Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. A Valsalva-like manoeuvre was used to elicit graded rises in total peripheral resistance (TPR) in conscious rabbits. The rises were reflex and mediated through sympathetic constrictors. Propranolol infused at different rates reaching plasma concentrations up to 240 (SEM 33) ng/ml had no effect on this reflex but reduced mean arterial pressure. However, the response was attenuated by clonidine in a dose-dependent manner. 2. Valsalva manoeuvres were used to elicit graded sympathetically mediated rises in TPR index in twenty-nine subjects with mean arterial pressure ranging from 75 to 165 mmHg. Absolute sensitivity of the constrictor response increased with rising resting TPR index, resulting in some enhancement of constrictor responses in the hypertensive subjects. It seems likely that non-autonomic factors (e.g. vessel structure) rather than hyperactive neural constrictor effects are involved in the enhanced constrictor responses in essential hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Valsalva vasoconstrictor reflex in human hypertension in after beta-adrenoreceptor blockade in conscious rabbits. 1 55

1. Haemodynamic responses to diazoxide (300 mg intravenously) were studied in 15 hypertensive patients before and after chronic beta-adrenoreceptor blockade by 320 mg of propranolol daily. After diazoxide alone, mean arterial pressure and total peripheral resistance were lowered by 24 +/- 3 and 35 +/- 5% (mean +/- SEM) respectively. Cardiac output and heart rate rose by 25 +/- 9 and 21 +/- 3%. During beta-adrenoreceptor blockade, the percentage changes of mean arterial pressure, heart rate, cardiac output and total peripheral resistance after vasodilatation were not significantly different from those after diazoxide alone. 2. Atropine, 0.04 mg/kg body weight, was given to 12 hypertensive patients chronically treated with beta-adrenoreceptor blockade, before acute vasodilatation by diazoxide. Diazoxide caused no increase in heart rate after combined beta-adrenoreceptor and parasympathetic blockade. However, cardiac output rose by 14 +/- 5%. 3. We conclude that withdrawal of parasympathetic tone is an important determinant of circulatory homeostasis after acute vasodilatation during beta-adrenoreceptor blockade.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Sympathetic and parasympathetic components of reflex cardiostimulation during vasodilator treatment of hypertension. 3 8

1. Intracellular electrolytes, and erythrocyte membrane adenosine triphosphatase (ATPase) activity, was studied in twenty patients after renal transplantation. 2. The mean ouabain-sensitive ATPase activity in the erythrocyte membranes of the transplant patients was 122 nmol of inorganic phosphorus (Pi) h-1 mg of tissue-1 (SEM 14), compared with 62 nmol of Pi h-1 mg of tissue-1 (SEM 8) in a group of paired, healthy controls. 3. The increase in ouabain-sensitive ATPase was most marked in the 4 months after transplantation. However, a significant increase in ouabain-sensitive ATPase persisted for more than 8 months after transplantation. 4. This increase in ouabain-sensitive ATPase was associated with a decrease in intracellular sodium in the erythrocytes of the transplant patients.
Clin Sci Mol Med 1975 Mar
PMID:Changes in erythrocyte membrane ouabain-sensitive adenosine triphosphatase after renal transplantation. 12 85

1. Administration of dexamethasone, 8 mg/day (0-02 mmol/day), for 5 days to normal subjects produced negative nitrogen balance, due to early and sustained increases in urinary urea nitrogen excretion 2. In eight subjects ingesting 0-9--1-6 g of protein day-1 kg-1 body weight the cumulative increment in urea nitrogen excretion averaged + 12-5 g (SEM 2-8, P less than 0-01) over the 5 days of glucocorticoid administration. 3. Increases in urinary urea nitrogen excretion could be related to both plasma alanine and blood glutamine changes by using a multiple regression equation. 4. These results suggest that corticosteroids induce increased release of alanine and glutamine by peripheral tissues, which may augment urea formation and negative nitrogen balance. 5. The correlation between increments in urea nitrogen excretion and increases in plasma arginine remains unexplained.
Clin Sci Mol Med 1977 Sep
PMID:The role of alanine and glutamine in steroid-induced nitrogen wasting in man. 91 44

