Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study aimed to assess and compare the effects of urapidil and clonidine on right ventricular volumes and function in 20 physical status ASA III patients, with a borderline untreated essential hypertension and with or without chronic coronary artery disease. The patients were randomly assigned to two equal groups to receive either urapidil (0.4 mg.kg-1) or clonidine (2.5 micrograms.kg-1). Neither patient had congestive heart failure, valvular heart disease, previous myocardial infarction, nor was any being treated with beta-blocking agents or with amiodarone. Usual anti-anginal medication (nifedipine and isosorbide) was maintained up to the time of the procedure. Monitoring was obtained from ECG, Swan-Ganz catheter fitted out with a fast response-thermistor, and radial artery cannula. Blood samples were withdrawn for plasma atrial natriuretic factor determination. Thirty minutes after catheter insertion, baseline data were collected in supine and 45 degrees head-up tilt positions. Following urapidil or clonidine i.v. injection, three series of measurements (3, 8 and 13 min) were made in supine and tilt positions according to a randomized sequence. The two groups were similar with regard to age, weight, height, coronary artery disease and treatment. Urapidil and clonidine elicited a similar decrease in mean arterial pressure of 14% in supine position and 20% in head-up tilt position, combined with an exclusive decrease in systolic index i.e. not associated with a change in peripheral vascular resistances. Despite the decrease in arterial pressure, heart rate remained unchanged. Right ventricular ejection fraction was maintained after both urapidil and clonidine, however end-diastolic and end-systolic volumes decreased, with no modification by tilting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Is urapidil a venodilator?]. 831 50

Among cardiovascular diseases, hypertension, angina pectoris, acute myocardial infarction and ischemic stroke present a circadian pattern with a greater incidence of unfavourable events between awakening and noon. Chronotherapy aims to use drugs that release their active principles at different times during the day, according to biological needs. In chronotherapy of cardiovascular diseases, a particular attention has been paid to slow-release drugs that assure a 24 hours therapeutic effect with once a day administration. In primary hypertension well controlled by monotherapy (dipper hypertensives), the morning administration of long-acting beta-blockers and calcium antagonists has shown to control blood pressure over 24 hours, whereas ACE-inhibitors have proved more effective when administered at evening. In secondary hypertension (non dipper hypertensives) the administration of calcium antagonists is more effective at evening. Patients with severe hypertension need polytherapy. In that case, at least one of the antihypertensive drugs should be given at evening to lower night blood pressure values, which are particularly elevated also during sleep, and so to prevent an excessive blood pressure rise on awakening. In chronic monotherapy of ischemic heart disease, long-acting beta-blockers and calcium antagonists have shown to be equally effective when they are administered at morning, whereas slow-release nitrates, which need a nitrate-free interval, are to be administered either at morning or at evening, according to the expected time of onset of anginal pain. ASA seems to reduce the morning incidence of acute myocardial infarction, while tissue-type plasminogen activator presents a circadian variation of its thrombolytic activity with a higher efficacy between noon and midnight.
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PMID:[Application of chronotherapy to cardiovascular diseases]. 979 79

A defective vascular activity of endothelial vasoactive substances is observed in essential hypertension and hypercholesterolemia, and is believed to participate in the vascular abnormalities characteristic of these conditions. The present study aimed to determine the role of cyclooxygenase (COX) products in the maintenance of vascular tone and in the endothelium-mediated vasodilation of healthy subjects, and to investigate their contribution to the endothelial dysfunction of essential hypertensive and hypercholesterolemic patients. The effects of intra-arterial aspirin (acetylsalicylic acid [ASA], 1, 3, and 10 mg/min) were assessed on basal forearm blood flow (strain gauge plethysmography) and on responses to acetylcholine (7.5, 15 and 30 microg/min) and sodium nitroprusside (0.8, 1.6 and 3.2 microg/min) in 24 normal, 23 hypertensive, and 24 hypercholesterolemic subjects. Basal forearm blood flow was not different among the 3 groups (p = 0.95). ASA resulted in a significant reduction of forearm blood flow from baseline in normal (p = 0.003), hypertensive (p = 0.001), and hypercholesterolemic subjects (p = 0.001), without any difference among the 3 groups (p = 0.90). ASA significantly improved the effect of acetylcholine in normal (p = 0.008), hypertensive (p = 0.008), and hypercholesterolemic subjects (p = 0.022), without significant difference among the 3 groups (p = 0.46). ASA did not significantly modify the vasodilator effect of sodium nitroprusside in any of the 3 groups. These findings suggest that in humans, vasodilator prostanoids actively contribute to the maintenance of basal vascular tone, whereas vasoconstrictor products of COX activity limit endothelium-dependent vasodilation. COX products do not appear to play a major role in the endothelial dysfunction of hypertensive or hypercholesterolemic patients.
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PMID:Role of cyclooxygenase products in the regulation of vascular tone and in the endothelial vasodilator function of normal, hypertensive, and hypercholesterolemic humans. 1223 Nov 11