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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma noradrenaline, plasma renin and pressor action of exogenous noradrenaline and angiotensin in normotensive subjects and patients with essential hypertension. In normotensive subjects an inverse correlation was observed between the index of sympathetic nervous activity, the plasma noradrenaline concentration during physical exercise, and reactivity to exogenous noradrenaline. The relationship between the index of sympathetic nervous activity and reactivity to noradrenaline was invariably disturbed in age-matched patients with essential hypertension. A multiple regression analysis revealed a highly significant correlation between the combination of both factors and the height of mean arterial blood pressure (r = 0.91). The data suggest that both factors combined, sympathetic nervous activity and pressor response to noradrenaline, are an important determinant of the arterial blood pressure level. An inverse relationship could also be demonstrated between plasma renin concentration and pressor response to angiotensin II in normotensives and hypertensives. However, this relationship was unaltered in the hypertensives. Therefore angiotensin II does not appear to contribute directly to the high blood pressure.
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PMID:[Pathogenesis of essential hypertension. Plasma noradrenaline, plasma renin and pressor effects of noradrenaline and angiotensin in normotensive patients and patients with essential hypertension]. 46 94

The effects of intraventricular and intraspinal administration of 6-hydroxydopamine (6-OH-DA) on the development and maintenance of DOCA-saline hypertension in rats have been investigated. Intraventricular administration of 6-OH-DA prevented the development of DOCA-saline hypertension in rats, but was ineffective in developed DOCA-saline hypertension. Treatment with intraventricular 6-OH-DA on rise in blood pressure was not secondary to a reduction in salt intake, however, since vehicle-treated rats given a similar reduced salt intake became fully hypertensive. The development of DOCA-saline hypertension was unaffected by pretreatment with intraspinal administration of 6-OH-DA, which produced a virtually complete loss of noradrenaline only in the spinal cord. It is suggested that brain adrenergic neurones may participate in the production of DOCA-saline hypertension but the noradrenergic projections in the spinal cords are not essential for this process.
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PMID:Effects of intraventricular and intraspinal 6-hydroxydopamine on blood pressure of DOCA-saline hypertensive rats. 48 4

Plasma catecholamine levels have been used experiemtally and clinically as the indices of the sympathetic nerve activity. We measured plasma catecholamines using high pressure liquid chromatography in rats to assess the significance of plasma catecholamines as an index of the sympathetic nerve activity and its role in hypertension. Pentobarbital anesthesia depressed plasma catecholamine levels, especially plasma adrenaline. Sodium loading for 5 weeks suppressed plasma noradrenaline, while administration of furosemide (1 mg/kg) produced the elevation of plasma noradrenaline. Experimental hypertension, one-kidney and two-kidney types of Goldblatt hypertension and DOCA-salt hypertension, raised plasma noradrenalines both in acute and chronic phases. The infusion of pressor doses of angiotensin II suppressed plasma noradrenaline by the reflex mechanism. Sar1, Ile8-angiotensin II and SQ 14,225 did not suppress plasma cathecholamine elevation due to hemorrhage. L-Hydroxyldopamine produced elevation of plasma catecholamines in experimental nypertension and controls in rats. After adrenal demedullation, plasma noradrenaline was decreased by the administration of 6-hydroxy-dopamine. Acute reduction of circulating blood volume and blood pressure fall produced the elevation of plasma catecholamine, especially plasma adrenaline. In rats, the adrenal medulla plays an important role in the regulation of blood pressure.
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PMID:Plasma catecholamines determination using high pressure liquid chromatography and their roles in blood pressure regulation and experimental hypertension in rats. 50 4

Reserpine was administered in purpose to determine the "Noradrenaline store" in sympathetic nerve endings. The marked increase of urinary noradrenaline excretion was observed by reserpine 0.4 mg/day administration. Total amount of noradrenaline in urine for first three days of 0.4 mg/day of reserpine administration was considered as a good indicators of "Noradrenaline store". There was no difference of "Noradrenaline store" between normal and hypertensive subjects. The increase % of urinary noradrenaline was higher in labile hypertension than in established hypertension as well as in normal subjects. Though the relationship between "Noradrenaline store" or the increase % of noradrenaline and sympathetic nerve activity was not clear, it is suspected that the releasable noradrenaline in sympathetic nerve granule was higher in labile hypertension than in established hypertension or normal subjects.
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PMID:Response of urinary noradrenaline excretion to reserpine administration in normal and hypertensive subjects. 50 5

Cardiovascular control was studied in five tetraplegic patients with physiologically complete cervical spinal cord transections. All had been injured less than two weeks previously and were in spinal shock. Blood pressure, heart rate, and plasma noradrenaline and adrenaline were measured at rest and during and after bladder stimulation and application of cold stimuli to skin below the level of the lesion. In three patients the cardiovascular responses to intravenously infused 1-noradrenaline and to the Valsalva manoeuvre were recorded. Measurements were also made in six chronic tetraplegic patients (in whom reflex spinal cord activity had returned) at rest, and during and after bladder stimulation, and in six normal subjects at rest. Average resting blood pressure in the recently injured tetraplegics was 130/57 (mean 81) mmHg, in the chronic tetraplegics 107/55 (mean 73) mmHg and in normal subjects 122/82 (mean 95) mmHg. Average resting heart rate was 64, 73 and 77 beats/min in the three groups respectively. Resting plasma noradrenaline and adrenaline levels in both the recently injured and chronic tetraplegics were lower than than in normal subjects. In the recently injured tetraplegics bladder stimulation caused minimal changes in blood pressure, heart rate and plasma noradrenaline and adrenaline levels. In the chronic tetraplegics similar stimulation caused marked hypertension, bradycardia and elevation in plasma noradrenaline but not adrenaline levels. Cold stimuli in the recently injured tetraplegics did not change blood pressure or heart rate. In the recently injured tetraplegics intravenous infusion of 1-noradrenaline resulted in greater elevation in blood pressure than normal. There was a decrease in heart rate. One patient was able to perform the Valsalva manoeuvre. His blood pressure responses were consistenly abnormal ('blocked' Valsalva).
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PMID:Cardiovascular control in recently injured tetraplegics in spinal shock. 50 51

