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. Noradrenaline content of several rat brain stem and hypothalamic nuclei falls transiently at 72 h after initiation of renovascular hypertension (one-kidney Goldblatt model). 2. Tyrosine hydroxylase activity is significantly reduced in posterior, paraventricular and periventricular nuclei of hypothalamus at this time but returns to control value by 7 days. 3. Treatment with hydrallazine, 5 mg/kg intraperitoneally, twice daily or methaoxamine, 5 mg/kg, three times daily for 3 days respectively raises and lowers the noradrenaline content of brain nuclei, suggesting that short-term changes in noradrenaline may be secondary to afferent baroreceptor input. 4. At later times after the development of renovascular hypertension (7 and 28 days) activity of phenylethanolamine-N-methyl transferase is increased in the nucleus of the solitary tract and the locus coeruleus. 5. Brain catecholamines may participate both early in the development and later in the maintenance of renovascular hypertension.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Brain catecholamines and catecholamine-synthesizing enzymes in renovascular hypertension in the rat. 3 99

1. Hypertension was induced in rats by renal artery clip with the contralateral kidney removed (Goldblatt I) or left intact (Goldblatt II). 2. Plasma noradrenaline was increased 62% in the Goldblatt I animals after 3 weeks. 3. Hypothalamic tyrosine hydroxylase and dopamine beta-hydroxylase activities, and the concentration of noradrenaline were increased in the Goldblatt I animals after 3 weeks. 4. Enhanced hypothalamic noradrenaline synthesis may be a pathogenic factor in Goldblatt I renovascular hypertension.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Enhanced hypothalamic noradrenaline biosynthesis in Goldblatt I renovascular hypertension. 3

1. Angiotensin I-generating activity of rat brain extract was separated into two components by affinity chromatography on a casein-Sepharose gel column. 2. The component without affinity to the gel was identified as true renin on the basis of its sensitivity to anti-renin antibody and the lack of protease activity. 3. The second renin-like component with affinity to the gel was a protease insensitive to the anti-renin antibody. Its renin-like activity examined with sheep substrate was pronounced compared with the rate of angiotensin I generation from the rat substrate. 4. It was concluded that rat brain contains true renin, which can be detected by the use of rat substrate but can be masked when examined with sheep substrate.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Definitive evidence for renin in rat brain by affinity chromatographic separation from protease. 3 1

1. Active and acid-activable inactive renin were measured in renal venous and arterial plasma of 18 patients with essential hypertension (EHT) and 19 patients with renovascular hypertension (RVHT). In seven patients with EHT and in 11 patients with RVHT measurements were made before and 25-35 min after an intravenous injection of 300 mg of diazoxide. 2. Under basal conditions the renal vein to artery ratios for active and inactive renin in EHT ranged from 0.71 to 1.96 and from 0.68 to 1.44 respectively. In 14 patients with RVHT the renal vein to artery ratio for active renin on the affected side was above the range found in EHT and in six of them the renal vein to artery ratio for inactive renin was also elevated. 3. The diazoxide-induced release of active renin from kidneys, which had a stenotic artery but were not seriously contracted, was associated with a fall of the renal vein to artery ratio for inactive renin to a value below 1.00. 4. The results indicate that changes in the release of active and inactive renin do not always run in parallel. The findings are compatible with the hypothesis that circulating inactive renin can be activated in the kidney.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Renal release of active and inactive renin in essential and renovascular hypertension. 3 2

1. The protease inhibitors Trasylol and soyabean trypsin inhibitor prevented the activation of plasma inactive renin by acid. 2. N-Ethylmaleimide inhibited acid-activation to some extent but o-phenathroline had no effect. 3. Acid-activation of the inactive renin in human plasma is mediated by a serine protease.
Clin Sci Mol Med Suppl 1978 Dec
PMID:An endogenous protease activating plasma inactive renin. 3 3

1. We have found that 'acid'-activation of inactive human plasma renin is a two-phase process. About 30% of activation occurs during dialysis to pH 3.3; the remaining 70% occurs at alkaline pH. 2. The 'alkaline phase' of activation has a pH optimum between 7.5 and 8.4. It is inhibited by unacidified plasma and by soya-bean or lima-bean trypsin inhibitors. 3. 'Cryoactivation' of inactive plasma renin, which occurs at -4 degrees C and alkaline pH, is also inhibited by soya-bean or lima-bean trypsin inhibitors and by the serine protease inhibitors diisopropylphosphorofluoridate and benzamidine. 4. Thus endogenous neutral serine proteases participate in the activation of inactive plasma renin in vitro. Their action is prevented in the circulation by inhibitors which are inactivated by acid or cold.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Activation of inactive plasma renin: evidence that both cryoactivation and acid-activation work by liberating a neutral serine protease from endogenous inhibitors. 3 4

1. The interaction between prazosin and clonidine was studied in anaesthetized rats, pithed rats and in anaesthetized cats. 2. Prazosin diminished the clonidine-induced hypotensive effect in anaesthetized rats, probably via an antagonism at the level of central alpha-adrenoreceptors. 3. In pithed rats, stimulation of the Nervi accelerantes caused tachycardia, which was diminished considerably by clonidine. The antagonism by clonidine was partly reversed by prazosin, suggesting that prazosin possesses a certain degree of presynaptic activity apart from its predominant effect at the postsynaptic alpha-receptor. Piperoxan was more active than prazosin. 4. The central hypotensive effect of clonidine, injected into the left vertebral artery of cats was significantly reduced by prazosin, administered before clonidine via the same route. Intravenously injected prazosin did not diminish the central hypotensive effect of clonidine. The antagonism is, therefore, caused by a central mechanism. 5. The combined application of clonidine and prazosin in antihypertensive treatment is probably not only irrational but ought to be discouraged in view of the interaction between the drugs, which leads to a reduced antihypertensive potency of clonidine.
Clin Sci Mol Med Suppl 1978 Dec
PMID:The interaction between prazosin and clonidine. 3 5

1. Eight hypertensive patients with angina pectoris had placebo added to their existing medications for 8 weeks, then incremental doses of active labetalol with simultaneous stepwise reduction in other medicines until blood pressure was satisfactorily controlled; after that only labetalol and thiazide (8 weeks) and finally labetalol-placebo together with previous beta-adrenoreceptor antagonists and thiazide for 4 weeks were administered. 2. During the labetalol plus thiazide period resting blood pressures and measurements obtained during isotonic exercise, isometric exercise and the cold pressor test were significantly lower than during the initial placebo addition period. Angina scores were significantly reduced during this period. 3. During the final treatment with placebo, beta-adrenoreceptor antagonist and thiazide, blood pressures remained reduced, but angina was significantly worse. 4. Labetalol which antagonizes both alpha- and beta-adrenoreceptors produced better relief of angina pectoris than beta-adrenoreceptor antagonists during improvement in blood pressure in hypertensive patients.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Labetalol in hypertensive patients with angina pectoris: beneficial effect of combined alpha- and beta-adrenoreceptor blockade. 3 6

1. Chlorothiazide twice a day plus atenolol, metoprolol, pindolol and propranolol in single daily doses administered to patients with essential hypertension achieved effective control of blood pressure. 2. Each beta-adrenoreceptor-blocking drug was associated with small, but significant, increases in plasma triglyceride concentrations and suppression of fasting immuno-reactive glucagon concentrations.
Clin Sci Mol Med Suppl 1978 Dec
PMID:beta-Adrenoreceptor-blocking agents and lipid metabolism. 3 7

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


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