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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have examined the effects of antihypertensive therapy on glomerular dynamics and on the clinical and morphologic features of a model of nephrotoxic serum nephritis (NSN) in which hypertension occurs. NSN was induced in uninephrectomized male Sprague Dawley rats, which drank 0.9% sodium chloride ad libitum. One-half were assigned randomly to a treated group whose blood pressure was normalized on a regimen of reserpine, hydralazine, and hydrochlorothiazide. Hypertension continued throughout the 6 weeks of study in untreated rats (blood pressure 148 +/- 5 vs. 103 +/- 3 mm Hg in treated rats, P less than 0.01). Urinary protein excretion was greater (437 +/- 110 vs. 254 +/- 81 mg/24 hr, P less than 0.005), and serum albumin lower (1.6 +/- 0.4 vs. 2.9 +/- 0.3 g/dl, P less than 0.01) in hypertensive animals. Diffuse glomerular endo- and extracapillary proliferation and arteriolar medial hypertrophy were observed frequently in nephritic rats with untreated hypertension. By contrast, structural abnormalities were limited primarily to focal segmental proliferation involving fewer than one-third of glomeruli in the absence of vascular changes in treated normotensive rats. Micropuncture studies performed 8 to 16 days after induction of nephritis showed a reduction in glomerular capillary pressure (46 +/- 1 vs. 55 +/- 1 mm Hg, P less than 0.001), glomerular plasma flow rate (115 +/- 20 vs. 160 +/- 20 nl/min, P less than 0.01), and single nephron filtration rate (42 +/- 4 vs. 56 +/- 5 nl/min, P less than 0.001) with antihypertensive treatment, suggesting that a hemodynamic mechanism may have been responsible for enhanced glomerular injury in the hypertensive nephritic animals.
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PMID:Nephrotoxic serum nephritis with hypertension: amelioration by antihypertensive therapy. 383 24

Acute hypertension induced by adrenergic agents opens up the blood-CSF barrier (choroid plexus) to nonelectrolyte and protein tracers. Sprague-Dawley adult rats anesthetized with ketamine were given an intravenous bolus of either epinephrine (10 micrograms/kg), phenylephrine (100 micrograms/kg), isoproterenol (10 micrograms/kg), or D,L-amphetamine (2 mg/kg). Tracers were injected simultaneously with test agents, and the animals killed 10 min later. Epinephrine raised MABP by 57 mm Hg, to a peak pressure of 160 mm Hg; and it increased the volume of distribution (Vd) of urea, mannitol, and 125I-bovine serum albumin in CSF by 1.5-, 2.7-, and 30-fold, respectively. There was enhanced uptake by lateral and fourth ventricle choroid plexuses, cerebral cortex, cerebellum, medulla, and thalamus. Phenylephrine also elevated MABP to 160 mm Hg, but it increased permeation of tracers into CSF (and several brain regions) to a lesser extent than epinephrine, attributable to protective vasoconstriction associated with alpha-agonist activity. Ratio analysis of Vd data provides evidence that augmented permeation of nonelectrolyte tracers in acute hypertension occurs predominantly by diffusion rather than vesicular transport. It is postulated that elevated MABP distends the central cores of choroid plexus villi and cerebral capillaries, with resultant stretching and opening of tight junctions in both barrier systems; with less hindrance to diffusion, urea and mannitol are cleared at rates closer to free diffusion. Neither isoproterenol (decreased MABP by 40 mm Hg) nor amphetamine (did not alter MABP) significantly opened the choroid plexus or blood-brain barrier to tracers.
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PMID:Adrenergic-induced enhancement of brain barrier system permeability to small nonelectrolytes: choroid plexus versus cerebral capillaries. 392 38

Ten patients with cirrhosis and protal hypertension received an initial 20 mg oral test dose of propranolol and subsequently 160 mg of a slow release preparation, orally, each day for seven days. Protein binding, serial plasma propranolol concentrations and effects on heart rate were studied. Protein binding was slightly reduced (mean 85%, range 78.9-88.1%) compared with four normals (mean 87.9%). In patients with severe liver disease (serum albumin less than 30 g/l) propranolol remained detectable in plasma 24 hours after the single 20 mg dose and high steady state concentrations (mean 266.5 ng/ml, range 84-406) were observed during regular dosing. At steady state there was a significant correlation between log total plasma propranolol concentrations and the percentage fall in heart rate (r = 0.659, p less than 0.05). We suggest that in patients with severe liver chronic disease (serum albumin less than 30 g/l), propranolol therapy should be initiated in hospital. The starting dose should be low (20 mg of the conventional formulation tds or 80 mg of the slow release preparation daily) and that regular monitoring of the heart rate should be carried out.
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PMID:Pharmacology of propranolol in patients with cirrhosis and portal hypertension. 396 62

