Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three case histories are described which highlight some of the predisposing risk factors and therapeutic strategies in the event of acute severe renal failure during treatment with ACEI. With appropriate therapy, renal function is usually restored within a few days. Renal artery stenosis, dehydration and diuretics stimulate the renin angiotensin system and make preservation of normal renal function, increasingly dependent on angiotensin II. The prevalence of renal artery stenosis is substantially increased in patients with peripheral vascular disease or with coronary artery disease with concomitant hypertension. Patients should be told about the increased risk of adverse effects to the kidneys if they become dehydrated. In these cases it is essential to reduce the dose diuretics and ACEI, and it may be necessary to give parenteral fluid substitution.
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PMID:[Severe renal failure during treatment with angiotensin-converting enzyme inhibitors]. 157 48

Sixty million Americans have hypertension, a major cardiovascular risk factor. Its presence accelerates the atherosclerotic process, producing strokes, heart attacks, heart failure, renal failure, and peripheral vascular disease. This article highlights the historical landmarks in the study of this disease from the first documented measurement of blood pressure in 1733, through the most recent pharmacologic approaches to treatment. In addition, the roles of the kidney and the renin-angiotensin-aldosterone system are examined.
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PMID:Historical reflections on hypertension. 194 83

The effects of iloprost, a stable analog derivative of prostacyclin, on heart rate, blood pressure, renal plasma flow (RPF), glomerular filtration rate, filtration fraction, urine flow, fractional excretion of sodium (FENa), proximal fractional sodium reabsorption (PFRNa), fractional sodium resorption at the ascending limb of Henle's loop (HFRNa), plasma renin activity (PRA), and plasma aldosterone concentration (PA) were evaluated in patients with peripheral vascular disease and normal renal function. In 10 patients the drug was administered intravenously for 6 hours daily for 6 days at a rate of 1 ng/kg/min. In 7 patients iloprost was also administered at a dose of 2 ng/kg/min for the same time. There was no significant change in heart rate and blood pressure at both iloprost doses. At the dose of 1 ng/kg/min the drug had no effect on renal hemodynamics and function, PRA, and PA. At the dose of 2 ng/kg/min iloprost significantly increased RPF (p less than 0.025) and FENa (p less than 0.025) and significantly decreased HFRNa (p less than 0.025) without affecting glomerular filtration rate, filtration fraction, urine flow, PFRNa, PRA, and PA. No correlation was found between the increase in RPF and FENa (r = 0.01). We conclude that at a dose of 2 ng/kg/min, but not 1 ng/kg/min, iloprost has a natriuretic effect secondary to inhibition of sodium reabsorption at the ascending limb of the Henle's loop and not related to the renal hemodynamic effect.
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PMID:Effects of iloprost, a prostacyclin analog derivative, on renal plasma flow, renal function, and renin-aldosterone system in humans. 245 74

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 saw three cases of severe reversible azotemia secondary to captopril therapy in hypertension. All patients had extensive peripheral vascular disease involving the renal arteries, and two patients (patients 2 and 3) had high levels of peripheral plasma renin activity. The azotemia occurred approximately two weeks after exposure to captopril, and fever, a maculopapular pruritic cutaneous rash, and eosinophilia developed in two patients (patients 2 and 3). The cause of the azotemia in our patients is not clearly known, since renal biopsies were not performed. The most likely cause for the azotemia was volume contraction with reduction in the glomerular filtration rate, although a direct insult to the kidney could not be excluded.
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PMID:Severe reversible azotemia from captopril therapy. Report of three cases and review of the literature. 633 47

In hypertensive emergencies, sublingual nifedipine (10 to 30 mg) is the treatment of choice. Nifedipine, however, may lead to reflex activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system as well as fluid retention when used as a monotherapy for a longer period of time. In chronic arterial hypertension, verapamil, and especially diltiazem seem to be superior to nifedipine. Verapamil (360 to 480 mg a day) and diltiazem (180 to 270 mg a day) produce a consistent antihypertensive effect throughout a 24-hour period. During dynamic or isometric exercise, their antihypertensive potency is equivalent to that of beta blockers. Overall response rate in patients with mild to moderate hypertension is 80 percent with monotherapy. In refractory hypertension, combination with thiazide, reserpine, or clonidine may be useful. Calcium blockers are preferred in older patients with chronic arterial hypertension, and in patients with low renin hypertension, coronary heart disease, peripheral vascular disease, or obstructive airways disease.
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PMID:Treatment of hypertension with calcium channel blockers: European data. 638 98

