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. In order to test whether the release of E-type prostaglandins from the kidney by various vasoconstrictor stimuli is related specifically to adrenoreceptor activation, we have compared release of prostaglandin E-like material from perfused rat kidneys during infusion of noradrenaline or vasopressin. 2. Concentrations of noradrenaline or vasopressin that produced comparable rises in renal perfusion pressure also released comparable amounts of prostaglandin E-like material. This effect was abolished by infusion of an inhibitor of prostaglandin synthesis into the kidney. 3. We conclude that liberation of E-type prostaglandins during renal vasoconstriction is probably related to the activation of intrarenal smooth muscle and odes not involve any specific hormonal receptor. Stimulation of release of prostaglandin E may explain certain reported renal actions of vasopressin.
Clin Sci Mol Med 1977 Jan
PMID:Release by vasopression of E-type prostaglandins from the rate kidney. 60 58

1. Noradrenaline, adrenaline and alpha-methylnoradrenaline administration into the nucleus tractus solitarii (NTS) of anaesthetized rats decreased blood pressure and heart rate in a dose-dependent fashion. 2. Bilateral injections were effective in lower doses than unilateral administration. alpha-Methylnoradrenaline given bilaterally produced hypotension in a dose of 0-08 nmol whereas after unilateral injection a dose of 0-32 nmol was needed to obtain the same degree of hypotension. 3. Electrical stimulation of the NTS caused hypotension and bradycardia. Conversely, bilateral electrolytic lesions or deafferentation of the NTS led to acute hypertension. Chronically such lesions caused neurogenic hypertension. 4. In spontaneously hypertensive rats increased concentrations of noradrenaline, adrenaline and dopamine were measured in the part of the NTS located just caudal to the obex (A2 region).
Clin Sci Mol Med Suppl 1976 Dec
PMID:Brain-stem structures and catecholamines in the control of arterial blood pressure in the rat. 79 55

1. Studies with a sensitive radioenzymatic assay for plasma noradrenaline suggest there is a selective overactivity of the sympathetic nerous system in essential hypertension. 2. Serotonin turnover in the mesenteric vessels is approximately twice that of noradrenaline and it is suggested that serotonin may interact with noradrenaline to maintain vascular resistance. 3. Methodology which allows the study of local sympathetic turnover in nuclei of the central nerous system and in peripheral blood vessels is decribed. This approach has been used to study non-innervated sympathetic turnover observed in phaceochromocytoma.
Clin Sci Mol Med Suppl 1976 Dec
PMID:The role of noradrenaline and other transmitter hormones in the pathogenesis of hypertension. 79 56

1. The interactions of dopamine, reserpine and methyldopa on blood pressure of normal subjects and of those with essential hypertension were examined. 2. When biosynthesis of noradrenaline from dopamine was blocked by reserpine, dopamine induced a prominent depressor effect in essential hypertension. 3. The long-term treatment with methyldopa induced a marked potentiateion of the pressor action of domapine in hypertension, although no significant pressor response was found in normal subjects. 4. It is suggested that methylnoradrenaline may accumulate in peripheral nerve endings of patients with essential hypertension in comparison with normal subjects, and this accumulated methylnoradrenaline potentiates the pressor response to dopamine in essential hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Interaction of dopamine, methyldopa and reserpine in the sympatho-adrenal system in essential hypertension. 79 57

1. Prazosin had a considerable anti-hypertensive effect in both lying and standing posture in a mixed group of twenty-four patients in an open clinical trial. The drug was well tolerated and side-effects were few. 2. Tested on rat blood vessels, prazosin was ten times more potent on a molar basis than phentolamine in blocking the vasoconstrictor effects of noradrenaline. In the absence of vasoconstrictor nervous activity, no vasodilatation was observed. 3. In genetically hypertensive rats, prazosin in large doses caused a substantial fall in blood pressure, total exchangeable sodium and extracellular fluid volume. Tolerance to these effects started to develop within 20 days. In normotensive rats, blood pressure was lowered but total exchangeable sodium and extracellular fluid volume were not affected.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Prazosin: preliminary clinical and pharmacological observations. 80 32

1. Mean plasma noradrenaline concentration was elevated in forty-four patients with established essential hypertension. Eighteen of the hypertensive patients had resting plasma noradrenaline concentrations in the normal range. 2. Patients with endogenous depression had higher mean plasma noradrenaline concentrations but significantly lower blood pressure than patients with essential hypertension. 3. Patients with phaeochromocytoma had plasma noradrenaline concentrations twenty-eight times greater than those found in essential hypertension, but blood pressures were less than 20% higher. 4. It is concluded that excess of sympathetic drive only partly explains the level of the blood pressure in essential hypertension.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Plasma noradrenaline concentration and blood pressure in essential hypertension, phaeochromocytoma and depression. 80 39

