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

Eleven beta-adrenergic receptor blocking agents and derivatives were evaluated for their ability to affect systolic arterial blood pressure and pulse rate in unanesthetized, male spontaneously hypertensive rats (SHRs) and normotensive Wistar Kyoto (WKY) controls. Animals ranged from 7 to 76 weeks of age. The subcutaneous injection of 5 and 45 mg/kg metoprolol in 52 to 64 week old SHRs and 45 mg/kg twice a day to 26 to 29 week old SHRs produced a significant decrease in blooc pressure. The subcutaneous injection of pindolol (0.1 and 1.0 mg/kg) produced a greater and more consistent depressor effect in mature SHRs. The subcutaneous administration of sotalol (100 mg/kg) and alprenolol (20 mg/kg) resulted in a depressor action which was significant 120 minutes after injection of the drug. In the doses used, propranolol, oxprenolol, 4-hydroxypropranolol and K9-1366 produced pressor effect in SHRs. Propranolol did not cause this pressor effect in prehypertensive (seven week old) SHRs. Practolol, dextro-propranolol and KO-1313 had no effect on blood pressure in the doses used. Propranolol, pindolol, metoprolol, dextro-propranolol, 4-hydroxypropranolol, practolol, oxprenolol, KO-1366 and KO-1313 produced no significant effects on blood pressure in normotensive WKY controls in the doses tested. Placing oral doses of 160 mg/kg/day of metoprolol in the drinking water for seven days significantly lowered blood pressure in 14 week old SHRs previously exposed to ineffective doses of 77 mg/kg/day for 24 days. The administration of oral doses of oxprenolol (40 mg/kg/day) in drinking water for three weeks had a slight but insignificant pressor effect. Smaller doses of metoprolol (15 and 39 mg/kg/day for three to four weeks) and practolol (70 to 85 mg/kg/day for two weeks) had no effect on 52 week old SHRs. Oral doses of pindolol, metoprolol, practolol and oxprenolol had no significant effect on blood pressure in WKY controls. There was no clear relationship between the effects of the drugs on blood pressure and their ability to affect the pulse rate. Similarly, there did not appear to be any consistent relationship between the potency of the beta-blocking drug and the blood pressure lowering action. In addition, neither cardioselective beta-blockade nor sympathomimetic properties allowed the prediction of blood pressure responses to the administration of those agents possessing these features. Although SHRs provide a valuable model of human essential hypertension, the variable effects reported here and elsewhere in the literature require caution as to the applicability and usefulness of testing and evaluating beta-adrenergic blocking drugs for theri potential anti-hypertensive effects in this particular form of experimental hypertension.
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PMID:Beta-adrenergic receptor blocking drugs in spontaneous hypertension. 1 Jul 29

1. In seventeen patients with untreated essential hypertension the sodium and water contents of leucocytes were significantly increased, whereas the rate constant for ouabain-sensitive sodium efflux was significantly reduced. 2. These abnormalities were not found in fourteen other patients with well-controlled hypertension. 3. Preliminary observations in accelerated hypertension suggest a different pattern of abnormality in leucocyte sodium metabolism.
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PMID:Abnormal sodium transport in leucocytes from patients with essential hypertension and the effect of treatment. 2 75

Cation transport and electrolyte composition were studied in leucocytes from 17 patients with uncomplicated essential hypertension. Significant increases in cell sodium and water contents, associated with a depression of the rate-constant for active sodium efflux, were found in the hypertensive patients. These abnormalities in cell sodium transport may possibly be related to mechanisms of hypertension.
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PMID:Abnormal leucocyte composition and sodium transport in essential hypertension. 4 73

Water and electrolyte excretion after a large water load and a small Na load was studied in a group of healthy volunteers (C) and in patients with renal arterial stenosis (S) and essential hypertension (EH). It was found that both groups of hypertensive patients reacted to this stimulus by higher Na, Cl, Ca and Mg excretion tan group C. In the two hypertension groups, cumulative Na excretion was comparable in size, but cumulative water excretion was significantly greater in group EH than in group S. The results indicate that these differences can be attributed to different localization of reduced Na reabsorption in the nephron. Signs of a decrease in Na resorption were found in the distal part of the nephron in both hypertension groups, but in the EH group they were also found in the proximal part.
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PMID:Effect of hydratation on renal water and sodium excretion in patients with renal arterial stenosis (S) and essential hypertension (EH). 16 27

