Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

We examined the relationship of hypertension and plasma renin activity to atherogenesis in 48 moderately hyperlipidemic (total serum cholesterol was about 200 mg/dl) baboons (Papio sp.). We used renal artery stenosis (two-kidney, one clip model) to produce hypertension associated with elevated plasma renin activity, and used cellophane wrapping of both kidneys (bilateral perinephritis model) to produce hypertension with normal renin activity. Renal artery stenosis and bilateral perinephritis increased both systolic and diastolic blood pressure by about 30 mm Hg. Renal artery stenosis approximately doubled, but bilateral perinephritis did not change plasma renin activity. Both hypertensive groups, to about the same degree, had significantly more extensive atherosclerosis than the control group in the abdominal aorta and brachial, iliac-femoral, and carotid arteries. The effect of hypertension was greatest in the carotid arteries where the extent of atherosclerosis was nearly tripled. Hypertension did not influence lesions in the thoracic aorta. By multiple regression analysis, very low plus low density lipoprotein cholesterol, high density lipoprotein cholesterol, and systolic blood pressure were consistently strong predictive variables for the extent of atherosclerotic lesions. Most of the effects of renal hypertension on atherosclerotic lesions appeared to be accounted for by the increase in blood pressure. In the carotid arteries, however, there was a suggestion of an effect above that due to increased blood pressure. Additional analyses indicated that these treatment effects were associated with serum potassium concentration, plasma renin activity, or other closely related variables.
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PMID:Effects of two forms of hypertension on atherosclerosis in the hyperlipidemic baboon. 389 70

The aging kidney suffers reduction both in mass and in glomerular filtration rate. These changes may be totally or partially due to atherosclerosis and hypertension, which reduce renal blood flow. Superimposed on these processes, and perhaps responsible for primary loss of renal mass irrespective of renal vascular disease, is glomerular damage and involution that is a consequence of adaptive increases in glomerular perfusion pressure that occurs as the number of nephrons decline with age. The data available at this time do not allow us to distinguish between these two potential mechanisms of renal senescence. The decline in GFR is in turn responsible for reduced renal acidification and the reduced renal clearance of drugs that are normally removed by the kidney. Certain renal functions, however, are depressed to a greater extent than is GFR. Both the ability to maximally dilute the urine and to maximally concentrate it are controlled by serum ADH concentrations and by the action of that hormone on the collecting duct. Aged rats do not maximally secrete ADH under conditions of dehydration and the effect of ADH on the kidney is also attenuated. Elderly humans also cannot maximally suppress ADH secretion when serum osmolality is reduced. Likewise, the renin-angiotensin-aldosterone axis is poorly responsive to volume depletion in aging subjects. As a result, elderly individuals cannot maximally retain sodium under conditions of plasma volume contraction out of proportion to reduction in GFR. The kidney is the site of vitamin D1 hydroxylation. Hydroxylation of vitamin D is reduced out of proportion to any reduction in GFR in the rat. There are no data as yet available on the effect of aging and the production of erythropoietin, a principal regulator of red blood cell mass. Neither are there data available on changes that might occur with advancing age in the ability of the aging kidney to metabolize various hormones, such as parathyroid hormone, glucagon, and insulin. The mechanisms and the full biochemical and physiologic consequences of renal senescence remain to be fully elucidated.
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PMID:The aging kidney. 391

Forty-six patients who underwent renal artery repair for presumptive renovascular hypertension are presented. Preoperative investigation included a rapid sequence IVP, a high quality angiogram and split function studies, as well as renin assays of renal venous blood in the more recent cases. Atherosclerosis was the causative pathological lesion in 60% of the patients, with fibromuscular dysplasia or miscellaneous causes of stenosis accounting for the remaining 40%.Surgical correction was usually obtained by bypass grafting (57%). Hypertension was cured or significantly improved in 36 patients (78%).Optimal results are dependent upon complete preoperative investigation and surgical repair of all the stenotic areas.
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PMID:Reconstructive vascular surgery for renovascular hypertension. 459 Jul 96

Propranolol (160--240 mg/24 h) and Oxprenolol (80--240 mg/24 h) were given for different periods of time to 13 and, respectively, 7 patients with essential arterial hypertension stage II. Both these beta-blocking drugs induced a significant fall in plasma renin activity : after ten days of treatment, platelet adhesiveness decreased in the patients with a basal level over 50% and increased in those with basal level below 30% (p < 0.01). When this treatment was given for 30 consecutive days, platelet adhesiveness decreased even in the latter patients. The drugs were also found to accelerate dilute blood clot lysis time in patients who presented a delayed lysis time before therapy. Thus, it is inferred that both propranolol and oxprenolol eliminate, at least partly, several factors involved in the pathogenesis of atherosclerosis, a frequent complication of essential arterial hypertension.
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PMID:[The effect of some beta-blocking drugs on plasma renin activity, platelet adhesiveness and dilute blood clot lysis time in patients with essential arterial hypertension]. 610 81