The activity of the adrenaline-forming enzyme, phenylethanolamine-N-methyltransferase (PNMT) and the levels of the catecholamines dopamine, noradrenaline and adrenaline were determined during the development of the DOCA-salt hypertension in selective areas of the rat brain stem and hypothalamus. Increases in PNMT activity were restricted to the A1 area and locus coeruleus after 2 weeks of DOCA-salt treatment and were extended to the A2 area after 9 weeks of treatment. Adrenaline concentrations were higher in these areas only after 9 weeks of treatment. Noradrenaline levels did not change, except in the nucleus tractus commissuralis. Dopamine levels were unchanged at all times and in all structures studied. These results implicate brain stem adrenaline neurons in the central response which occurs during the DOCA-salt experimental hypertension.
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PMID:Brain catecholamines during development of DOCA-salt hypertension in rats. 50 25

The effect of acute hypertension and hypotension on serum TSH concentration was studied in anesthetized male rats. I.v. infusions (10 and 30 min) of Na-nitroprusside and dihydralazine induced a profound hypotension, and angiotensin amide and noradrenaline increased blood pressure, but none of the treatments significantly modified serum TSH concentrations. Also clonidine and noradrenaline, when given i.p., caused hypertension, but again the increase of serum TSH levels was not consistent. When the whole material was analysed, there was a scarcely significant correlation between the change of blood pressure and the change of serum TSH level. It is inferred that the drugs affecting TSH secretion, do not exert their action solely by changing the blood pressure.
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PMID:Effects of acute hypotension and hypertension on serum TSH concentrations in male rats. 52 73

The central noradrenaline (NA) and adrenaline (A) turnover in 15--16-week-old stroke prone, spontaneously hypertensive (sp-SH) female rats in an advanced stage of hypertension was found to differ from that of normotensive Wistar-Kyoto (WKy) control rats. The catecholamine (CA) levels were measured after inhibition of dopamine-beta-hydroxylase (DBH) or phenylethanolamine-N-methyltransferase (PNMT). in the hypertensive rats the dopamine (DA) and NA levels and the NA turnover were reduced in the hypothalamus, while in the dorsal part of the caudal medulla oblongata NA levels and A turnover were reduced. Changes in hypothalamic DA and NA mechanisms and in A mechanisms in medulla oblongata may therefore be of importance in the blood pressure regulation of sp-SH rats.
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PMID:Catecholamine turnover changes in hypothalamus and dorsal midline area of the caudal medulla oblongata of spontaneously hypertensive rats. 53 May 33

1. Twelve subjects (mean age 46.3 +/- 12.5 years) with mild to moderate hypertension were studied before, during and after bicycle ergometer exercise. 2. Baroreflex sensitivity was determined by the Oxford phenylephrine method; sensitivity at rest was inversely related to intra-arterial pressure and age. Age and resting arterial pressure were not related. 3. Exercise for 5 min at 50 W and 5 min at 75 W raised the mean arterial pressure from 116.4 +/- 18.0 to 150.0 +/- 25.4 mmHg, the heart rate from 73.2 to 126.7 beats/min and the plasma noradrenaline from 541 +/- 142.7 to 1309.8 +/- 543.5 pg/ml (P less than 0.001). 4. The increase in noradrenaline during exercise and the maximum mean pressure achieved were inversely related to resting baroreflex sensitivity (r = -0.68 and -0.77 respectively). Resting values of noradrenaline were not related to baroreflex sensitivity, age, or resting blood pressure. 5. It is possible that the rise in both plasma noradrenaline and arterial blood pressure produced by exercise is controlled by the baroreceptor reflexes; these are less effective in hypertensive subjects and thus the increases in noradrenaline and arterial pressure during exercise are greater in subjects with raised blood pressure.
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PMID:Baroreflex control of blood pressure and plasma noradrenaline during exercise in essential hypertension. 54 Apr 26

1. Neonatal sympathectomy with 6 hydroxy-dopamine (6-OHDA) was used as a tool to assess the significance of an increased sympathetic vascular tone for the development of high blood pressure in stroke-prone spontaneously hypertensive rats. After administration of 6-OHDA the rise in blood pressure was blunted for the following 9 weeks until innervation was re-established. 6-OHDA-treated rats retained more sodium and had larger plasma and blood volumes than sham-treated rats. 2. Catecholamines in plasma were increased 2-10-fold immediately after sympathectomy, but their concentrations were subnormal on day 7. Eight weeks after sympathectomy plasma noradrenaline and dopamine were not elevated, but plasma adrenaline has increased twofold. 3. The reactivity of resistance vessels to noradrenaline was markedly enhanced and the neuronal uptake and metabolism of noradrenaline were still reduced 8 weeks after neonatal sympathectomy. 4. These results confirm the significance of an intact sympathetic nervous system for the development in these rats. Sodium retention and increased plasma and blood volume may be considered as a compensatory mechanism for the vasodilatation resulting from decreased vasomotor tone.
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PMID:Effect of neonatal sympathectomy by 6-hydroxydopamine on volume and resistance regulation in stroke-prone spontaneously hypertensive rats. 54 Apr 31


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