The incidence of renal artery stenosis (RAS) was prospectively evaluated by aortofemoral angiography in 100 patients with peripheral vascular disease (PVD) to find whether RAS was a more common finding in hypertensive than in normotensive patients. For a possible association with RAS, risk factors, clinical and angiographical variables were evaluated. Nephrotoxicity of the contrast medium Iohexol was elucidated. A follow-up of six month was performed in patients with severe stenosis or total occlusion of the renal arteries. Of the 49 patients with a renal artery lesion 26.5% were normotensive and 73.5% hypertensive. Hypertension was significantly correlated to RAS. Reconstructive vascular procedures were during the follow-up performed in 47.3% of the patients with severe RAS or occluded renal arteries, two patients underwent a renal artery revascularization, none of them got a postoperative blood pressure decrease. Hypertension in patients with peripheral vascular disease is predictive for renal artery stenosis and a possible renovascular hypertension should be evaluated. Surgery for renal artery stenosis in peripheral vascular diseased patients should, however, probably be performed firstly to reduce the risk for occlusion. The effect on the blood pressure can not be predicted without a more careful analysis that the blood pressure is renin-dependent. Iohexol showed low nephrotoxicity, also in patients with renal artery disease.
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PMID:To what extent does peripheral vascular disease and hypertension predict renal artery stenosis? 796 68

A 67-yr-old female patient with accelerated hypertension, severe peripheral vascular disease, diabetes mellitus, and coronary artery disease had an abnormal renal scan, renal angiogram, and renal vein renin determination with lateralization to the left kidney. Angiography demonstrated a very tight, eccentric plaque obstructing the left renal artery of approximately 99%. Because of the anatomy of the plaque, balloon dilatation was deemed inadvisable. Subsequently, a Simpson 7F graft DCA atherocath through a four-curved 10F right bypass graft guiding catheter was used to successfully debulk the left renal artery. After debulking, the artery was dilated with a 5 mm Meditech balloon on a wire through a Cobra guiding catheter. The patient's blood pressure responded immediately and there were no complications. A large amount of atherosclerotic plaque was removed from the renal artery.
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PMID:Successful directional atherectomy of eccentric renal artery stenosis using the Simpson directional coronary atherocath as a primary therapy. 834 97

Diabetes mellitus is associated with an inordinately high risk of virtually all manifestations of cardiovascular-renal disease including atherosclerotic coronary and peripheral vascular disease, congestive heart failure, stroke, nephropathy, and cardiomyopathy unassociated with coronary heart disease. Abnormalities in the renin-angiotensin-aldosterone-kinin (RAAK) cascade have been implicated in the pathogenesis and clinical expression of these cardiovascular-renal sequelae. Thus, pharmacological modulation of the RAAK system is an attractive therapeutic target in diabetes mellitus. Indeed, emerging data from human clinical studies appear to confirm this thesis.
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PMID:Renin-angiotensin-aldosterone-kinin system influences on diabetic vascular disease and cardiomyopathy. 993 Mar 81

Hypertension is currently defined in terms of levels of blood pressure associated with increased cardiovascular risk. A cut-off of 140/90 mm Hg is accepted as a threshold level above which treatment should at least be considered. This would give a prevalence of hypertension of about 20% of the adult population in most developed countries. Hypertension is associated with increased risk of stroke, myocardial infarction, atrial fibrillation, heart failure, peripheral vascular disease and renal impairment. Hypertension results from the complex interaction of genetic factors and environmental influences. Many of the genetic factors remain to be discovered, but environmental influences such as salt intake, diet and alcohol form the basis of nonpharmacological methods of blood pressure reduction. Investigation of the individual hypertensive patient aims to identify possible secondary causes of hypertension and also to assess the individual's overall cardiovascular risk, which determines the need for prompt and aggressive therapy. Cardiovascular risk can be determined from (i) target organ damage to the eyes, heart and kidneys; (ii) other medical conditions associated with increased risk; and (iii) lifestyle factors such as obesity and smoking. Secondary causes of hypertension are individually rare. Screening tests should be initially simple, with more expensive and invasive tests reserved for those in whom a secondary cause is suspected or who have atypical features to their presentation. The main determinants of blood pressure are cardiac output and peripheral resistance. The typical haemodynamic finding in patients with established hypertension is of normal cardiac output and increased peripheral resistance. Treatment of hypertension should initially use nonpharmacological methods. Selection of initial drug therapy should be based upon the strength of evidence for reduction of cardiovascular mortality in controlled clinical trials, and should also take into account coexisting medical conditions that favour or limit the usefulness of any given drug. Given this approach, it would be reasonable to use a thiazide diuretic and/or a beta-blocker as first-line therapy unless there are indications to the contrary. Individual response to given drug classes is highly variable and is related to the underlying variability in the abnormal pathophysiology. There are data to suggest that the renin-angiotensin system is more important in young patients. The targeting of this system in patients under the age of 50 years with a beta-blocker (or ACE inhibitor), and the use of a thiazide diuretic (or calcium antagonist) in patients over 50 years, may enable blood pressure to be controlled more quickly.
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PMID:Pathoaetiology, epidemiology and diagnosis of hypertension. 1067 92


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