1. Catecholamine plasma concentrations and urinary excretion were measured together with plasma renin activity in ten patients with essential hypertension and in five normal control subjects before and after a frusemide challenge. 2. The same procedure was repeated in the same subjects 3--4 days later after pretreatment with oxprenolol. 3. Noradrenaline plasma concentrations and urinary excretion increased significantly after frusemide in all cases, returning to normal values at 30 and 60 min. Adrenaline plasma concentrations and urinary excretion were unchanged. 4. Plasma renin activity increased significantly in seven patients with hypertension and normal renin basal values, remaining unchanged in three hypertensive patients with low-renin basal values. 5. Oxprenolol suppressed the response of noradrenaline and plasma renin activity to frusemide in all cases.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Effect of oxprenolol on catecholamines and plasma renin activity: acute response to frusemide in hypertensive patients. 80 48

1. Plasma noradrenaline concentrations and dopamine beta-hydroxylase activity have been measured at various stages in the development of hypertension in the one-kidney Goldblatt rat (unilateral renal arterial constriction and contralateral nephrectomy). 2. Although plasma noradrenaline concentrations were significantly elevated from control values at 7, 14 and 28 days, plasma dopamine beta-hydroxylase activity was not significantly different from control values except at 24 h. 3. These findings suggest that peripheral sympathetic activity is increased in the one-kidney Goldblatt model of experimental hypertension but that plasma dopamine beta-hydroxylase activity is poor index of this increase. 4. Both the rise in blood pressure and the rise in plasma noradrenaline concentrations were prevented by pretreatment with intracisternal 6-hydroxydopamine, suggesting that the increased sympathetic activity is at least in part centrally mediated.
Clin Sci Mol Med 1977 May
PMID:Plasma noradrenaline concentrations in experimental renovascular hypertension in the rat. 86 41

1. A single oral dose of clonidine hydrochloride (300 microgram) lowered systolic blood pressure by 20+/-2 mmHg and diastolic blood pressure by 15+/-2 mmHg in seven healthy normotensive subjects. 2. Resting supine plasma noradrenaline concentration fell from 2-42+/-0-47 nmol/l before dosing to a minimum of 0-59+/-0-18 nmol/l at 6 h. The value subsequently rose and was not significantly different from that before the dose at 12 h. There was a significant reduction in urinary free catecholamine excretion in the first 12 h after dosing. 3. Resting supine plasma renin activity before dosing was 0-95+/-0-16 pmol of angiotensin I h-1 ml-1 of plasma and rose significantly after clonidine to 3-50+/-0-39 pmol of angiotensin I h-1 ml-1 of plasma at 6 h. By 12 h plasma renin activity had returned to control values. 4. When the same subjects were studied on a control, drug-free, day under the same conditions, there was no significant change in blood pressure or plasma noradrenaline. Although plasma renin activity rose during this control day, it was significantly lower than after clonidine. 5. In normotensive subjects single doses of clonidine lower blood pressure and are associated with a reduction of sympathetic nervous activity. Delayed elevation of plasma renin activity may be secondary to the fall in blood pressure. There is no evidence for an overshoot of sympathetic activity after a single dose of clonidine.
Clin Sci Mol Med 1977 Jul
PMID:Effects of clonidine on biochemical indices of sympathetic function and plasma renin activity in normotensive man. 87 20

1. The concentrations of plasma total and unconjugated bilirubin and of serum nonesterified fatty acids (NEFA) have been measured in two healthy subjects during fasts of up to 21 h. 2. Fasting was either continuous or interrupted by various procedures that altered the concentrations of NEFA and total bilirubin. 3. When NEFA concentrations were increased by the administration of noradrenaline, heparin or caffeine, bilirubin concentrations also rose. 4. When NEFA concentrations were lowered by insulin, bilirubin concentrations fell. 5. Meals of 3-138 kJ and more, taken during the fasting period, lowered total bilirubin and NEFA concentrations in both subjects, whereas the effects of smaller meals were less consistent. 6. These studies demonstrate a statistically significant correlation between total bilirubin and NEFA during uninterrupted fasting and an association between these variables under other experimental conditions. They suggest that the control of bilirubin concentrations in the blood is linked to lipid metabolism.
Clin Sci Mol Med 1977 Aug
PMID:The association between fasting hyperbilirubinaemia and serum non-esterified fatty acids in man. 89 Nov 4


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