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

Clinical, experimental and pathologic studies strongly indicate that hypertension is a major factor in coronary heart disease, sudden death, stroke congestive heart failure and renal insufficiency. The deleterious effect of the elevated blood pressure on the cardiovascular system appears to be due mainly to the mechanical stress placed on the heart and blood vessels. Humoral factors and vasoactive hormones such as angiotensin, catecholamines and prostaglandins may play a role in the pathogenesis of hypertensive cardiovascular disease but this role has not yet been defined and is probably secondary. Hypertension and the resulting increase in tangential tension on the myocardial and arterial walls, leads to the development of hypertensive heart disease and congestive heart failure as well as hypertensive vascular disease that affects not only the kidneys but also the heart and brain. Hypertensive vascular disease involves both large and small arteries as well as arterioles and is characterized by fibromuscular thickening of the intima and media with luminal narrowing of the small arteries and arterioles. The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis. Thus the patient with hypertension is a candidate for both hypertensive and atherosclerotic vascular disease of the coronary and cerebral vessels leading to occlusive disease of both the large and small arteries and resulting in myocardial infarction and stroke. Other major complications of hypertensive vascular disease include rupture and thrombotic occlusion of blood vessels, especially in the brain. Disease of the arterial media, which begins in childhood with the deposition of calcium in the vessels, may be an important cause of arterial hypertension. This form of hypertension may manifest itself in adults as arteriosclerotic hypertension and lead to cardiovascular complications very similar to those of essential hypertension. The relation of arteriosclerotic hypertension to nutritional factors, including dietary salt intake, deserves study.
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PMID:Role of hypertension in atherosclerosis and cardiovascular disease. 13 91

The content of calcium bound to the erythrocyte membrane and the effect of intracellular calcium concentration on the activity of Na+, K+-ATPase in the reconstituted erythrocytes were studied in 20 patients with essential hypertension and in 20 individuals with normal pressure. In incubation of the erythrocytes in a solution containing EDTA much more calcium is removed from the outer surface of their membrane in patients with essential hypertension than in the control group (60 +/- 5 mEq/l and 41 +/- 3 mEq/l, respectively). When the intracellular calcium concentration varies from 0 to 500 mumol/l, which corresponds to a rise in the free calcium (Ca2f+-3) concentration to 41 mumol/l, a difference in the changes of Na+, K+-ATPase activity of the reconstituted erythrocytes is noted. When intracellular calcium concentration is 50 mumol/l (Ca2f+-3 mumol/l), ATP-ase activity in patients with essential hypertension is 21% less than that in individuals with normal pressure (P less than 0.005). The authors explain the difference in the kinetics of Na+, K+-ATPase changes by the different degree of calcium depletion of the inner surface of the erythrocyte membrane in relatively low Ca2f+ values in the internal medium. The data obtained are evidence of the altered calcium-binding capacity of the erythrocyte membrane, which may cause the increased permeability of the erythrocyte membrane to sodium and potassium ions in patients with essential hypertension, which the authors had revealed earlier. The authors consider the revealed changes to be a fragment of a more extensive membrane defect which may be the principal cause of activation of the servomechanisms which maintain arterial pressure.
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PMID:[Role of membrane-bound calcium in the changes of ion permeability and Na+, 5+ and ATPase activity of the erythrocytes in hypertension]. 14 18

The data presented establish that in early or mild essential hypertension there is a state of inappropriate hypermineralocorticoid activity represented by the sum of aldosterone and 18-hydroxy-11-deoxycorticosterone concentrations in the plasma. This disturbance, associated with a "normal" or excessive salt intake, would produce the arteriolar cationic changes in sodium, potassium, calcium, or magnesium leading to hypersensitivity or hyperresponsiveness of the arteriolar actomyosin to normal levels of circulating norepinephrine or angiotensin. The nature of the cationic changes in the arteriolar cells responsible for the increased tonicity of the arteriolar actomyosin, which is the fundamental cause of essential hypertension, remains to be elucidated.
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PMID:The role of the adrenal cortex in human essential hypertension: keynote address. 19 54

A new hypouricemic diuretic (tienilic acid) was compared with hydrochlorothiazide in a double-blind study in 8 patients with mild essential hypertension. After a two-week placebo period the patients received either 250 mg tienilic acid or 50 mg hydrochlorothiazide in a single daily dose for 3 weeks. After a second placebo period of 2 weeks the patients received, in a crossover design, either tienilic acid or hydrochlorothiazide for a further 3 weeks. The reduction of blood pressure and of body weight was similar for both drugs. When treatment was started diuresis and natriuresis increased with tienilic acid and with hydrochlorothiazide. Whereas serum sodium levels showed only minor variations, serum potassium levels fell with both diuretics and urinary potassium excretion increased. Urinary calcium excretion decreased and serum calcium levels slightly increased under both treatments. Both diuretics induced similar increases of plasma renin activity, plasma aldosterone concentration and aldosterone-18-glucuronide excretion. Blood urea nitrogen and, to a lesser extent, serum creatinine levels were raised slightly under both drug regimens. Whereas the serum uric acid level rose and remained elevated for the duration of hydrochlorothiazide treatment, it fell significantly and remained lowered during treatment with tienilic acid. Uric acid clearance was about twice as high with tienilic acid as with hydrochlorothiazide. Tienilic acid therefore appears to be a therapeutic alternative to thiazides and other hyperuricemic diuretics in hypertensive patients in whom hyperuricemia should be avoided or corrected.
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PMID:[Experiences with a new hypouricemic diuretic (tienilic acid): comparison with hydrochlorothiazide]. 37

1. Nifedipine, a calcium antagonist drug, was given sublingually (10 mg) to seven normal subjects and 19 patients with essential hypertension. In addition, 12 of the hypertensive subjects then received nifedipine (10 mg thrice daily) for 3 weeks. 2. Sublingual administration of nifedipine in hypertensive patients induced a prompt and sustained reduction of blood pressure, without a significant increase of heart rate; in normotensive subjects blood pressure did not change, and heart rate was significantly increased. After chronic treatment, blood pressure remained reduced and heart rate did not rise. 3. Plasma catecholamines and plasma renin activity increased significantly in normotensive subjects after acute administration. 4. After both acute and chronic administration, only plasma noradrenaline was significantly increased in hypertensive patients; in long-term treatment, it was increased in both the lying and standing positions. 5. Nifedipine is an active antihypertensive drug, which may induce some degree of sympathetic activation.
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PMID:Acute and chronic effects of nifedipine on plasma renin activity and plasma adrenaline and noradrenaline in controls and hypertensive patients. 39 62

Under conditions of physiological concentration of free calcium in the incubation medium (Ca2+f = 1.5 mM), the outer surface of the membrane of human and Wistar rat erythrocytes binds 435 +/- and 359 +/- 32 nmol calcium per 1 ml cells, respectively. The external surface of erythrocytes in patients with essential hypertension and in rats with spontaneous hypertension (SHR, Kyoto Wistar) also binds such amounts of calcium. With the concentration of calcium corresponding to its concentration in the intracellular space (Ca2+f less than 1 mcM), the inner membrane surface of eritrocyte ghosts binds only 3.53 +/- 0.16 and 4.28 +/- 0.39 nmol calcium per 1 mg protein of human and rat eritrocyte ghosts, respectively. The noted decrease in the calcium-binding capacity of the inner part of the erythrocyte membrane, being probably a characteristic feature of membrane alteration displayed also in other cellular structure, may determine the changes in tissue sensitivity to the effect of hormones and catecholamines in both types of hypertension.
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PMID:[Disorder of erythrocyte membrane calcium binding in hypertension and experimental genetic hypertension]. 67 4

The Ca2+ antagonistic coronary vasodilator, Nifedipine, was sublingually administered by a dose of 30 mg to 19 patients with hypertension. Blood pressure of patients with with essential hypertension (n=14) decreased from 177 +/- 24 to 123 +/- 13 mmHg systolic and from 108 +/- 12 to 80 +/- 11 mmHg diastolic (mean +/- SD) (p less than 0.01). Plasma renin activity (PRA) increased significantly from 0.73 +/- 0.62 to 1.50 +/- 1.02 ng/ml/h (p less than 0.05). The same tendency was observed in malignant and renovascular hypertension. In primary aldosteronism (n = 2), blood pressure decreased but PRA did not increase. Hypotensive action and increased plasma renin activity by Ca2+ antagonist, Nifedipine, were clearly demonstrated in patients with hypertension.
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PMID:Hypotensive action and increased plasma renin activity by Ca2+ antagonist (Nifedipine) in hypertensive patients. 96 84

