. Cardiac output (but not index) was higher and peripheral resistance lower in obese than in lean subjects, except in borderline hypertension. Intravascular volume was increased in obese patients, and more so when corrected for body height; correction for body weight led to relative volume contraction. Intravascular volume correlated directly with cardiac output in the entire population, as well as in the subgroups. Intravascular volume correlated inversely with total peripheral resistance in all subjects and in each subgroup. Both correlations remained significant when an approximation was used to correct influences of obesity on total blood volume. Sodium excretion was higher in obese than in lean subjects. Thus, despite the expanded intravascular volume in obesity, the pathophysiologic relationship between systemic hemodynamics and intravascular volumes remains unchanged. Relatively low peripheral resistance in obesity may decrease the risk of systemic vascular disease. Nevertheless, since circulating volume is increased, the greater venous return adds an additional load to a left ventricle that is already burdened by a high afterload caused by arterial hypertension.
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PMID:Obesity and essential hypertension. Hemodynamics, intravascular volume, sodium excretion, and plasma renin activity. 700 72

Antihypertensive effects of captopril, an orally active converting enzyme inhibitor were examined in the young and adult stroke-prone SHR (SHRSP) rats. The treatment was initiated at 6-7 and 14-18 weeks of age, and was continued for 12 and 17 weeks, respectively. The dosage of captopril was changed stepwise 3-30 and 3-100 mg/kg, orally per day in the young and adult rats, respectively. The effects of hydralazine were also determined for comparison. Captopril had a chronic antihypertensive effect when given in doses of 30 mg/kg in the young and 100 mg/kg in the adult rats. Captopril had no significant effect on heart rate throughout the experiments, while hydralazine increased the heart rate. Treatment with captopril decreased the incidence of vascular disease in the young and the severity in the adult rats, respectively. A decrease in incidence of cerebral stroke in the adult SHRSP was also apparent. More than a ten fold increase in plasma renin activity and about a two fold increase in kidney renin activity were observed in both the young and adult SHRSP at the end of the treatments. The results demonstrate the efficacy of long-term treatment with captopril in the management of hypertensive disease in SHRSP rats.
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PMID:Effects of long-term treatments with captopril on blood pressure and renin activity in the stroke-prone spontaneously hypertensive rats. 701 11

Polycystic kidney disease (PKD) is the fourth most common cause of end-stage renal disease and is a common cause of hypertension and associated vascular morbidity. Activity of the renin angiotensin system has been identified as a major component of hypertension and altered fluid and electrolyte physiology in PKD. Activity of this pathway also has been proposed as a potential modulator of structural change in both tubules and the interstitium of the kidney. Cilazapril is a long-acting angiotensin-converting enzyme inhibitor that has been effective in producing vascular remodelling in hypertensive vascular disease. We undertook a study to determine whether therapy with cilazapril would modify the expression of PKD in the Han:SPRD-cy rat, a model of autosomal dominant PKD that closely resembles human disease. Male rats were treated for 4 months, starting at 1 month of age. Control animals were hypertensive by 3 months of age, whereas treated animals were noted to be hypertensive only at the exit assessment (P < 0.001 at 3 months, P = 0.005 at 5 months). At 5 months of age, cilazapril-treated animals had modest but statistically significant reductions in serum creatinine (mean, 1.77 mg/dL v 1.97 mg/dL; P = 0.0006) and morphometrically assessed cyst volume (mean, 0.32 mL v 0.67 mL; P = 0.036). Cilazapril is an effective treatment for hypertension in this model of progressive renal disease and may have benefits beyond the prevention of cardiovascular morbidity.
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PMID:Cilazapril delays progression of hypertension and uremia in rat polycystic kidney disease. 750 69

The kidney and hypertension are critically linked. They appear to be linked particularly by the renin angiotensin system and the control of sodium balance. There are other mechanisms by which the kidney controls hypertension, but there are not as important as the above. In people with intrinsic renal disease hypertension increases the rate of deterioration and such hypertension should be treated energetically to prevent this deterioration. Long-standing chronic mild impairment of renal function leads to hypertension and vascular disease. This hypertension and vascular disease causes further deterioration of renal function, setting up a vicious cycle and an irreversible process unless measures are taken to interrupt the cycle.
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PMID:[The kidney and hypertension]. 753 Oct 84

NG-nitro-L-arginine methyl ester (L-NAME) and 11-desoxycorticosterone plus salt intake (DOCA-salt) hypertensive rat models were compared to study the possible involvement of model-specific factors in the development of renal angiopathy and left ventricular hypertrophy (LVH). Blood pressure was measured in L-NAME, DOCA-salt hypertensive, and control Wistar rats, and the lesions of nephroangiosclerosis and left ventricular hypertrophy were evaluated after 7 weeks. Arterial wall cyclic guanosine monophosphate, plasma renin activity (PRA), and renal renin storage were assessed in parallel. For the same level of hypertension in the two models, the renal arterial fibrinoid necrotic lesions were significantly more frequent in L-NAME than in DOCA-salt hypertensive rats. In DOCA-salt hypertensive rats, PRA was decreased and arterial cGMP increased compared to controls. In the L-NAME model, arterial cGMP decreased and PRA showed a bimodal distribution in this intermediate stage of hypertensive disease. LVH was observed in DOCA-salt rats and only in the L-NAME rats with a high level of PRA. There was a close correlation between the lesions of nephroangiosclerosis, left ventricular index, and plasma renin activity in L-NAME rats. We therefore suggest that the activation of the renin-angiotensin system participates specifically in the development of the second stage of hypertension during chronic blockade of NO synthase involving nephroangiosclerosis and LVH.
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PMID:Renal hypertensive angiopathy. Comparison between chronic NO suppression and DOCA-salt intoxication. 775 45

The present study examines the effects of dietary magnesium on the development of hypertension and hypertensive vascular lesions in deoxycorticosterone acetate and salt induced (DOCA-salt) and 2 kidney one clip (2K1C) hypertensive as well as normotensive control rats. Animals received a regular (0.12% Mg), high (0.4% Mg) or low (0.03% Mg) magnesium diet for 6 wks. Dietary magnesium did not alter the growth or blood pressure in control, DOCA-salt and 2K1C rats even though the plasma magnesium concentration was significantly altered by the diets (ANOVA, p < 0.05 in control, DOCA-salt and 2K1C, respectively). Dietary magnesium did not alter the urinary potassium excretion, plasma sodium, potassium, total calcium concentration and plasma renin activity in any group, while the high magnesium diet significantly increased the urinary sodium excretion in DOCA-salt (p < 0.05) but not in control and 2K1C rats when compared with the regular magnesium diet. In histological studies, dietary magnesium did not alter the percentage media area of intramyocardial arteries, or glomerular and renal arterial and arteriolar lesions in DOCA-salt and 2K1C rats. This study suggests that moderate alterations of dietary magnesium do not modify blood pressure in normotensive control, DOCA-salt and 2K1C hypertensive rats, nor do they modify vascular disease in these 2 hypertensive models.
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PMID:Effects of dietary magnesium on blood pressure and vascular lesions in hypertensive rats. 789 33


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