ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

The effect of mental arithmetic (MA) on α 2- and β 2-adrenoceptors on platelets and lymphocytes, respectively, and on plasma catecholamines was studied in normotensive (NT) and essential hypertensive (HT) subjects. There were no significant differences in responses of blood pressure, forearm blood flow (FBF) and heart rate to MA between the two groups. Baseline values and changes in adrenaline and noradrenaline levels during MA were similar in NT and HT. Alpha2-adrenoceptor density and antagonist affinity did not differ between NT and HT and was not influenced by MA. Baseline values of β 2-adrenoceptor density also did not differ between NT and HT and increased similarly after MA in both groups. Antagonist affinity to the β 2-adrenoceptors under baseline conditions was lower in HT and did not change during MA in either group. Our results indicate that there are no differences between NT and HT in α 2- and β 2-adrenoceptor density, either under baseline conditions or after mental stress.

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Male spontaneously hypertensive fawn-hooded (FH) rats can be divided into two classes on the basis of their proteinuria. We investigated the relationship between early proteinuria and the impairment of renal function later in life. Urinary protein excretion (UpV), systolic blood pressure (SBP) and parameters of renal function were sequentially determined in male FH rats. A significant difference in UpV was already present from the age of 10 weeks. Class I rats excreted less protein than class II animals. Initially, the glomerular filtration rate (GFR) of class II animals was somewhat higher than that of class I rats, but from week 50 onwards a decrease in GFR of class II rats was noted and from then on rats died due to uraemia. The GFR of class I animals fell from week 75. The fall in GFR was preceded by a concomitant increase in UpV and SBP. The increase occurred earlier and the rate of increase was higher in class II rats. We conclude that a number of hypertensive FH rats die prematurely from end-stage renal failure. The presence of an increased UpV at an early age is an early marker for the development of renal failure.

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

The contractile responses to various endogenous vasoactive agents were investigated in isolated human uteroplacental arteries from normotensive (NT) patients and patients with pre-eclampsia (PE) undergoing caesarian section. Tissue samples were obtained from the uterine incision and from macroscopically normal cotyledons. Vascular ring preparations of intramyometrial and stem villous arteries (length 1.0–1.3 mm, outer diameter 400–600 µm) were dissected and mounted in organ baths and isometric tension was recorded. Concentration-response relationships for vasopressin (VP), oxytocin (OX), angiotensin II (Ang II), noradrenaline (NA), 5-hydroxytryptamine (5-HT), prostaglandin F2α(PGF2α) and prostaglandin E2(PGE2) were assessed. For each compound, the mean maximum contractile effect (Emax) and the drug concentration producing half-maximal response (EC50) were determined. In intramyometrial arteries from NT and PE patients, VP, Ang II, NA, 5-HT and PGF2αinduced contraction while OX and PGE2produced weak or no responses. Preparations from PE patients showed higher Emaxvalues, while no differences in EC50were found between the two groups. In fetal stem villous arteries, Ang II, 5-HT, PGF2αand PGE2induced contractions, while VP, NA and OX produced weak responses. No differences in Emaxor EC50values were found between the fetal vessels of PE and NT patients. No qualitative differences were demonstrated in response to the agents tested between the vessels (fetal and maternal) from NT women at term and PE patients. However, the results may reflect quantitative differences, suggesting increased contractility of maternal uteroplacental arteries from women with PE.

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

In previous studies, administration of adrenocorticotrophin (ACTH; 0.5 mg i.m. b.d. for 5 days) to normal subjects produced an adrenally dependent rise in blood pressure (BP) of some 20mmHg, accompanied by an increase in cardiac output and an increase in plasma volume [1]. The BP and metabolic effects of ACTH (increase in plasma glucose, fall in eosinophils, increase in body weight and urine sodium retention) were reproduced by infusion of the glucocorticoid (GC) cortisol at rates (6-8mg/h) which reproduced the blood concentrations of the steroid achieved with ACTH administration [2]. Oral administration (hydrocortisone 200 mg daily) produced similar changes qualitatively, although the cortisol concentrations and increase in pressure (12mmHg) were less. Plasma volume was increased [3].To determine the role of urine sodium retention and plasma volume expansion in the hypertension, we gave synthetic steroids to six normal subjects for 5 days, at doses which were calculated to be similar for GC activity, but which had little or no mineralocorticoid (MC) activity.Prednisolone (40mg/day), methylprednisolone (32mg/day), triamcinolone (40mg/day) and dexamethasone (8mg/day) all produced equivalent GC effects (increase in plasma glucose, increase in total white cell count, fall in direct eosinophil count). There were no MC effects with any of the steroids. Body weight did not increase and urinary sodium excretion increased rather than decreased. Plasma volume (125I human serum albumin) and haematocrit were unchanged. BP rose with all four steroids: systolic BP rose by 13mmHg with prednisolone, by 9mmHg with methylprednisolone, by lOmmHg with triamcinolone, and by 6mmHg with dexamethasone. Diastolic BP increases were 8, 11, 8 and 7mmHg, respectively.Thus, neither MC activity nor an increase in plasma volume is essential for steroids to induce an increase in blood pressure. Therefore, screening of synthetic GCs to minimize MC activity will not prevent hypertensive complications.