Sprague-Dawley rats susceptible (DS) to NaCl-induced hypertension suffer higher mortality when exposed daily to 2.0 ppm ozone than do hypertension-resistant (DR) rats, independent of salt in the diet or systemic blood pressure. To investigate one possible contribution to this differential sensitivity to ozone, alveolar permeabilities to serum albumin were measured both in ozone-exposed and in control DS and DR rats. Female rats aged 5-7 weeks maintained on a low-salt (0.4% NaCl) diet were injected intravenously with 125I-bovine serum albumin and were then exposed to either 2.0 ppm ozone or air for 5 h. After pentobarbital anesthesia, the rats were exsanguinated and their lungs were lavaged in situ with saline. Lavage fluids and blood samples were measured for radioactivity using a NaI-well gamma counter. The results indicated that while DS and DR control rats have similar pulmonary permeabilities to 125I-albumin, the lungs of the ozone-exposed DS animals were 63% (p less than 0.02) more permeable than those of DR rats exposed to ozone. Sloughing of epithelial tissue, mucous formation and an accumulation of macrophages in the end-airways were more pronounced among ozone-exposed DS animals than in DR-ozone-exposed rats. This increased damage among DS rats correlated well with the increased protein permeability levels. In similar studies, Sprague-Dawley (D) rats were more variable in their response to ozone than either inbred strain. However, the results appeared generally more like those of the DS animals, suggesting that the trait selected by inbreeding may have been resistance rather than sensitivity to ozone-induced lung injury.
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PMID:Alveolar permeability to protein in rats differentially susceptible to ozone. 400 66

The autoregulation theory of essential hypertension states that the characteristic haemodynamic derangement of this disease, i.e. increased vascular resistance, is a homeostatic response to abnormal sodium retention by the kidneys. The postulated relationship between arterial pressure and urinary sodium excretion is disturbed in such a way that a higher than normal pressure is required for sodium excretion to keep up with intake. This will initially expand plasma volume and raise cardiac output. However, hyperperfusion of the tissues will ultimately induce vasoconstriction, presumably by greater than normal wash-out of vasodilator metabolic products. Thus, cardiac output will be restored. Some elements of this theory are not supported by current evidence, but the key element, i.e. the assumption that increased vascular resistance is somehow dependent on abnormal renal sodium handling, is consistent with the following clinical observations: Arterial pressure and urinary sodium excretion are directly correlated over a wide range of pressures in patients with autonomic failure, both acutely during titling and chronically with changes in posture during a 24-h period. The failure to demonstrate pressure-natriuresis in normal subjects may therefore be related to the amplifying effect of the sympathetic nervous system on this mechanism, so that small changes in pressure are capable of inducing large changes in sodium excretion. The pressure-natriuresis curve in patients with autonomic failure is shifted to higher pressures by administration of aldosterone, which is consistent with an important role of renal sodium retention in mineralocorticoid hypertension. Measurements of total extracellular fluid volume, plasma volume/interstitial fluid volume ratio, transcapillary escape rate of serum albumin, cardiac output and arterial pressure at timed intervals during the development of hypertension, in patients exposed to mineralocorticoid excess, or during the reversal of hypertension in nephrectomized patients treated with ultrafiltration haemodialysis, revealed an association of increased total peripheral resistance with a reduced plasma volume/interstitial fluid volume ratio and an increased transcapillary escape rate of serum albumin. This association has also been observed in cross-sectional studies of patients with essential hypertension and suggests that part of the increase in resistance is located at a post-capillary level. It may be related to compression of collapsible venules and veins due to abnormally increased interstitial fluid pressure, not only in sodium-dependent secondary forms of hypertension but also in essential hypertension.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The second Sir George Pickering memorial lecture. What regulates whole body autoregulation? Clinical observations. 402 Jan 27