Many avian species demonstrate atherosclerosis and high blood pressure (BP) that are influenced by age, sex, diet, and environment, but show no arteriosclerosis in small vessels. Thus, we aimed to define neural and humoral control of BP in conscious, 32-wk-old female chickens, Gallus gallus. Mean aortic pressure (determined by chronically implanted catheter) was 137.6 +/- 2.0 mm Hg; heart rate was 295 +/- 4 beats/min. Plasma renin activity (PRA), measured by radioimmunoassay of fowl angiotensin I ([Asp1, Val5, Ser9]AI), and plasma angiotensinogen levels were 3.55 +/- 0.31 ng/ml/hr and 1229 +/- 66 ng/ml respectively. Repeated injection of propranolol (4 to 8 mg/kg/day, i.m.) decreased (p less than 0.01) the BP 19.1 +/- 3.0 mm Hg and heart rate 76 +/- 6 beats/min. Acute infusion of propranolol also markedly reduced BP and heart rate, and increased plasma levels of norepinephrine and epinephrine. SQ 14,225 (20 mg/kg/day) reduced BP (p less than 0.01), but BP returned towards original levels unless a higher dose was given. PRA increased 2- to 6-fold. BP also decreased 31.0 +/- 2.1 mm Hg after reserpine treatment, but not after [Sar1, Ile8]AII. These results suggest that in maintaining BP in fowl the beta-adrenergic function is important, whereas the renin-angiotensin system may not have a primary role.
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PMID:Renin-angiotensin and adrenergic mechanisms in control of blood pressure in fowl. 626 58

In order to evaluate the effect of the angiotensin I-converting enzyme inhibitor, captopril, on lipid metabolism, we measured serum lipoperoxides concentration ( LPX ) as well as plasma levels of renin activity (PRA), aldosterone (PAC) and bradykinin ( PBK ) before and after captopril administration in 15 hypertensive patients. Captopril significantly lowered the LPX (p less than 0.05 by repeated measures ANOVA) from the control value of 3.25 +/- 1.16 (mean +/- S.D.) to 2.92 +/- 0.94, 2.83 +/- 1.10, and 2.89 +/- 1.31 nmol/ml 30, 60, and 120 min after the administration, respectively. A significant reduction of blood pressure (p less than 0.0001) and PAC (p less than 0.01) was observed following captopril administration, while PBK increased significantly (p less than 0.001) from a baseline level of 10.85 +/- 4.07 to 13.95 +/- 5.29, 16.25 +/- 6.85, and 15.71 +/- 7.65 pg/ml 30, 60, and 120 min after captopril administration, respectively. There was no significant correlation between changes in serum LPX and in mean blood pressure, PRA and PAC, though a significant inverse relationship was found between changes in serum LPX and in PBK 120 min after the administration (r = -0.576, p less than 0.05, n = 13). Although the mechanisms by which serum LPX is decreased by captopril are not clear, it is suggested from the results that captopril is a beneficial antihypertensive agent for preventing LPX -induced atherosclerosis in hypertensive patients.
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PMID:[The effects of the angiotensin I-converting enzyme inhibitor, captopril, on serum lipoperoxides level and the renin-angiotensin-aldosterone and kallikrein-kinin systems in hypertensive patients]. 637 99

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, an orally active angiotensin-converting enzyme inhibitor, was administered to 15 patients with essential hypertension. The serum lipid peroxides level, aldosterone concentration in plasma and blood pressure decreased rapidly after administration, while plasma renin activity was not significantly changed. It is suggested that inhibition of angiotensin-converting enzyme by captopril offers a possible therapeutic approach to the treatment of atherosclerosis complicated with hypertension.
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PMID:Acute effect of captopril on serum lipid peroxides level in hypertensive patients. 637 87

Atherosclerosis and hypertension begin in childhood. Studies of children have identified black-white differences in anthropometric, hormonal, enzymatic, and renal mechanisms related to the development of coronary artery disease and hypertension. Black children have greater body density, higher blood pressure, and higher serum total cholesterol, alpha-lipoprotein cholesterol, and insulin levels, whereas white children have a higher percentage of body fat, a faster heart rate, and higher hemoglobin, serum triglyceride, pre-beta-lipoprotein cholesterol, plasma renin, and dopamine-beta-hydroxylase levels. At puberty, white male children have decreased high-density lipoprotein (HDL) levels and increased low-density lipoprotein/HDL ratios. Black children have lower urinary K+ excretion and demonstrate natriuresis when K+ is administered orally. These black-white contrasts provide clues for studying disease development early in life. Rational approaches to primary prevention of atherosclerosis and hypertension may require a diversity of strategies because of these black-white differences.
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PMID:Black-white contrasts as determinants of cardiovascular risk in childhood: precursors of coronary artery and primary hypertensive diseases. 638 95


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