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

Plasma noradrenaline and plasma renin activity were measured as indices of sympathetic activity and renin angiotensin system in similar groups of hypertensive patients receiving either propranolol, bendrofluazide or methyldopa. Plasma renin activity was similar in the propranolol and methyldopa groups and significantly lower (p less than 0.01) in both these groups than the diuretic treated subjects. Plasma noradrenaline was significantly lower (p less than 0.01) on methyldopa than either propranolol or bendrofluazide. These different effects on the renin angiotensin system and the sympathetic nervous system of these drugs may be relevant in the choice of long term therapy in hypertension.
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PMID:Sympathetic nervous function and renin activity in hypertensives on long term drug treatment with propranolol, methyldopa or bendrofluazide. 75 41

Neonates of male stroke-prone spontaneously hypertensive rats (SHRSP) were treated with 6-hydroxydopamine (6-OHDA) on two different schedules. Peripheral sympathectomy, which was evaluated by the pressor response to exogenous noradrenaline (NA) or by the decrease in NA content of the spleen, was more evident in the NB-8 group (treated on 8th and 15th day after birth) than in the NB-1 group (treated at 6, 24 and 72 h after birth). The reduction of the NA content in the cerebral cortex was more prominent in the NB-1 group than in the NB-8 group. The blood pressure from 7 to 23 weeks of age was lower in the treated groups: NB-8 less than NB-1 less than control. Therefore, the reduction of blood pressure in the treated groups could be related to the severity of peripheral sympathectomy. The incidence of sroke was also lower in the treated groups: 38, 11 and 0% in the control NB-1 and NB-8 groups, respectively. Loading with 1% NaCl solution from 11 weeks of age enhanced the rise in blood pressure and increased the incidence of stroke in each group of rats: 100, 20 and 40% in the control. NB-1 and NB-8 groups, respectively. However, the onset of stroke after exhibiting a severe hypertension (greater than 200 mmHg) was delayed in the treated groups. It seems that the activated tone in the peripheral sympathetic nerve is likely to participate in the development of spontaneous hypertension. In addition to the high blood pressure level, the activated tone of sympathetic nerve innervating the cerebral vasculature may be partly involved in the development of stroke in the new strain of the SHR rats, SHRSP.
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PMID:Effects of chemical sympathectomy on hypertension and stroke in stroke-prone spontaneously hypertensive rats. 75 97

In Europe, about 1% of the women using oral contraceptives develop hypertension. Predisposing factors seem to be age, hypertension problems in past pregnancies, family history of hypertension, personal histories of kidney disorders, diabetes mellitus or adipositas, or diastolic pressure over 80 mm Hg. An overactive renin-angiotensin-aldosterone system may be an important factor in the etiology of this type of hypertension. Oterh possible factors are: reduced excretion of angiotensin 2, increased sensitivity of the arterioles to substances such as angiotensin 2 and noradrenaline, direct effect of ethinyl estradiol and mestranol on the sodium and water system, cardiovascular changes, disorders in the adrenergic system (e.g., catecholamine metabolism). Blood pressure should be checked before beginning any treatment with oral contraceptives and every 3 months after that. For the purpose of differential diagnosis angiotensin 2 in the plasma and catecholanin and its by-products should be checked (24-hour urine samples). In cases of serious hypertension hormone therapy should be discontinued at once. Primary aldosteronism and renal artery stenosis must be excluded in the differential diagnosis, for although these hypertensive disorders exhibit similar biochemical changes, they should be treated by surgical intervention. Usually hypertension is reversible after cessation of therapy with contraceptive steroids. However, some cases of irreversible hypertention, kidney failure, and malignant nephrosclerosis have been described. Hypertensive somen who wish to use oral contraceptives may, under medical supervision try a modified hormonal contraceptive (minipill without estrogen) or sequential or lower dosages.
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PMID:[Clinical aspects of hypertension under contraceptive steroids]. 79 66

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).
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PMID:Brain-stem structures and catecholamines in the control of arterial blood pressure in the rat. 79 55

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.
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PMID:Interaction of dopamine, methyldopa and reserpine in the sympatho-adrenal system in essential hypertension. 79 57

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.
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PMID:Effect of oxprenolol on catecholamines and plasma renin activity: acute response to frusemide in hypertensive patients. 80 48