Endocrine activity in patients with essential hypertension was studied by measuring the urinary excretion of catecholamines, prostaglandin E (PGE) and cyclic adenosine monophosphate (cAMP). Simultaneously, plasma renin activity, concentrations of serum sodium, potassium, blood urea nitrogen (BUN) and creatinine were determined. Systolic blood pressure and BUN increased progressively with age until the sixth decade. Urinary excretion of norepinephrine was correlated with the systolic blood pressure. In contrast, plasma renin activity and urinary excretion of PGE decreased progressively with the increase in systolic blood pressure. Although the cause of essential hypertension is not known, it is suggested that hypertension accelerates the aging process in the kidney and thus decreases renal PGE synthesis. This decrease of PGE in turn causes a reduction of plasma renin activity, possibly either by accelerating the retention of sodium and water or by failing to stimulate renin synthesis. A decrease of PGE may also potentiate the vasopressor action of norepinephrine.
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PMID:Changes in hormonal activities relative to the severity of essential hypertension. 21 51

1. Indomethacin was administered alone or in addition to either diuretic or propranolol therapy to three groups of patients with essential hypertension on a free sodium diet. 2. Indomethacin administration reduced renin secretion by about 30% in untreated uncomplicated hypertensive patients and by about 75% in those whose renin secretion had either been stimulated or suppressed by maintained diuretic or beta-adrenoreceptor-blockade therapy. 3. Indomethacin administration produced no net effect on blood pressure in untreated patients with uncomplicated hypertension but it blunted or reversed the antihypertensive effect of either diuretic or propranolol therapy. 4. Salt and water retention may be an important factor in the blood pressure-raising effect of indomethacin during diuretic or propranolol therapy: In addition, prostaglandin synthesis may be important in counteracting increased alpha-adrenergic tone, which may limit the blood pressure-lowering effect of beta-adrenoreceptor-blockade. 5. Because of these interactions and their pressor potential indomethacin should be used with caution when combined with either diuretics or beta-adrenoreceptor blockers.
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PMID:Effects of indomethacin alone and during diuretic or beta-adrenoreceptor-blockade therapy on blood pressure and the renin system in essential hypertension. 28 51

In acute experiments in the stomach of dogs electrocoagulation with simultaneous instillation of water (EHT-electrode i.e. electro-hydro-thermo-electrode) proved the most effective electrocoagulation method for controlling standardized bleeding: Optimal visibility at the bleeding site, extension of the therapeutic range as well as the avoidance of charring at the bleeding site are its major advantages. Disturbing adhesion of coagulated material on the electrode is also avoided. The electro-hydro-thermo-electrode is a cheap and portable means of controlling bleeding.
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PMID:Modified electrocoagulation and its possibilities in the control of gastrointestinal bleeding. 31 95

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

Venous distensibility in essential hypertension has been reported to be unchanged or decreased; its pathophysiologic role is uncertain. In 27 male hypertensive patients and 21 normotensive control subjects, forearm venous distensibility and capillary filtration rate at 30 cm of H2O distending pressure were measured by strain gauge plethysmography. Plasma renin activity (PRA), plasma volume (PV) by the Evans blue dye dilution technique, mean arterial pressure (MAP) by cuff, and cardiac output (CO) by the CO2 rebreathing method were also measured. Compared to values in normotensive control subjects, forearm venous distensibility in hypertensive subjects was decreased (P less than 0.05); the forearm venous pressure-volume curves (deflation phase) were shifted in the direction of the pressure axis (P less than 0.02); and the capillary filtration rate was increased (P less than 0.05). Venous distensibility changes in hypertensive subjects were unrelated to PRA, MAP, PV, CO, stroke volume, and total peripheral resistance. These findings confirm previous reports of decreased venous distensibility in hypertension and provide direct evidence for increased capillary filtration rate. In view of the lack of significant correlation between venous distensibility and the measured hemodynamic parameters, a patho-physiologic role for venous distensibility in hypertension could not be established.
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PMID:Decreased venous distensibility in essential hypertension: lack of systemic hemodynamic correlates. 37 15

The safety and efficacy of tienilic acid have been evaluated in studies of patients with mild to moderate essential hypertension, salt and water retention states and hyperuricaemia associated with gout. During the course of these studies 675 patients were treated with tienilic acid, 310 were treated with hydrochlorothiazide, 43 were treated with probenecid and 34 were treated with placebo. Overall, adverse reactions characterized as probably drug-related or questinably drug-related were reported in 28% of patients treated with tienilic acid, 24% treated with hydrochlorothiazide, 25% of patients treated with probenecid and 33% treated with placebo. The side effects encountered were mild in severity, reversible and represented extensions of the pharmacological activity of tienilic acid, hydrochlorothiazide and probenecid. These initial studies demonstrate that tienilic acid is safe and effective in the treatment of mild to moderate essential hypertension, salt and water retention states, including oedema associated with congestive cardiac failure or mild to moderate renal dysfunction, and in the management of elevated serum uric acid levels associated with gout.
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PMID:Safety of tienilic acid. 38 98


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