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

In a randomized, double-blind study (n=58) with parallel groups, the effects of diltiazem (mean dose 329mg/day) and atenolol (mean dose 67mg/day) on carbohydrate and lipoprotein metabolism in hypertensive patients were compared. The mean systolic blood pressure (SBP)/diastolic blood pressure (DBP) reductions in the supine position were similar and satisfactory, 9/11 and 11/9 mmHg during atenolol and diltiazem treatment, respectively. Insulin-mediated glucose uptake, measured with the euglycaemic insulin clamp technique, decreased during atenolol treatment, from 7.1 to 5.6mg/kg per min (P=0.005) but not during treatment with diltiazem (initial value 6.8, final value 6.7mg/kg per min;P> 0.8). Treatment differences between groups were statistically significant (P< 0.05).During atenolol treatment there was a slight but significant increase in plasma glucose in the fasting state (P<0.05) and at the end of an intravenous glucose tolerance test (IVGTT;P< 0.01), and in plasma insulin at the end of IVGTT (P< 0.05). Despite increased insulin resistance the increase in insulin response was small, suggesting inhibition of insulin release. The insulin peak was decreased by 13% during diltiazem treatment (P < 0.05). The concentrations of very-low- and low-density lipoprotein triglycerides increased, whereas high-density lipoprotein cholesterol decreased and low-density lipoprotein cholesterol was unaffected during atenolol treatment. In conclusion, there was no difference between the antihypertensive effects of atenolol and diltiazem, but atenolol decreased insulin sensitivity and altered the lipid profile, thus possibly increasing the risk of diabetes mellitus and theoretically reducing the benefits of blood pressure reduction with regard to risk of coronary heart disease.

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Noradrenaline hydrochloride (160 µg base/kg perh) or vehicle were infused subcutaneously for 11 days into 35 male Wistar-Furth rats using osmotic minipumps. Chronic noradrenaline infusion produced moderate hypertrophy of both ventricles without causing tissue oedema. Left ventricular (LV) hypertrophy was concentric with no change in cavity volume, increased mass: volume ratio (approximately 50%) and increased fibre diameter (approximately 25%). In the conscious rat, noradrenaline produced only a slight increase in mean arterial pressure (13%) and heart rate (11%) but a marked increase in the variability of mean blood pressure (250%). The extent of LV hypertrophy was not related to the level of mean blood pressure or to its variability. In the anaesthetized rat, peak cardiac pumping ability was normal before and after cardiac autonomic blockade. Peak pressure-generating ability during aortic occlusion was increased in hypertrophied hearts before autonomic blockade but was similar to control rats after autonomic blockade. Chronic noradrenaline administration produces cardiac hypertrophy which has many similarities to hypertensive cardiac hypertrophy but no clear association with the level of blood pressure.

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

The effects of theophylline and cyclic adenosine 3',5'-monophosphate (cAMP) on renin release by afferent arterioles were studied. Rabbit afferent arterioles (seven to 10), obtained by a microdissection technique, were incubated for three consecutive 20min periods in 100(µ of Medium 199 with 0.1% bovine serum albumin (BSA). Afferent arterioles exposed to theophylline, 1 x 10-4mol/l, produced a>100% increase in renin release (0.18 ± 0.04 to 0.42 ± 0.05 ng angiotensin l/h per arteriole per h incubation). The renin release stimulated by theophylline was completely abolished by indomethacin and meclofenamate. The stimulation of renin secretion was also blocked when extracellular calcium concentration was decreased to 10~7 mol/l and the arterioles were permeabilized with calcium ionophore. Dibutyryl cAMP (db-cAMP), 1 x 10-4mol/l, and forskolin, 1 µ.mol/1 or 100µmol/l, failed to stimulate renin release by afferent arterioles. The results of this study therefore suggest that theophylline-stimulated renin release may be mediated through a prostaglandin pathway. The stimulation of renin secretion is also dependent on the extracellular concentration of calcium.

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID