Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Enhanced hypothalamic noradrenaline biosynthesis in Goldblatt I renovascular hypertension. 3

Chronic treatment with beta-blockers was interrupted abruptly in six patients with arterial hypertension. Three patients, who had experienced symptoms during a previous withdrawal, again complained of transient palpitations, tremor, sweating, headache and general malaise. A significant increase in standing blood pressure (BP) and heart rate (HR) was noted after 24 h. The standing HR reached a maximum after 48 h and had decreased significantly on the 7th day (p less than 0.005). There was a strong tendency to greater increase in standing BP and HR in the patients who experienced symptoms than in those who did not. Plasma concentrations of noradrenaline, adrenaline and prolactin did not change significantly. Thus, beta-blocker withdrawal symptoms are reproducible and are indicative of a transient sympathetic hyperresponse. The increased activity is not likely to be caused by increased production of circulating catecholamines, but rather by increased sensitivity of the beta-receptor.
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PMID:Abrupt withdrawal of beta-blocking agents in patients with arterial hypertension. Effect on blood pressure, heart rate and plasma catecholamines and prolactin. 3 93

1. Chronic hypertension was induced in Wistar rats with intact kidneys by subcutaneous implantation of 50 mg of deoxycorticosterone acetate (DOCA) in wax and addition of sodium chloride (9 g/l) to the drinking water. 2. The development of DOCA/salt hypertension, as monitored by tail-cuff plethysmography, was prevented by: (a) destruction of the peripheral adrenergic nerves with neonatal administration of guanethidine (80 mg/kg subcutaneously for the first 14 days postnatally); (b) bilateral stellate ganglionectomy; (c) oral administration of the beta-adrenoreceptor antagonists propranolol or atenolol (1 mg day-1 kg-1) during the period of DOCA/salt treatment. 3. The dose of DOCA used was sufficient to inhibit the atrial Uptake2 pathway completely: this process appears to participate in termination of action of neurally released noradrenaline in the heart. 4. It is suggested that this model of DOCA/salt hypertension is due to adrenergic enhancement of cardiac output in the presence of an increased sodium load. The enhancement may be partly due to deficient myocardial inactivation of noradrenaline.
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PMID:Dependence of deoxycorticosterone/salt hypertension in the rat on the activity of adrenergic cardiac nerves. 3 42

Acute hypertension was induced by adrenaline, noradrenaline or angiotensin in awake unrestrained rats with chronic indwelling catheters in a jugular vein and in the aorta. The leakage of 125IHSA (human serum albumin) into the brains from rats given adrenaline was significantly larger than in the brains from rats given noradrenaline or angiotensin. It is likely that the enhanced vulnerability of the blood-brain barrier to an adrenaline-induced increase in blood pressure is due to the beta-adrenergic stimulating effect of adrenaline.
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PMID:Blood-brain barrier to albumin in awake rats in acute hypertension induced by adrenaline, noradrenaline or angiotensin. 4 64

The relationship between the severity of hypertensive disease and sodium excretion and sympathetic activity has been studied in subjects of the same age and sex derived from screening a total population. 19 untreated subjects with casual blood-pressure (B.P.) above 175/115 mm Hg on two separate occasions made up the hypertensive group. A normotensive group (n =19) was obtained by selecting a 5% random sample from all subjects with casual B.P. below 160/95. Sympathetic activity was determined from noradrenaline excretion and the severity of hypertension assessed by recording resting diastolic B.P., signs of left ventricular hypertrophy on orthogonal E.C.G., and the glomerular filtration-rate. In the hypertensive group the resting B.P. correlated well both with signs of left ventricular hypertrophy and with the glomerular filtration-rate--i.e., the degree of severity of the hypertension. Up to the level of 90 mm Hg resting diastolic B.P., sodium excretion rose in complete agreement with the theory of pressure diuresis. Above 90 mm Hg, however, sodium and noradrenaline excretion fell with increase of B.P. These two findings indicated that with increasing severity of hypertension the sodium balance overrides the sympathetic activity in the long-term regulation of B.P. This may have both prognostic and therapeutic implications.
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PMID:Sodium excretion and sympathetic activity in relation to severity of hypertensive disease. 5 37

Experiments have been done on rats, rabbits and baboons to elucidate the role of the cranial sympathetic nerves originating in the superior cervical ganglia in the regulation of local cerebral blood flow, including its autoregulation, and in blood-brain barrier functions. Flow was measured by the [14C] ethanol technique, thermoclearance, and xenon-133 clearance. Blood-brain barrier functions were studied by the extravasation of an Evan's blue-albumin complex and by calculation of brain uptake index for two compounds (noradrenaline and inulin). Electrical stimulation of the sympathetic nerves reduces regional flow to a degree that is related to the amount of local perivascular innervation. The breakthrough of autoregulation during induced systemic hypertension is prevented by bilateral stimulation of the superior cervical ganglia. Acute sympathectomy markedly enhances the vascular penetration both at normotension (tested by brain uptake index for noradrenaline and inulin) and rapidly induced hypertension (evidenced by extravasation of Evans' blue). This extravasation of Evans' blud during acute hypertension can be counteracted by sympathetic nerve stimulation. The results give further support for the view that the cranial sympathetic nerves afford an efficient control of the cerebrovascular bed.
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PMID:Influence of the cerebrovascular sympathetic innervation on regional flow, autoregulation, and blood-brain barrier function. 9 65

