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

Hypertension constitutes a major health problem and the challenge is to identify patients having 'surgically' curable renal vascular disease among the majority with so-called essential hypertension. The best of unsatisfactory diagnostic tests are renography and plasma renin activity both before and during angiotensin II blockade. The necessity of better screening tests has increased because of the recent advances in surgical techniques and especially percutaneous transluminal renal angioplasty. The latter has definitely become the method of choice for correction of suspected hemodynamically significant artery stenoses whenever technically feasible. With improved angioplasty techniques the risk of treating renal artery stenosis without hemodynamic and clinical importance (so-called cosmetic repair) has increased. Unfortunately randomized trials including surgery versus angioplasty are not available. It should be kept in mind that only after correction of the stenosis is achieved and the blood pressure has become normal, can the diagnosis of renovascular hypertension be made with certainty.
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PMID:Renovascular hypertension. Diagnosis and intervention. 252 9

Endothelial injury and platelet activation may be involved in the pathogenesis of hypertensive vascular disease. The aim of this study was to evaluate the change in endothelial cell and platelet activation plasma markers after an acute physiological increase in blood pressure. Plasma renin activity (PRA), serum angiotensin-converting enzyme (ACE), plasma factor VIIIR:Ag, and plasma beta-thromboglobulin (BTG) were determined before and after handgrip in subjects with borderline (n = 8) and established (n = 11) hypertension and in age-matched normal volunteers (n = 10). A significant mean increase in ACE, factor VIIIR:Ag, and BTG was observed after handgrip in all groups of subjects. A greater response in BTG changes was found in hypertensive subjects when compared with normal subjects. No correlations were found between the blood pressure response after handgrip and the handgrip-induced changes in plasma markers of endothelial cells and platelet activation. Changes in endothelial cells and platelet activity occurring after handgrip did not appear to depend on the associated blood pressure elevations.
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PMID:Plasma markers of endothelial cells and platelet activation following handgrip in normals and hypertensive patients. 283 26

Adverse effects of converting enzyme inhibitors are either substance-specific (neutropenia, proteinuria, skin rashes, taste disturbances) or due to the converting enzyme inhibition (hypotension, functional renal insufficiency, hyperkalemia, cough, angioedema). They are rare nowadays because of better knowledge of the pharmacokinetics and -dynamics of the converting enzyme inhibitors, resulting in lower dosage, and because of identifying patients at high risk. The dosage must be adjusted according to renal function, in order to prevent accumulation and toxicity. In addition to patients with renal insufficiency, patients at high risk are those with a stimulated renin-angiotensin-aldosterone system, i.e. patients with renovascular hypertension or heart failure. Patients with collagen vascular disease, for example, systemic lupus erythematosus or scleroderma, should not be considered for long-term therapy with converting enzyme inhibitors because of the increased risk of neutropenia. Life-threatening angioedema may develop, mainly during the first few hours after drug administration.
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PMID:[Angiotensin-converting enzyme inhibition: side effects and risks]. 285 Jun 87

The blood pressure and endocrine responses to cigarette smoking were studied in 19 hypertensive patients to determine whether smoking activates the renin-aldosterone axis. Blood pressure rose from 140 +/- 7/99 +/- 3 (mean +/- SEM) to 151 +/- 5/108 +/- 2 mm Hg (p less than 0.01) within 10 minutes after smoking, and pulse rate also increased significantly (69 +/- 2 to 96 +/- 4 beats per minute). Plasma renin activity did not change but rose 15 minutes after ambulation. In contrast, plasma aldosterone and plasma cortisol levels increased significantly after smoking and peaked at 20 minutes: 13.9 +/- 0.9 to 20.2 +/- 2.0 ng/dl (p less than 0.01) and 10.2 +/- 1.0 to 22.0 +/- 2.2 micrograms/dl (p less than 0.01), respectively. These responses were closely correlated (r = 0.6467, p less than 0.01), suggesting a pituitary-adrenal mechanism is activated during smoking. Plasma ACTH levels rose from 58 +/- 6 to 87 +/- 10 pg/ml in 10 minutes (p less than 0.001) and to 90 +/- 14 pg/ml at 20 minutes (p less than 0.01). Total plasma catecholamine levels also rose from 468 +/- 60 to 624 +/- 73 pg/ml 10 minutes after smoking (p less than 0.01) and to 724 +/- 69 pg/ml (p less than 0.01) 15 minutes after ambulation. In hypertensive smokers, cigarette smoking is associated with an increase in blood pressure, pulse rate, and plasma ACTH, cortisol, aldosterone, and plasma catecholamine levels. The long-term significance of these acute hormonal changes in regard to blood pressure homeostasis and vascular disease in cigarette smokers remains to be determined. Smoking should be avoided prior to blood pressure and endocrine determinations.
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PMID:Cigarette smoking in hypertensive patients. Blood pressure and endocrine responses. 298 31