1. Cholesterol intake (about 0-25 mmol/day) and the faecal excretion of cholesterol, coprostanol and coprostanone were determined in normolipidaemic control subjects and hyperlipidaemic patients, whose bile acid kinetics had been previously studied. 2. The combined excretion of the neutral steroids (excluding plant sterol and plant sterol metabolites) averaged 1-07 +/- 0-13 (+/-SEM)mmol/day in the control subjects (n=14). The corresponding values in patients with hyperlipoproteinaemia type IIa (n=19), IIb (n=12) and IV (n=23) were 0-86 +/- 0-10, 0-93 +/- 0-11 and 1-48 +/- 0-17 mmol/day respectively. 3. The mean values for the net steroid "balance", defined as the combined amount of bile acid synthesized (determined by an isotope-dilution technique) and the faecal excretion of neutral steroids minus cholesterol intake, were 1-83 +/- 0-22 mmol/day in the control subjects and 1-60 +/- 0-15, 1-81 +/- 0-19 and 3-53 +/- 0-23 mmol/day in patients with type IIa, IIb and IV lipoprotein patterns respectively. 4. No significant correlations between net steroid "balance" and sex, age, serum lipid concentrations, body weight or body surface area were found in any of the groups of subjects. 5. It is concluded that patients with type II hyperlipoproteinaemia eliminate cholesterol as bile acids and neutral faecal steroids normally. The type IV lipoprotein pattern is associated with increased bile acid synthesis and/or elevated faecal excretion of neutral steroids, so that the net steroid "balance" is usually above the normal limit.
Clin Sci Mol Med 1976 Oct
PMID:Elimination of cholesterol in hyperlipoproteinaemia. 97 79

1. Indomethacin inhibits prostaglandin synthesis and interferes with renin release; these effects were studied in rabbit renovascular hypertension. 2. Ten intravenous injections (3 mg day-1 kg-1 after two initial doses of 9 mg/kg) of indomethacin were given daily to ten normal rabbits, ten rabbits with two-kidney Goldblatt hypertension (2KH), tension (1KH). Twelve appropriate control rabbits received diluent phosphate buffer without indomethacin. Plasma renin activity and plasma prostaglandin E2 were measured by radioimmunoassay. 3. In the normal group, indomethacin significantly decreased plasma prostaglandin E2 (1-15 to 0-2 ng/ml, SEM 0-2; P less than 0-01) and plasma renin activity (20 to 3 ng h-1 ml-1, SEM 1, P less than 0-01). Plasma creatinine increased slightly but the mean blood pressure was not significantly changed by indomethacin. 4. Six of ten rabbits with 2KH showed results similar to those in the normal rabbits. In four of ten rabbits in which development of 2KH was accompanied by increments in plasma renin activity (18 to 31-5 ng h-1 ml-1, SEM 3 and 4 respectively; P less than 0-01) and plasma prostaglandin E2 (1-2 to 3-4 ng/ml, SEM 0-2 and 0-4 respectively; P less than 0-05), treatment with indomethacin produced renal failure (plasma creatinine increasing to 7-6 mg/100 ml), oliguria, malignant hypertension (mean blood pressure, 168 mmHg, SEM 7-7) and death within 5 days. 5. In 1KH, indomethacin decreased plasma renin activity and plasma prostaglandin E2, but caused increased mean blood pressure (102 to 121 mmHg, SEM 4 and 6 respectively; P less than 0-01) and decreased renal function (plasma creatinine 0-9 +/- 0-04 to 3-5 +/- 1 mg/100 ml, SEM 0-04 and 1 respectively; P less than 0-01). 6. Aggravation of hypertension was conditioned by pre-existing levels of renal function and, to a lesser extent, by plasma renin activities. 7. These results suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Effects of indomethacin in rabbit renovascular hypertension. 107 20

1. Serum dopamine beta-hydroxylase activity was determined in normotensive control subjects and patients with labile or established essential hypertension. The enzyme activity was 25-9 +/- 1-9 (SEM) 29-6 +/- 2-5 and 25-1 +/- 1-9 micronmol min-1 1-1, for control, labile and established hypertensive subjects respectively. 2. Neither blood pressure nor serum dopamine beta-hydroxylase activity was changed in normotensive control subjects by administration of phentolamine; however, in patients with essential hypertension blood pressure was significantly decreased (P is less than 0-01) and serum dopamine beta-hydroxylase activity was slightly increased. With propranolol administration, blood pressure and the serum enzyme activity were not significantly changed in normotensive or hypertensive subjects. 3. Our results suggest that there is no correlation between serum dopamine beta-hydroxylase activity and blood pressure.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Serum dopamine beta-hydroxylase activity in essential hypertension. 107 65