A combined retrospective and prospective study of 86 patients with IgA nephropathy was conducted to determine whether the level of proteinuria was a good predictive index of progressive disease. The patients fell into three groups: Group A, 31 patients with proteinuria of less than 1 g/day, Group B, 31 patients with proteinuria of 1 to 3.5 g/day; and Group C, 24 patients with proteinuria of more than 3.5 g/day. The groups are comparable in age of presentation, sex ratio, and duration of study and showed no difference in serum creatinine levels, creatinine clearance, incidence of hypertension or incidence of impaired renal function. Compared with the patients in the other groups, those in Group C did not have increased incidence of progressive disease. Nevertheless, they have a higher incidence of nephrotic syndrome (p less than 0.001), a lower incidence of macroscopic haematuria (p less than 0.05), lower serum albumin (p less than 0.05) and heavier proteinuria (p less than 0.01). Severity of proteinuria had no significant correlation with the severity of renal histopathologic changes. Clinical observations divided the 24 patients with nephrotic range proteinuria into three well-defined groups with different prognoses. Six patients had progressive disease with decreasing proteinuria. Five of these remained hypertensive and their initial renal biopsy showed advanced pathologic changes. Thirteen patients had persistent proteinuria although the renal function remained unchanged. Three of these were treated with steroid but failed to respond, and their renal histopathologic changes were usually moderate. The remaining five patients showed good response to steroid treatment although two became steroid-dependent. Their renal histopathology showed mild alteration. Our findings suggest that severe proteinuria in IgA nephropathy does not inevitably indicate a poor prognosis.
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PMID:Nephrotic range proteinuria--a good predictive index of disease in IgA nephropathy? 408 Sep 57

Nineteen patients with nephrotic syndrome, 13 with histological diagnosis, were studied throughout 31 pregnancies. Eight were diagnosed for the first time during pregnancy.Antenatal problems due to severe oedema, urinary tract infection, and refractory orthochromic anaemia were encountered. Eight patients were hypertensive at booking, and in two of these pregnancy was terminated; three others had a significant increase in blood pressure. In 12 of the remaining pregnancies a rise in blood pressure of 20 mm. Hg or more occurred towards term.There were 29 live births (including one set of twins), one stillbirth due to a cord accident, and one neonatal death. The infant birth weight, apart from being affected by hypertension, was related to the maternal serum albumin level.The patients have been under observation for up to 20 years. Fifteen have not shown any deterioration of renal function during the prolonged period of observation. One developed oliguric renal failure immediately post partum and three others died, two, four, and 12 years after their pregnancies.
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PMID:Pregnancy and the nephrotic syndrome. 576 44

The effects of oral administration of 2 mg prazosin on several metabolic and endocrine variables were evaluated in 12 patients with hypertension (6 with normal and 6 with abnormal glucose tolerance). Prazosin was followed by a rise in plasma glucose and serum free fatty acids (FFA) in both normal and diabetic subjects; there was a trend upward in serum albumin (IRI), but growth hormone (GH), prolactin (PRL), and gastrin did not change. Although these results are in general agreement with metabolic effects of other alpha adrenergic blockers already reported, the rise in plasma glucose is at variance with studies performed with phentolamine.
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PMID:Metabolic effects of prazosin. 610

Rats were subjected to adrenaline-induced acute hypertension during either the day or night. Albumin leakage into the brain was studied with Evans blue and 125I labeled serum albumin. The leakage was significantly lower during the night than during the day (P less than 0.001). d,1-propranolol had a protective effect (P less than 0.001) during the day and a slight reduction of the radioactivity (P less than 0.05 in some parts of the brain) was obtained by metoprolol (10 mg/kg) but not by butoxamine (10 mg/kg). None of the drugs reduced the tracer leakage during the night. The results suggest that the degree of alertness is of importance for the function of the blood-brain barrier in acute hypertension. However, the present experimental situation does not allow a separation of the effect of alertness per se and dark/light cycles. The changed vulnerability during the night could be related to enhanced neuronal activity, altered beta-adrenoreceptor sensitivity or to hormonal factors.
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PMID:The blood-brain barrier in adrenaline-induced hypertension. Circadian variations and modification by beta-adrenoreceptor antagonists. 611 Nov 72

The phenothiazine dixyrazine (5 mg . kg-1 i.v.) had minimal, transient hypotensive effects but significantly reduced the leakage of 125I labelled serum albumin in conscious rats subjected to acute hypertension provoked by i.v. adrenaline or bicuculline. By contrast, dixyrazine did not protect the blood-brain barrier during osmotic stress induced by intracarotid infusion of 2 M urea. The diameters of pial arteries and veins were continuously measured with a multichannel videoangiometer through a closed cranial window in anesthetized rats before and after i.v. injection of dixyrazine (5 mg . kg-1). No change in vessel diameter was observed except for a transient autoregulatory dilatation of arteries in response to a slight transitory decrease in the blood pressure. It is concluded that dixyrazine probably protects the blood-brain barrier during mechanical stress by modifying the endothelial cell membrane.
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PMID:Phenothiazine-mediated protection of the blood-brain barrier during acute hypertension. 612 2


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