Antihypertensive effect of enalapril (MK-421), an orally active non-sulfhydryl-containing converting enzyme inhibitor, was examined in stroke-prone spontaneously hypertensive (SHRSP) rats. The treatment was started at 14-15 weeks of age with tail blood pressure over 240 mmHg and was continued for 11 weeks. We used captopril as the reference drug. The dose of enalapril and captopril was 10 and 30 mg/kg per day, p.o., respectively. Enalapril showed a sustained antihypertensive effect from the 1st to the 11th week of the treatment. This antihypertensive effect was substantiated by the good increase in body weight; decrease in heart weight; decrease in incidences of vascular disease, nephrosclerosis, stroke and death. Enalapril treatment also prevented the increases in urine volume, and excretion of osmotically active solutes, Na, Cl and K with age. Captopril treatment showed about the same antihypertensive effect. No side effects were seen in the enalapril or captopril treated group. The antihypertensive potency of enalapril was about 3 times more than that of captopril. Enalapril and captopril slightly increased plasma renin concentration. Urinary excretion of PGE2 was not changed by enalapril or captopril treatment. These results clearly demonstrate the efficacy of long-term treatment with enalapril to prevent development of malignant hypertensive cardiovascular disease in SHRSP rats.
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PMID:Chronic effects of enalapril on blood pressure, stroke, plasma renin, urinary electrolytes and PGE2 excretion in stroke-prone spontaneously hypertensive rats. 299 88

Teprotide, a nonapeptide isolated from the venom of a Brazilian pit viper, Bothrops jararaca, was the first angiotensin converting enzyme (ACE) inhibitor to be discovered and tested. It was found to be an effective, non-toxic antihypertensive agent as well as an afterload-reducing agent for patients with congestive heart failure (CHF). The primary activity of teprotide resulted from blockade of the angiotensin I converting enzyme--the pivotal step in the renin-angiotensin-aldosterone system (RAAS), and consequent reductions in angiotensin II levels. There was limited clinical testing for teprotide because of: its scarcity; the need for parenteral administration; and the subsequent discovery and synthesis of captopril, the first orally active angiotensin converting enzyme inhibitor. Captopril is the prototype oral angiotensin converting enzyme inhibitor and has been extensively studied since the initiation of formal studies in 1976. Perhaps one of the most closely researched drugs in modern times, the experience with captopril now includes more than 12,000 patients studied in formalized trials and over 4,000,000 patients treated world-wide by physicians for hypertension and congestive heart failure. Enalapril (MK421) is the first of what appears to be a growing number of analogues which are structurally and pharmacodynamically different from captopril; yet, they possess the same capacity for inhibiting the activity of angiotensin converting enzyme. The side effect profile of enalapril (and presumably future) angiotensin converting enzyme inhibitors appears to be similar to captopril, though clearly more experience is needed with newer agents. The initial use of captopril was troubled by a relatively high incidence of side effects which will form the focus of this discussion. Partially the result of incomplete pharmacokinetic information, captopril was administered in early studies at dosages now recognised to be far in excess of those necessary for drug action. In addition, dosages were given without regard for deficiencies of renal function, now known to be the main excretory route of captopril. The population of those patients studied frequently had chronic, treatment-resistant hypertension, often associated with concomitant end-organ disease (especially renal disease); and many additional factors further complicating the clinical setting, e.g. a relatively high incidence of collagen vascular disease and immunosuppressive treatments.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adverse reactions with angiotensin converting enzyme (ACE) inhibitors. 302 83