To study limb vascular responses in man to elevations in plasma calcium concentrations, we infused test isosmolar solutions of CaCl2 (0.115, 0.230, and 0.460 meq calcium/min) and NaCl and control isosmolar solutions of NaCl into the brachial arteries of 10 normotensive men and eight men with essential hypertension of mild to moderate severity. Limb blood pressures were monitored, limb blood flow was measured by indicator-dilution, and limb vascular resistance was calculated as mm Hg/ml flow/min/100 cm3 limb volume. Measured concentration of calcium in limb venous plasma during infusion of 0.460 meq calcium/min was 11.5 +/- 0.8 meq/liter (mean +/- SEM) with individual values ranging up to 20 meq/liter. Changes in limb venous serum sodium, potassium, magnesium, and osmolality were similar during control and CaCl2 infusions. Decreases in limb venous blood hematocrit during CaCl2 infusions were the same or greater than those during control infusions. The infusions did not significantly change systemic blood calcium concentration or blood pressures. Limb blood flow decreased and resistance increased in response to CaCl2. Increments averaging as little as 2.2 meq/liter elevated limb resistance by about 45%. Log dose-response curves were linear. Responses did not differ in normotensives and hypertensives (P greater than 0.8). We conclude that the vascular response to acute elevation of plasma calcium concentrations up to 20 meq/liter in the limb oman is an impressive vasoconstriction. We found no evidence for abnormal vascular responses to calcium in essential hypertensive men.
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PMID:Similar vasoconstrictor responses to calcium in normotensive and esssential hypertensive men. 109 55

Animal experiments have shown that the administration of calcium antagonists can prevent or slow the progression of atherosclerosis by inhibiting calcium overload and interfering with lipid metabolism and deposition. These encouraging results have prompted clinical trials to evaluate the effects of calcium antagonists (dihydropyridines and diphenylalkylamines) on atherosclerotic plaque formation. In patients with coronary heart disease, several studies have already shown that calcium antagonists can have a positive effect on plaque evolution, while in hypertensive patients no such study has been published to date. The Verapamil in Hypertension Atherosclerosis Study is an ongoing multicentre randomised double-blind parallel group trial comparing the antihypertensive efficacy of verapamil SR 240 mg/day with that of chlorthalidone 25 mg/day in 1464 patients with essential hypertension aged 40 to 65 years. In a randomised subgroup of patients (n = 550), who will be followed up for 3 years, B-mode ultrasonography is being employed to evaluate the effects of the 2 drugs on carotid wall thickness and carotid plaque development. Ultrasonographic evaluations are performed at baseline, after 3 months, and 1, 2 and 3 years after a standardised protocol to determine intimal-medial thickness in 4 segments of the extracranial carotid tree. The most interesting result to date is the high incidence of carotid alterations, with plaques present in 35% and arterial wall thickening in 31.8% of the 311 asymptomatic hypertensive patients processed so far. A preliminary evaluation of the antihypertensive efficacy of the trial medications after 6 months of double-blind treatment indicates a 63.5% response rate to monotherapy and a 7.8% drop-out rate because of drug inefficacy or intolerance.
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PMID:Preliminary clinical experience with calcium antagonists in atherosclerosis. Verapamil in Hypertension Atherosclerosis Study Investigators. 128 76

Patients with essential arterial hypertension demonstrate abnormal vasodilator capacity either during increased cardiac metabolic demand or during pharmacological vasodilation. Structural and functional damage to the coronary microcirculation has been proposed as one of the major causes of impaired coronary reserve in this disease. To assess the role of microvascular impairment in regional myocardial blood flow (MBF), 27 patients with essential hypertension were evaluated by dynamic positron emission tomography (PET) at rest, during atrial pacing and after dipyridamole infusion and compared with 13 healthy subjects. All patients had normal coronary arteries, 17 had moderate to severe hypertension and 10 had mild hypertension. Baseline mean MBF of 0.97 +/- 0.25 ml/min/g was significantly increased to 1.60 +/- 0.38 during atrial pacing and 2.35 +/- 0.95 after dipyridamole infusion (p < 0.01); however, mean flow during atrial pacing and after dipyridamole infusion was significantly lower than in healthy subjects (2.15 +/- 0.73 and 3.71 +/- 0.86 ml/min/g, p < 0.05 and p < 0.01, respectively). The MBF response to atrial pacing and dipyridamole infusion was similarly depressed in patients with mild and severe hypertension. The study was repeated after 6 months of antihypertensive treatment with the calcium antagonist verapamil or the angiotensin converting enzyme (ACE) inhibitor enalapril in a subgroup of 20 patients as part of a randomised, single-blind clinical trial. This study is still in progress; the initial 16 patients treated with verapamil or enalapril showed an obvious improvement in MBF values during atrial pacing and after dipyridamole infusion after 6 months of therapy (mean MBF: 2.10 +/- 0.64 and 2.99 +/- 1.63 ml/min/g, respectively, p < 0.05 vs pretreatment values). In conclusion, obvious impairment of MBF during atrial pacing and after dipyridamole infusion was observed in hypertensive patients with normal coronary arteries and this appeared unrelated to the severity of hypertension. Therapy with verapamil or enalapril improved coronary reserve and MBF response to an increase in myocardial oxygen demand.
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PMID:Regional myocardial blood flow and coronary reserve in hypertensive patients. The effect of therapy. 128 84


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