Phentolamine, dihydroergocristine and isoxsuprine were compared for their effects on the blood pressure in anaesthetized normotensive rats, in rats made hypotensive by ganglionic blockade or by pithing and in rats with noradrenaline-induced hypertension. Their ability to inhibit pressor responses elicited by electrical stimulation of the posterior hypothalamus and of the sympathetic outflow from the spinal cord was also investigated. All three drugs appeared very potent in inhibiting noradrenaline-induced hypertension and caused a dose-dependent fall in blood pressure in normotensive rats, which however was less pronounced with dihydroergocristine than with phentolamine and isoxsuprine. In hypotensive rats, dihydroergocristine caused a rise in blood pressure. At higher doses than those required to block noradrenaline-induced hypertension, the three drugs inhibited pressor responses elicited by electrical stimulation and were equally active on peripherally- and centrally-evoked responses. Simultaneous recording of heart rate and blood pressure, both in anaesthetized and in pithed rats, indicated a reflex origin for phentolamine-induced tachycardia and a direct cardiac stimulation for isoxsuprine. Reflex changes of heart rate were not observed with dihydroergocristine.
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PMID:Effects of phentolamine, dihydroergocristine and isoxsuprine on the blood pressure and heart rate in normotensive, hypotensive and hypertensive rats. 81 97

In five baboons and 11 cats cerebral ischaemia was produced either by inflating an epidural balloon and or by ligating major arteries supplying the brain. Fifteen of the animals developed intracranial hypertension after cerebral ischaemia. If ICP were high, but still significantly lower than MABP, elevation of MABP by noradrenaline infusions was accompanied by a proportional increase of ICP. However, the increase of ICP was lower than that of MABP so that CPP was raised. CBF measured by the 133Xenon clearance technique was significantly increased by arterial hypertension in eight cases. The proportional increase of CPP and CBF by elevation of arterial blood pressure was substantially greater, the lower ICP was immediately after ischaemia. There was no effect of MABP in cases in which ICP equalled MABP.
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PMID:Effect of systemic arterial blood pressure on cerebral blood flow in intracranial hypertension. 81 13

Using specific anesthetic agents, permanent segmental occlusion of the proximal middle cerebral artery (MCA) causes ischemic infarction limited to the putamen and other deep hemispheral structures in primates. Using this model, 25 rhesus monkeys were subjected to acute arterial hypertension before, during and up to 5 days after onset of MCA occlusion in order to reevaluate the possible role of the ischemic process in pathogenesis of cerebral hemorrhage. Norepinephrine infusion induced prompt rapid rise in mean arterial pressure (MAP) and intracranial pressure (ICP) limited to the duration of infusion. This procedure produced acute ischemic lesions which were totally bland but topographically more extensive than untreated controls; in chronic lesions, however, deep nuclear masses showed hemorrhagic infarction. Animals given 5% CO2 air had slowly progressive elevation in ICP and MAP. Acute specimens showed intact, widely-dilan hypercarbia was induced 5 days after MCA occlusion, animals developed intracerebral hematoma involving putamen, external capsule and claustrum, occasionally dissecting through to ipsilateral ventricle. In acute cerebral ischemia, elevated MAP produced only quantiative changes in lesion size. In the vasoproliferative stages of mature infarction, MAP elevation induced by a cerebral vasoconstrictor caused hemorrhagic infarctions while cerebral vasodilation caused intracerebral hematomas.
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PMID:Primate model of cerebral hematoma. 82 36

1. Renal prostaglandins act primarily as local hormones, having their effects at, or near to, sites of synthesis. PGE2 is a major determinant of renal vascular reactivity; it opposes the vasoconstrictor and natriuretic actions of pressor hormones and brakes the release of noradrenaline from adrenergic nerves. In the unanaesthetized rabbit prolonged inhibition of prostaglandin synthesis results in hypertension. In the rat, however, renal prostaglandins augment pressor stimuli. 2. Basal efflux of renal prostaglandins is positively correlated with blood flow to the inner cortex and medulla. Those stimuli which increase renal medullary blood flow do so primarily by activating prostaglandin synthetase. 3. Kinins increase prostaglandin synthesis which action modifies the renal effects of kinins. Thus, one or more renal prostaglandins contribute to the renal vasodilator action of bradykinin and mediate its effect on excretion of water as well as possibly attenuating the natriuretic action of the polypeptide. Kinins in addition to stimulating prostaglandin synthesis may determine the principal product of synthetase by regulating the enzyme PGE 9-ketoreductase, which converts PGE to PGF. The coupling of these systems within the kidney appears unique--prostaglandins mediate some of the actions of kinins and modulate others, whereas they depend on the intrarenal generation of kinins to set their level and type of activity.
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PMID:Renal prostaglandins. 82 36


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