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C. G. Isles

Bio: C. G. Isles is an academic researcher. The author has contributed to research in topics: Atenolol & Nifedipine. The author has an hindex of 1, co-authored 1 publications receiving 17 citations.

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Journal ArticleDOI
TL;DR: Recommendations that most patients with malignant hypertension can be managed without recourse to parenteral therapy are supported.
Abstract: We have compared the efficacy and safety of slow release nifedipine and atenolol given orally as initial treatment for malignant hypertension. Twenty consecutive black patients with untreated malignant hypertension, whose diastolic pressure remained greater than 120 mm Hg after 3 h bed rest, were randomized to receive either slow release nifedipine 40 mg at 1 and 12 h, or atenolol 100 mg at 0 h only. Patients remained supine throughout the study. Blood pressure was measured using a semi-automatic recorder (Omega 1000) at 15 min intervals from -3 to 24 h. Baseline blood pressure was similar in the nifedipine (233/142 mm Hg) and atenolol (226/141 mm Hg) groups. The rate of fall of pressure was greater after nifedipine whose maximum hypotensive effect occurred 4-5 h after each dose. Blood pressure decreased more slowly and more enduringly after atenolol, although the extent of fall was the same (delta BP 5 h after first dose nifedipine = 67/41 mm Hg; delta BP 16 h after atenolol = 64/40 mm Hg). There were no precipitous falls in pressure. No patient developed focal neurological signs, nor was heart failure precipitated by either form of treatment. These results support recommendations that most patients with malignant hypertension can be managed without recourse to parenteral therapy.

18 citations


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Journal ArticleDOI
01 May 1991-Drugs
TL;DR: Preliminary findings indicate that sustained release nifedipine formulations are useful and established cardiovascular therapeutic agents which have demonstrable efficacy in various forms of angina, mild to moderate hypertension and Raynaud’s phenomenon.
Abstract: Nifedipine antagonises influx of calcium through cell membrane slow channels, and sustained release formulations of the calcium channel blocker have been shown to be effective in the treatment of mild to moderate hypertension and both stable and variant angina pectoris. Preliminary findings also indicate that these formulations are effective in the treatment of Raynaud's phenomenon and hypertension in pregnancy, and that they reduce the frequency of ischaemic episodes in some patients with silent myocardial ischaemia. The exact mechanism of action of nifedipine in all of these disorders has not been defined. However, its potent peripheral and coronary arterial dilator properties, together with improvements in oxygen supply/demand, are of particular importance. A major goal of sustained release therapy is to permit reductions in the frequency of nifedipine administration, preferably to once daily, and thus improve patient compliance. Two new once-daily formulations--the nifedipine gastrointestinal therapeutic system (GITS) and a fixed combination capsule comprising sustained release nifedipine 20 mg and atenolol 50 mg--have exhibited marked antihypertensive efficacy. The GITS preparation has also been used effectively in the treatment of stable angina pectoris, and both formulations appear to be well tolerated. Sustained release nifedipine formulations are generally better tolerated than their conventionally formulated counterparts, particularly with regard to reflex tachycardia. Adverse effects seem to be dose related, are mainly associated with the drug's potent vasodilatory action, and include headache, flushing and dizziness. Generally, these effects are mild to moderate in severity and transient, usually diminishing with continued treatment. Thus, sustained release nifedipine formulations are useful and established cardiovascular therapeutic agents which have demonstrable efficacy in various forms of angina, mild to moderate hypertension and Raynaud's phenomenon. Further, promising results shown by the nifedipine GITS formulation, with its advantage of once daily administration suggest that it is likely to become one of the preferred nifedipine formulations for the treatment of hypertension and the various forms of angina.

62 citations

01 Jan 2005
TL;DR: Renoprotective effect of losartan in comparison to amlodipine in patients with chronic kidney disease and hypertension: a report from Japan intended for the global renal protection in hypertensive patients (jlight study).
Abstract: s). Iino Y and Kawaguchi Y. Renoprotective effect of losartan in comparison to amlodipine in patients with chronic kidney disease and hypertension: a report from japanese losartan therapy intended for the global renal protection in hypertensive patients (jlight study). Nephrology Dialysis Transplantation 2003;18(Supplement

43 citations

Journal ArticleDOI
TL;DR: There is important evidence in favor of the use of angiotensin-converting enzyme inhibitors for treating hypertensive urgencies, compared with calcium channel blockers, considering the better effectiveness and the lower frequency of adverse effects (like headache and flushing).
Abstract: CONTEXT AND OBJECTIVE: Hypertensive urgencies are defined as severe elevations in blood pressure without evidence of acute or progressive target-organ damage. The need for treatment is considered urgent but allows for slow control using oral or sublingual drugs. If the increase in blood pressure is not associated with risk to life or acute target-organ damage, blood pressure control must be implemented slowly over 24 hours. For hypertensive urgencies, it is not known which class of antihypertensive drug provides the best results and there is controversy regarding when to use antihypertensive drugs and which ones to use in these situations. The aim of this review was to assess the effectiveness and safety of oral drugs for hypertensive urgencies. METHODS: This systematic review of the literature was developed at the Brazilian Cochrane Center, and in the Discipline of Emergency Medicine and Evidence-Based Medicine at the Universidade Federal de Sao Paulo — Escola Paulista de Medicina (Unifesp-EPM), in accordance with the methodology of the Cochrane Collaboration.RESULTS: Sixteen randomized clinical trials including 769 participants were selected. They showed that angiotensin-converting enzyme inhibitors had a superior effect in treating hypertensive urgencies, evaluated among 223 participants. The commonest adverse event for calcium channel blockers were headache (35/206), flushing (17/172) and palpitations (14/189). For angiotensin-converting enzyme inhibitors, the principal side effect was bad taste (25/38). CONCLUSIONS: There is important evidence in favor of the use of angiotensin-converting enzyme inhibitors for treating hypertensive urgencies, compared with calcium channel blockers, considering the better effectiveness and the lower frequency of adverse effects (like headache and flushing).

31 citations

Book ChapterDOI
TL;DR: The variation in properties of beta adrenoceptor blocking drugs can be used as a basis for classification and beta1 selective drugs have been previously termed ‘cardioselective’ reflecting their preferential effect on the heart in contrast to certain other tissues, such as bronchial smooth muscle.
Abstract: The variation in properties of beta adrenoceptor blocking drugs can be used as a basis for classification. There are those which are non-selective, those which have a selective action on the beta1receptors, and then those drugs which in addition possess vasodilator or alpha receptor blocking properties. They may be further sub-divided into various groups according to the presence or absence of intrinsic sympathomimetic activity (I.S.A) or partial agonist activity and membrance stabilising activity (M.S.A) [1, 2, 3] (Table 1). Beta1 selective drugs have been previously termed ‘cardioselective’ reflecting their preferential effect on the heart in contrast to certain other tissues, such as bronchial smooth muscle, however as beta1 and beta2 receptors are found in the heart the term ‘cardioselective’ is inaccurate.

26 citations

Journal ArticleDOI
TL;DR: 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.
Abstract: 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 β-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 β-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 α-adrenergic blockers, β-adrenergic blockers, digoxin, quinidine, and disopyramide. Combination therapy of calcium antagonists with β-blockers is increasingly common, and is probably safest in the case of the dihydropyridines. Other combinations being explored are with angiotensin-converting enzyme inhibitors and diuretics. With the correct selection of drug and patient, the calcium antagonists as a group can be remarkably effective at relatively low cost of serious side effects.

20 citations