Renin and prorenin, the latter after conversion to renin, are usually measured by indirect RIA using antibodies against angiotensin I. They can now also be measured by direct RIA using monoclonal antibodies reacting with total immunoreactive renin (renin plus prorenin) or with renin alone. Results of measurements in renal and peripheral venous plasma indicate that normally a large proportion of prorenin in plasma is of renal origin and they support the concept of separate pathways for prorenin and renin secretion by the JG-cells. Acute stimulation causes a prompt increase of plasma renin without any change in prorenin. During chronic stimulation both renin and prorenin are increased, in such a way that the ratio between the two is higher the stronger the stimulus. Thus, with acute stimulation only the release of stored renin appears to be increased (regulated pathway), whereas during chronic stimulation the synthesis and secretion of prorenin are also (constitutive pathway). During pregnancy, in the early luteal phase of the menstrual cycle and after ovarian hyperstimulation with gonadotropins, a normal or somewhat elevated plasma level of renin is associated with a disproportionally high level of prorenin. This is an indication of extrarenal production of prorenin and in these conditions the ovary, probably corpus luteum, seems to be the main source. In most patients with renin-producing tumors plasma prorenin is also disproportionally high. In diabetes mellitus complicated by micro-angiopathy plasma prorenin is also elevated whereas renin is normal or even low. In diabetics with end-stage nephropathy we found no significant veno-arterial difference in prorenin across the kidneys, despite high circulating prorenin and a very low blood flow through these kidneys, suggesting that also in these patients part of the increased prorenin in plasma is of extrarenal origin. Thus, measurements of prorenin in plasma in various pathological conditions may contribute to a better understanding of the physiological role of the renal and extrarenal renin-angiotensin systems.
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PMID:Human prorenin: pathophysiology and clinical implications. 306 28

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

Antihypertensive effects of three beta-adrenergic blocking drugs, acebutolol, propranolol, and practolol were studied for 11 weeks. Spontaneously (SHR); one-clip, two-kidney (CLIP); and deoxycorticosterone and salt (DOC) hypertensive rats were used. The drugs were given orally, 100 mg/kg per day, 5 days per week before development of hypertension. Propranolol inhibited blood pressure (BP) increase significantly in SHR. Acebutolol and practolol also lowered BP in SHR. Three drugs did not affect BP in CLIP, but an apparent inhibition was seen when the results were analyzed including the cases of which BP stayed below 150 mmHg. Either of three drugs did not show antihypertensive effects in DOC. Acebutolol rather increased BP more rapidly. Practolol also increased BP slightly more rapidly. Cerebral stroke was seen in DOC. The incidences of the stroke in the groups given the solvent, acebutolol, propranolol, and practolol were 3/6, 4/7, 2/6, and 3/6, respectively. Acebutolol seemed to cause stroke earlier with the more rapid BP elevation. Acebutolol, propranolol, and practolol decreased incidence of the vascular disease in CLIP. Propranolol also decreased it in DOC. Plasma renin activity was suppressed by these drugs in SHR and CLIP. The mechanisms of antihypertensive effects of beta-adrenergic blocking drugs are unknown. The present study denies those due to inhibition of cardiac function, or renin release from the kidney. A better experimental model is necessary to study this. The possibility that acebutolol and other beta-blockers might accelerate BP elevation and incidence of stroke must be reexamined.
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PMID:Effects of beta-adrenergic blocking drugs in hypertensive rats. 611 Jul 12

The authors describe a juxtaglomerular cell tumor (JGCT) which caused severe hypertension in a 58-year-old man. Light microscopy showed a circumscribed tumor composed of interlacing cords and occasional nodules of relatively uniform cells with no mitotic activity. Rhomboid crystals characteristic of "prerenin" were present within the cytoplasm of tumor cells, and there was a close relationship between the tumor and unmyelinated nerve axons. Intracytoplasmic renin was demonstrated by immunofluorescence, and tumor granules were shown to contain zinc by electron-beam microanalysis. Review of 14 prior cases, with additional follow-up of 9, showed that no patient had developed recurrence, metastasis, or another tumor. Four patients, however, are hypertensive but probably because of secondary tumor effects rather than recurrent hyperreninism. The distinction of JGCT from hemangiopericytoma with renal involvement is important because of the high mortality associated with the latter. The authors conclude that JGCT is benign, but patients with JGCT may remain hypertensive postnephrectomy because of hypertensive angiopathy.
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PMID:Juxtaglomerular cell tumor of the kidney. 636 18


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