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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies on the Kyoto (SHR) and the New Zealand (GHR) strains of genetically predisposed hypertensive rats have shown that in the SHR neurogenic influences, primarily of higher central origin, play an important role in the initiation of hypertension. Studies on human essential hypertension indicate that this may also be true for man, although it is far from being the sole explanation. Brookhaven hypertension-prone rats illustrate the interaction between genetic and exogenous factors since they require an overload of salt for the development of high blood pressure. The Milan hypertensive rats (MHS), on the other hand, illustrate a genetic deviation of renal function with imbalance between glomerular filtration and tubular resorption of sodium and water, which may simulate at least some variants of the relatively mild forms of low renin hypertension in man. Structural adaptive vascular changes have been demonstrated in SHR and GHR and in nongenetic renal hypertension in rats, and there are several indications of their presence in MHS. Thus, regardless of the nature of the initiating factors, these secondary but rapidly established changes occur and greatly contribute to the maintenance and acceleration of the hypertensive state. The vascular changes can even be regarded as a common denominator for chronic hypertension and serve as an element which, in fact, reinforces the initiating mechanisms. The progress of the vascular changes can be interfered with by reducing the pressure load. Lowering the blood pressure by pharmacologic treatment is most effective when the treatment is initiated as such an early age when the cardiovascular structural adaptation is still minimal. Treatment in later phases is less successful since the adaptive increases in cardiac and vessel wall thickness can then no longer be fully normalized by pressure reduction because of increased amounts of collagen and other connective tissue elements in the vessel wall, which regress poorly. An increased wall thickness of the resistance vessels implies a vascular hyperreactivity to constricting influences which, in turn, rapidly brings the blood pressure back to supranormal levels as soon as therapy is stopped.
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PMID:Mechanisms of spontaneous hypertension in rats. 32

Diabetes mellitus is commonly associated with systolic and diastolic hypertension, and a wealth of epidemiological data suggest that this association is independent of age and obesity. Much evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive patients, whether obese or of normal body weight, are compared with age- and weight-matched normotensive controls, a heightened plasma insulin response to a glucose challenge is found consistently. A state of cellular resistance to insulin action subtends the observed hyperinsulinism. Using the insulin/glucose clamp technique in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms: sodium retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and proliferation of vascular smooth-muscle cells. Physiological maneuvers, such as caloric restriction (in the overweight patient) and regular physical exercise, can improve tissue sensitivity to insulin; good evidence indicates that these maneuvers also can lower blood pressure in both normotensive and hypertensive individuals. Insulin resistance and hyperinsulinemia also are associated with an atherogenic plasma lipid profile. Elevated plasma insulin concentrations enhance very-low-density lipoprotein (VLDL) synthesis, leading to hypertriglyceridemia. Progressive elimination of lipid and apolipoproteins from the VLDL particle leads to an increased formation of intermediate density and low-density lipoproteins, both of which are atherogenic. Last, insulin per se, independent of its effects on blood pressure and plasma lipids, is known to be atherogenic. The hormone enhances cholesterol transport into arteriolar smooth-muscle cells and increases endogenous lipid synthesis by these cells. Insulin also stimulates the proliferation of arteriolar smooth-muscle cells, augments collagen synthesis in the vascular wall, increases the formation of and decreases the regression of lipid plaques, and stimulates the production of a variety of growth factors. In summary, insulin resistance appears to be a syndrome that is associated with a clustering of metabolic disorders, including type II diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic cardiovascular disease.
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PMID:Insulin resistance, hyperinsulinemia, and coronary artery disease: a complex metabolic web. 128 37

Prazosin which is a selective alfa-1 blocking drug has a very good antihypertensive effect. Its hemorheological effects were studied in 20 patients with essential hypertension (I and II degree according to WHO classification). After 6 weeks of the therapy with prazosin, hematocrit and viscosity of the whole blood and plasma were significantly reduced, because of hemodilution, while aggregability of erythrocyte and "Tk" values were not significantly reduced. Platelet aggregation induced by collagen, ADP and adrenaline, showed a decrease after the treatment. Assuming the hemorheological effects not to be crucial in choosing an antihypertensive agent, we must not, however, neglect them, especially in patients with compromised hemorheological profile, and we should take advantage of the positive hemorheological effect of prazosin, particularly in a long antihypertensive treatment.
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PMID:[Hemorheologic changes in patients with essential hypertension treated with prazosin]. 134 59

