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)

Lisinopril is an orally active angiotensin-converting enzyme (ACE) inhibitor which at dosages of 20 to 80 mg once daily is effective in lowering blood pressure in all grades of essential hypertension. It is at least as effective as usual therapeutic dosages of hydrochlorothiazide, atenolol, metoprolol and nifedipine while direct comparisons with other ACE inhibitors have not been reported. Many patients achieve an adequate blood pressure reduction with lisinopril alone, and in those who do not, most will with the addition of hydrochlorothiazide; lisinopril also attenuates hypokalaemia induced by thiazide diuretics. In patients with congestive heart failure resistant to conventional therapy, lisinopril 2.5 to 20 mg once daily improved indices of cardiac function and appeared to produce greater benefit than captopril in one controlled study. Lisinopril is well tolerated, with few serious adverse effects being reported. Thus, lisinopril is a suitable treatment for essential hypertension and shows promise in the treatment of congestive heart failure. If additional studies confirm these preliminary findings, then lisinopril will have a similar profile of indications to other ACE inhibitors, and like some other drugs in this class it offers the convenience of once daily administration.
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PMID:Lisinopril. A preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic use in hypertension and congestive heart failure. 284 97

Multiclinic controlled studies have shown that enalapril alone 10 to 40 mg/day orally is effective in lowering blood pressure in patients with essential hypertension. Enalapril has been compared with thiazides and beta-blockers (propranolol, metoprolol and atenolol). The effect on systolic blood pressure has been greater with enalapril than with beta-blockers. The proportion of patients who respond to enalapril alone with a decrease in diastolic blood pressure (greater than or equal to 10mm Hg) is around 70%. When a thiazide is added to the treatment, the proportion is above 90%. Enalapril improves the signs and symptoms associated with congestive heart failure. Patients increased their exercise tolerance by an average of 148 sec and improved in their NYHA cardiac status and prognosis classification. The overall incidence of side effects is similar to that seen in the placebo control groups. Side effects such as agranulocytosis, taste loss, rash, proteinuria were not characteristic of enalapril. This supports the hypothesis that the improved safety profile of enalapril is the result of being a nonsulphydryl angiotensin-converting enzyme (ACE) inhibitor. The most common side effects reported were dizziness, headache and asthenia. Abnormalities in electrolytes, uric acid, glucose or in lipids have generally not been associated with enalapril.
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PMID:Enalapril in hypertension and congestive heart failure. Overall review of efficacy and safety. 286 29

Terazosin is a post-synaptic alpha 1-adrenoceptor antagonist with a similar pharmacodynamic profile to prazosin. It differs from prazosin in having a longer duration of action, with an elimination half-life some 2 to 3 times that of prazosin, allowing the convenience of once daily administration. Moreover, its absorption from the gastrointestinal tract is more complete and predictable than that of prazosin which may facilitate dose titration. Terazosin therapy results in a significant reduction in blood pressure in patients with mild to moderate essential hypertension, with little influence on heart rate. The drug is an effective antihypertensive when administered as monotherapy or in combination with a range of antihypertensive agents including beta-blockers, diuretics and combinations of the two. In the few patients with congestive heart failure studied, terazosin produced an increase in cardiac output with a reduction in ventricular filling pressure and systemic vascular resistance, but no studies have been performed to assess the therapeutic potential of terazosin in this indication. Reductions in total plasma cholesterol and low density plus very low density lipoprotein cholesterol fractions have been reported after terazosin therapy, while high density lipoprotein cholesterol concentrations have tended to increase. Should such beneficial changes be confirmed in long term clinical studies they would suggest a therapeutic advantage of terazosin over some other antihypertensive drugs, particularly diuretics, which have been reported to adversely affect the plasma lipid profile. The most common side effects associated with terazosin treatment are dizziness, headache, asthenia and nasal congestion, but these are usually mild and do not require treatment discontinuation. Terazosin is normally administered once daily, starting at a dose of 1 mg/day and gradually titrating upwards as the blood pressure stabilises at each new dose, until blood pressure is adequately controlled or to a maximum dose of 20mg daily. First-dose syncope occurs rarely after terazosin, and can largely be avoided by giving the first dose at bedtime. Thus, terazosin offers a useful alternative to the drugs currently available for the management of mild to moderate essential hypertension either as monotherapy or in combination with other antihypertensive drugs.
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PMID:Terazosin. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in essential hypertension. 288 69

Drug-induced reduction of elevated blood pressure decreases cardiovascular mortality and morbidity in patients with moderate and severe hypertension. Furthermore, antihypertensive drug studies in mild hypertensive subjects (diastolic blood pressure 90 to 104 mm Hg) have shown protection against stroke, left ventricular hypertrophy, congestive heart failure and progression of renal damage, as well as improved patient longevity. The Hypertension Detection and Follow-up Program trial, recently carried out in the U.S., documented reduced coronary artery disease events (fatal and nonfatal) in special drug-treated patients with mild hypertension. From the standpoint of practical management and considering the ubiquity of essential hypertension, a modified stepped-care regimen advocating initial drug therapy with a beta blocker and addition of low-dose thiazide diuretic when necessary constitutes a judicious approach for widespread application. Although there are 8 orally active beta blockers currently approved in the U.S. for clinical use in systemic hypertension, only acebutolol possesses all of the salutary pharmacologic properties of cardioselectivity, intrinsic sympathomimetic activity and hydrophilicity, thereby making this compound an effective and safe beta-blocking agent for first-order management of a broad segment of the hypertensive population.
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PMID:Antihypertensive therapy and the concept of total cardiovascular protection. 288 51

This survey covers the classification and subdivisions of alpha- and beta-adrenoceptors, including alpha 1 and alpha 2, beta 1 and beta 2, and pre-and postsynaptic receptor subtypes, together with the distribution and functional relevance of the various adrenoceptor subtypes. The emphasis will be on their relevance in circulatory regulatory processes, especially those of the blood vessels. The alpha- and beta-adrenoceptor antagonists that interact with various receptor subtypes are briefly discussed. The control of alpha 2-adrenoceptors concerned with blood pressure regulation is an important target for centrally acting antihypertensive drugs (such as clonidine or alpha-methyldopa). Changes in adrenoceptor density, particularly the down-regulation of beta 1- adrenoceptors (but not beta 2), are found in congestive heart failure. However, the experimental findings about alpha-and beta-adrenoceptors in essential hypertension remain controversial. Finally, the influence of alpha- and beta-adrenoceptor antagonists on plasma lipids and carbohydrate metabolism is briefly reviewed. The changes found may be only partly explained on the basis of alpha- or beta-receptor blockade.
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PMID:The role of adrenoceptors in circulatory and metabolic regulation. 290 48

The presence of alpha-hANP immunoreactive material in human heart and plasma was investigated with a specific and sensitive radioimmunoassay and immunohistochemical method. It was found that alpha-hANP immunoreactive staining of specific atrial granules was located around the nucleus of atrial cardiocytes. No immunoreactive staining was found in the ventricle. The content of immunoreactive hANP was 0.5 pmol/mg protein in the atria and 0.11 +/- 0.01 pmol/ml in the plasma of 26 normal volunteers. In 16 patients with congestive heart failure and 26 patients with essential hypertension, the plasma level of immunoreactive alpha-hANP was significantly lower than that in normal humans. The above evidence indicate that alpha-hANP is a putative hormone secreted by human atrium. A relative shortage of alpha-hANP in the circulatory system may be involved in the mechanism of heart failure and hypertension.
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PMID:Alpha-human atrial natriuretic polypeptide (alpha-hANP) in normal volunteers and patients with heart failure or hypertension. 294 May 20

Hypertension and obesity are two disorders that are closely related; each occurs more frequently with the other than in an otherwise normal population. These two disorders, however, exert disparate effects on cardiovascular structure and function. The hallmark of essential hypertension is an increased total peripheral resistance, and hypertensive patients have a contracted intravascular volume and normal cardiac output but an increased left ventricular stroke work due to a high afterload. In contrast, obese patients have an increased intravascular volume, left ventricular filling pressure, cardiac output and a lower total peripheral and renal vascular resistance. Left ventricular adaptation will consist of eccentric hypertrophy in obesity regardless of the level of arterial pressure and concentric hypertrophy in lean hypertensive patients. Although obesity may mitigate the harmful effect of a chronically elevated total peripheral and renal vascular resistance and lessen target organ damage in essential hypertension, the combination of obesity and hypertension presents a double burden to the left ventricle and is associated with systolic and diastolic dysfunction and a propensity for high grade ventricular dysrhythmias. It is not surprising that congestive heart failure and sudden death are common sequelae of obesity hypertension. Weight reduction reduces arterial pressure by decreasing intravascular volume and cardiac output associated with a fall in sympathetic activity and reversal of cardiac hypertrophy. Therefore, weight loss unloads the heart from the two-fold burden caused by obesity and hypertension and should become a major goal in the prevention and treatment of heart disease.
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PMID:Cardiovascular adaptation to obesity and hypertension. 294 41

Using a radioimmunoassay for atrial natriuretic peptide (ANP) we studied plasma concentrations of immunoreactive ANP in order to investigate the pathophysiological role of ANP in patients with various diseases. Plasma ANP levels were elevated in patients with congestive heart failure (394 +/- 260 pg/ml, n = 8) and chronic renal failure (219 +/- 86 pg/ml, n = 11). In patients undergoing hemodialysis plasma ANP levels were markedly high and decreased after hemodialysis from 433 +/- 166 pg/ml to 204 +/- 92 pg/ml (n = 11). ANP was removed from blood to dialysate (21 +/- 13 pg/ml of dialysate, n = 6, dialysate flow: 500 ml/min). Plasma ANP level was conversely correlated with creatinine clearance (r = -0.812, p less than 0.001) in patients with renal diseases (n = 29). In patients with atrial fibrillation, pace maker implantation, lung disease, chronic glomerulonephritis, nephrotic syndrome, essential hypertension, liver disease and cerebrovascular disease, plasma ANP levels were not significantly different from those in normal subjects (70 +/- 32 pg/ml, n = 28). These results suggest that ANP may be a circulating hormone playing pathophysiological roles in congestive heart failure and chronic renal failure.
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PMID:Plasma concentrations of atrial natriuretic peptide in various diseases. 294 55

A sensitive and specific radioimmunoassay for alpha-human atrial natriuretic polypeptide (alpha-hANP) was developed to determine its plasma level. Anti-alpha-hANP rabbit serum was specific for the N-terminus and ring structure of alpha-hANP, and showed no appreciable cross-reactions with other neuropeptides. The lowest level of alpha-hANP detectable by this radioimmunoassay was 4 pg per tube. The intra- and inter-assay coefficients of variation were 4.6-11.4% and 7.9-11.8%, respectively, and the recovery rates at 4 concentrations were 62.6-74.0%. The fasting plasma alpha-hANP concentration in normal subjects were 19.3 +/- 1.0 ng/l (mean +/- SE; n = 54), and there was no sex difference. The plasma alpha-hANP level in normal subjects fell significantly during water deprivation and increased significantly on infusion of hypertonic saline. The mean plasma levels of alpha-hANP were higher than normal in patients with essential hypertension, liver cirrhosis, congestive heart failure and chronic renal failure. Our results indicate that this radioimmunoassay is suitable for determining the alpha-hANP concentration in human plasma and can assess changes in pathological and physiological states.
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PMID:Radioimmunoassay for atrial natriuretic peptide: method and results in normal subjects and patients with various diseases. 294 73

Essential hypertension, with pressure overload leading to left ventricular hypertrophy, often results in coronary artery disease and congestive heart failure. The spontaneously hypertensive rat (SHR) is an attractive model for studying the effects of long-term antihypertensive therapy on the contractile properties of the myocardium. In this study we investigated differences in mechanical and biochemical characteristics of papillary muscles from SHR and normal (Wistar-Kyoto [WKY]) rats as a function of age and treatment. We found that the rate of delayed force redevelopment after rapid stretch was less in SHR than in WKY in every age group studied, even at 2 wk of age, before hypertension was evident in the SHR. In the treated SHR, blood pressure was lower, hypertrophy was reduced and the rate of delayed force redevelopment was increased compared with the untreated SHR. Finally, the pattern of myosin isoenzymes was different in treated than in untreated SHR, being shifted to more of the fast V1 and less of the slow V3 isomyosin. We conclude that long-term antihypertensive therapy not only prevents the development of left ventricular hypertrophy, but may do so by preventing the shift in myosin isoenzyme pattern normally found in hearts subjected to a long-term pressure overload.
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PMID:Rapid transient analysis of myosin cross-bridge kinetics in hypertrophied hearts. 294 68


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