The sympathetic nervous system is of major importance for the regulation of several physiological functions. Drugs which inhibit the actions of catecholamines and adrenergic drugs are used in the treatment of many clinical disorders. The potential role of catecholamines in a number of human diseases has, however, until recent years been studied to a limited extent only due to lack of methods for quantitation of sympathetic nervous activity. After the development of enzymatic isotope-derivative assays, reliable measurements of noradrenaline and adrenaline in plasma became available. Studies in man have shown that plasma noradrenaline is an index of sympathetic nervous activity. The present survey deals with sympathetic nervous activity and plasma adrenaline in a number of clinical disorders viz. arterial hypertension, duodenal ulcer, thyrotoxicosis, diabetes mellitus and ketotic hypoglycemia.
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PMID:The role of catecholamines in clinical medicine. 10 29

Cardiovascular 'reactivity' to graded splanchnic nerve stimulation was compared in adult spontaneously hypertensive rats (SHR) and normotensive controls (NCR), during abolished adrenal medullary secretion and neurogenic cardiac control and depressed reflex vascular adjustments. Arterial pressure, heart rate and cardiac output were measured, and total peripheral resistance (TPR) and stroke volume (SV) computed before, during and after nerve stimulation. The neurogenic resistance increases in the major gastrointestinal-renal-hepatic circuits expressed themselves as TPR elevations, which were much accentuated in SHR. This reflects an increased w/ri of SHR resistance vessels rather than any altered effector sensitivity, since the responses were particularly accentuated at high discharge rates when noradrenaline junction concentrations approach maximal levels. The splanchnic capacitance responses expressed themselves as SV increases, being the most relevant aspect of capacitance control. SV increased less in SHR, mainly reflecting the reduced diastolic compliance of the hypertrophied SHR left ventricle and the consequent rightward shift of its Frank-Starling curve. The results indicate that an elevated resistance may well be maintained by a normal sympathetic discharge in established SHR hypertension. There seems, however, to be an increasing need for accentuated discharge to the capacitance side to maintain proper cardiac filling of the hypertrophied left ventricle.
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PMID:Cardiovascular 'reactivity' to graded splanchnic nerve stimulation in spontaneously hypertensive and normotensive control rats. 15

Changes in the arterial pressure, in the heart and respiratory rate evoked by the gastrocnemuis nerve stimulation were studied on conscious cats before and during intravenous injection of noradrenaline. Stimulation of the gastrocnemius nerve increased the arterial pressure, the heart and respiratory rates. The same stimulation of the nerve during hypertension caused by noradrenaline injection led to the fall of arterial pressure and tachycardia. The depressor response failed to change under the effect of the beta-adrenoreceptor block and disappeared after the m-cholinoreceptor block with methylatropine. The depressor response was absent in the unanesthetized decerebrated cats. It is supposed that the depressor response of the arterial pressure depended on the strong cholinergic vasodilatation, reflexively evoked by stimulation of the motor nerve in the intact cats.
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PMID:[Depressor reactions to sural nerve stimulation in intact unanesthetized cats]. 19 91

In two fractions obtained from the bovine A. coronaria adenylate cyclase activity was identified and characterized. The adenylate cyclase activity of the 75,000 X g sediment shows a pH optimum at 7.4. The temperature dependence of this adenylate cyclase activity is linear when represented in the Arrhenius plot, and an Arrhenius activation energy of 13.2 kcal Mol-1 can be calculated for the enzyme reaction. The Km-value of the enzyme to ATP is 6 +/- 0.6 - 10(-4) M. The adenylate cyclase activity of the 75,000 X g sediment can be stimulated by NaF. 5'AMP and adenosine inhibit the adenylate cyclase activity of the 75,000 X g sediment. With regard to the enzyme activity, Mn++ and Co++ replace Mg++, but not Ca++. The monovalentcations Na+ and K+ do not influence the adenylate cyclase activity. In a particulate fraction containing plasma membranes, adenylate cyclase activity was also identified. This adenylate cyclase activity can be stimulated by catecholamines, noradrenaline, and isoproterenol. This stimulation can, however, only be proved for the enzyme in the coronaries of 9-week-old and 2-year-old animals. The adenylate cyclase activity from the coronaries of adult animals is not affected by catecholamines. These findings are discussed with regard to hypertension frequently found in adult animals.
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PMID:[Proof of adenylate cyclase activity in the coronary artery of cattle]. 19 28


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