1. The National Blood Pressure Study (NBPS) is a single blind trial designed to test the efficacy of active drug treatment in reducing complications from mild hypertension (mean diastolic pressure = 95-109 mmHg). 2. Between 1973 and 1975, four centres screened about 104 000 subjects aged 30-69 years, yielding an estimated prevalence of hypertension (greater than or equal to 95 mmHg diastolic) of 16% and of moderate-to-severe hypertension (greater than of equal to 110 mmHg diastolic) of 1-3%. 3. Some 4000 subjects selected for untreated uncomplicated mild hypertension were randomized to either active treatment (cholorothiazide +alpha-methyldopa and/or a beta-adrenoreceptor antagonist as required) or to matching placebos. 4. At 1 year mean pressures had fallen significantly below entry pressures in both groups but in the active group the fall was greater by a margin of 14-4+/-1-3 (SEM) mmHg systolic and 7-1+/-0-7 mmHg diastolic. At 1 year 5% of subjects in the placebo group had been placed on active treatment on the ethical grounds that pressure had exceeded the mild hypertension limit. 5. Trial end-points (death, morbidity from stroke, hypertensive heart and renal disease, and ischaemic heart disease) number 106 (nine deaths) thus far, of which ischaemic heart disease accounts for 71% and stroke 19%. 6. The duration of trial may need to be extended beyond the original estimate of 5 years.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Report on progress in the Australian National Blood Pressure Study (NBPS). 107 98

1. Systolic blood pressure was measured by a Doppler ultrasound technique in twenty normal babies on 6 successive days after the day of delivery. In three babies blood pressure was recorded every 15 min for 24 h. 2. Systolic blood pressure during the first 6 days of life was 95 (SEM = 2) mmHg. 3. Systolic blood pressure increased on average by 2 mmHg/day, but increased most between the second and third days of life. 4. Systolic blood pressure was 11 mmHg higher when awake than when the babies were asleep. 5. There was marked within-baby variation in the systolic blood pressure of neonates, which could not be accounted for by age or recognizable changes in level in consciousness.
Clin Sci Mol Med 1975 Dec
PMID:Systolic blood pressure variation during the first 6 days of life. 120 86

We studied lung explants in submersion organ culture to examine the role of the developing fetal alveolar epithelium in the production of lung fluid. Fourteen-day-gestation fetal rat lungs were grown in a collagen gel matrix supplemented with F-12 media and 10% fetal calf serum. In this model, the lung continues to grow, secrete fluid, and become progressively cystic in morphology. There is gradual thinning of the distal epithelial layer, which is lined by alveolar type II cells and their precursors. After 6 to 8 days in culture, we impaled the cyst walls with a microelectrode and continuously recorded the transepithelial potential (psi t). Stable, baseline transepithelial potentials of -1.1 to -6.2 mV (mean +/- SEM = -3.3 +/- 0.11 mV, lumen negative, n = 34) were measured in bicarbonate-buffered Ringer's solution, suggesting active electrolyte transport. When bumetanide, an inhibitor of chloride secretion in other systems, was added to the bathing solution, psi t decreased from a baseline of -3.5 +/- 0.07 mV (mean +/- SEM) to a value of -2.2 +/- 0.07 mV, suggesting chloride transport contributes to the voltage (n = 18, P less than 0.0005). Isoproterenol hyperpolarized psi t from a baseline of -4.3 +/- 1.0 mV to -6.5 +/- 1.0 mV (n = 7, P less than 0.005). 8-(4-Chlorophenylthio) adenosine 3':5'cyclic monophosphate (CPT-cAMP) plus isobutylmethylxanthine (IBMX) similarly hyperpolarized psi t from a baseline of -4.6 +/- 0.4 mV to -7.3 +/- 0.7 mV (n = 11, P less than 0.005). Addition of bumetanide after stimulation with isoproterenol or CPT-cAMP/IBMX depolarized psi t.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Respir Cell Mol Biol 1992 Jun
PMID:Secretion of lung fluid by the developing fetal rat alveolar epithelium in organ culture. 131 92


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