Diastolic dysfunction is often present in patients with arterial hypertension. It is not only the consequence of an increased left ventricular muscle mass but also due to a progressive fibrosis of the cardiac interstitium. Experimental studies have shown a close relationship between the degree of interstitial cardiac fibrosis and the activity of the renin-angiotensin system (RAS). Reversal of collagen deposition can be induced by inhibition of the RAS. The purpose of this study was to evaluate the therapeutic potential of ACE inhibitors not only in lowering blood pressure in patients with essential hypertension, but also in normalizing an impaired diastolic filling pattern in the left ventricle. Monotherapy with a single dose of 2.5-5 mg Cilazapril for a period of 6 months was effective in reducing mean arterial blood pressure by about 10 mmHg over the entire 24-h interval. The main reduction occurred throughout the day, but lower blood pressure values during the night were hardly affected at all. The pre- and post-treatment values of the 24-h blood pressure were subjected to a modified Fourier analysis, which did not reveal any disturbances in the circadian blood pressure rhythm by the ACE inhibitor. Left ventricular mass, as calculated from echocardiographic measurements, was reduced by 30% after 6 months of treatment. The degree of regression of LV hypertrophy was closely related to the drug-induced fall in mean arterial pressure. The abnormal left ventricular filling pattern before treatment with a predominance of the late diastolic filling period was corrected by 6 months of ACE inhibitor treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Reparative effects of ACE inhibitors on the heart]. 153 2

The effect of various antihypertensive medications on platelet function is of increasing interest. Conflicting effects of captopril on platelet function are reported and the impact of angiotensin converting enzyme (ACE) inhibitors not containing a sulfhydryl group such as enalapril, lisinopril, and quinapril on platelet function remains unstudied. Therefore, the aim of the present study was to examine the effect of antihypertensive treatment with quinapril, a novel ACE inhibitor not containing a sulfhydryl group, on platelet function. Ten white men (age range of 32-61 years) with untreated mild-to-moderate essential hypertension (supine diastolic blood pressure greater than 95 mm Hg) were treated with 4 weeks each of placebo and quinapril in a double-blind, randomized, crossover design. Quinapril (20 mg twice a day) significantly lowered systolic (p less than 0.01) and diastolic blood pressure (p less than 0.01) without any significant effect on heart rate or plasma catecholamines. No significant change was noted for in vitro platelet aggregation induced by epinephrine, ADP, or collagen. Plasma concentrations of the platelet release factors beta-thromboglobulin and platelet factor 4 did not change, nor did the platelet content of norepinephrine, platelet weight (mg/10 ml of blood), circulating platelet count, or platelet size. Thus, as assessed by a broad spectrum of platelet parameters, we found that antihypertensive treatment with quinapril has no significant effect on platelet function in patients with mild-to-moderate essential hypertension. These "platelet-neutral" properties of quinapril suggest that quinapril, both from a thromboembolic and a hemostatic point of view, may be a rather safe agent for treatment of hypertension.
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PMID:Platelet function during antihypertensive treatment with quinapril, a novel angiotensin converting enzyme inhibitor. 170 46

Eighteen patients with a mean age of 54.7 years were included in the study. All patients had a diagnosis of mild or moderate essential hypertension (sitting diastolic blood pressure of 96 to 114 mm Hg). The study design was single blind and in two phases: phase I, placebo (4 weeks), and phase II, the active treatment (8 weeks) with increasing doses, if needed, of doxazosin every 2 weeks (1, 2, 4, and 8 mg/day). Results show that doxazosin has an antihypertensive effect that is dose dependent. Systolic, diastolic, and mean blood pressures were decreased significantly, and no effect on heart rate was observed. Doxazosin significantly inhibited the platelet aggregation induced by epinephrine, adenosine diphosphate, and collagen in a dose-dependent manner. In addition, treatment with doxazosin lowered total serum cholesterol and triglyceride levels, without changing other standard biochemical parameters. This indicates that doxazosin could offer a distinct therapeutic advantage in the modulation of atherogenic and thromboembolic factors associated with coronary heart disease.
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PMID:Evidence of an antiplatelet aggregation action of doxazosin in patients with hypertension: an ex vivo study. 182 66

In essential hypertension, ventricular function is determined primarily by the degree of hypertrophy (myocardial factor) and by organic complications in the coronary artery (coronary factor). Ventricular function is inversely correlated with ventricular size and systolic wall stress, inasmuch as ventricular function diminishes when these two variables increase. Even the young hypertensive heart of normal size with no angiographic abnormalities appears to be prone to ischemia, because the coronary reserve is seriously limited even in the absence of coronary stenosis. Unlike ventricular distensibility, myocardial compliance may be normal, even in the presence of pronounced myocardial hypertrophy. As myocardial compliance decreases, systolic wall stress increases and ventricular function is reduced. The hypertensive heart, the most common form of an irregular hypertrophy of the ventricular wall, is found in 14% of such cases. Analysis of the degree of hypertrophy shows that the hypertrophy can be inappropriately high (high mass-to-volume ratio, reduced wall stress), appropriate, or inappropriately low (normal mass-to-volume ratio, increased wall stress). One of the profound mechanisms influencing both myocardial and coronary function in hypertensive heart disease is the pressure-dependent development of smooth vascular hypertrophy (media) or coronary resistance vessels. Consequently, the oxygen supply to the myocardium is impaired and secondary lesions occur such as fibrosis, increased myocardial and perivascular collagen content and scars within the heart muscle. Diastolic dysfunction develops, as well as an increase in myocardial stiffness, thus promoting the transition from the concentric (compensated) to the eccentric or dilated (decompensated) state, with the consequence of the occurrence of cardiac failure. On the basis of both functional and morphological criteria, evidence is presented in this report that coronary small vessel disease is one of the underlying mechanism for the development of cardiac failure in hypertensive heart disease.
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PMID:Development of cardiac failure by coronary small vessel disease in hypertensive heart disease? 183 64

Diabetes mellitus is commonly associated with systolic/diastolic hypertension, and a wealth of epidemiological data suggest that this association is independent of age and obesity. Much evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive patients, whether obese or of normal body weight, are compared with age- and weight-matched normotensive control subjects, a heightened plasma insulin response to a glucose challenge is consistently found. A state of cellular resistance to insulin action subtends the observed hyperinsulinism. With the insulin/glucose-clamp technique, in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms: Na+ retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and proliferation of vascular smooth muscle cells. Physiological maneuvers, such as calorie restriction (in the overweight patient) and regular physical exercise, can improve tissue sensitivity to insulin; evidence indicates that these maneuvers can also lower blood pressure in both normotensive and hypertensive individuals. Insulin resistance and hyperinsulinemia are also associated with an atherogenic plasma lipid profile. Elevated plasma insulin concentrations enhance very-low-density lipoprotein (VLDL) synthesis, leading to hypertriglyceridemia. Progressive elimination of lipid and apolipoproteins from the VLDL particle leads to an increased formation of intermediate-density and low-density lipoproteins, both of which are atherogenic. Last, insulin, independent of its effects on blood pressure and plasma lipids, is known to be atherogenic. The hormone enhances cholesterol transport into arteriolar smooth muscle cells and increases endogenous lipid synthesis by these cells. Insulin also stimulates the proliferation of arteriolar smooth muscle cells, augments collagen synthesis in the vascular wall, increases the formation of and decreases the regression of lipid plaques, and stimulates the production of various growth factors. In summary, insulin resistance appears to be a syndrome that is associated with a clustering of metabolic disorders, including non-insulin-dependent diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic cardiovascular disease.
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PMID:Insulin resistance. A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. 204 34

Lowering blood pressure is not totally effective in preventing the atherosclerotic complications of systemic hypertension. In hypertensive patients both platelet hyperaggregation and dyslipidemia have been suggested as important risk factors. The effect of 8 weeks' treatment with ketanserin on blood pressure, serum lipid parameters (cholesterol, triglycerides, LDL, HDL-C, apolipoprotein A1 and B) and platelet aggregation, induced by collagen, ADP, arachidonic acid, was evaluated in 10 patients with essential hypertension. Ketanserin was effective in lowering blood pressure in all patients, 6 of whom became normotensive. Both CHOL and TG levels and APO B were significantly reduced, whereas HDL-C and APO A1 were significantly increased after treatment. These results might be attributed to the antagonistic activity of ketanserin on alpha-1 adrenoceptors with a consequent inhibition of phosphodiesterase. Platelet aggregation, after stimulation with collagen and arachidonic acid, was significantly reduced secondary to the inhibition of intraplatelet serotonin synthesis and release. These results suggest that keranserin is effective in reducing blood pressure and in achieving normal serum lipid pattern and platelet aggregation. Therefore, this drug might be helpful in controlling the main risk factors for cardiovascular damage.
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PMID:Effects of ketanserin administration on lipid metabolism and platelet aggregation in hypertensive patients. 227 4

The safety of 738 high-risk patients treated with enalapril under various clinical programs was evaluated. High risk was defined as the presence of a collagen vascular disease; a renal disease, including renovascular hypertension; or either hypertension or refractory cardiac failure with serum creatinine greater than or equal to 1.7 mg/dl at baseline. Essential hypertension was the primary diagnosis in most of these patients. Treatment with enalapril in these patients usually continued without interruption for the length of the particular protocol. The incidence of adverse reactions resulting in discontinuation of treatment was comparable to that observed with other standard antihypertensive therapies in patients with milder forms of disease. No enalapril-related neutropenia, proteinuria, dysgeusia or ageusia were reported in these high-risk patients. The incidence of discontinuation due to rash was less than 0.5%. Resolution and/or improvement of captopril-related adverse effects was observed in many patients crossed over to treatment with enalapril. In patients with collagen vascular diseases and those with severe impairment of renal function (serum creatinine greater than or equal to 3.0 mg/dl), the incidence of discontinuation due to adverse experiences or death as well as the profile of reported adverse experiences was similar to those for the total group of high-risk patients. The data suggest that enalapril is efficacious and well tolerated by the high-risk patients.
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PMID:High-risk patients treated with enalapril maleate: safety considerations. 253 44


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