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

The authors discuss the radiological signs in 18 patients with an adrenal tumour. 7 of them had a Cushing's syndrome, 10 others a phaechromocytoma and the last had primary hyperaldosteronism. The diagnosis was made from the history, the clinical picture, hormone estimations and pharmacodynamic tests, whilts in the majority of cases the tumour was localised by radiodiagnosis. In all cases, there was hypertension, permanent in tumours of the adrenal cortex, paroxysmal or permanent in the cases of pheochromocytomas. We emphasise the importance of retro-pneumoperitoneum, as the radiological investigation of choice, in the localisation of adrenal tumours, especially pheochromocytomas, and in Cushing's syndrome. In cases of pheochromocytoma, one should follow carefully the blood pressure, during special radiological investigations, in view of the danger of a sudden rise or fall in blood pressure, the first is treated with phentolamine, the second with noradrenaline solution. Finally, a scan using I 131 19-iodocholesterol may be valuable in diagnosis and localisation of adrenal tumours; it has in particular given very encouraging results in the differential diagnosis of adrenal tumours with the clinical presentation of Cushing's disease.
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PMID:[Radiological signs of tumours of the adrenal glands (author's transl)]. 21 64

1. Pressor responses to angiotensin II, noradrenaline and tyramine were examined in sheep prior to and during the development of corticotrophin-induced hypertension. 2. Pressor responses to angiotensin II amide did not change with corticotrophin (ACTH) administration. Small significant increases in pressor responses to noradrenaline occurred at low doses only (0.27 and 1.06 mumol/h). Significant increases in response to tyramine occurred after 24h of ACTH administration, but were not maintained after 6 days of ACTH. These changes are quantitatively small and do not suggest that changes in pressor sensitivity contribute significantly to the rise in blood pressure following ACTH administration. 3. Sodium depletion significantly reduced the pressor responses to angiotensin II amide at all doses and to tyramine in the middle range only, but did not affect the responses to noradrenaline.
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PMID:The effect of corticotrophin (ACTH) administration on the pressor action of angiotensin II, noradrenaline and tyramine in sheep. 21 61

1. Seven latent hypertensive patients and seven matched controls were subjected to standardized mental stress and orthostatic provocation. 2. Mental stress increased blood pressure by approximately 25%, heart rate by 25 beats/min, plasma glycerol by 50% and plasma cyclic AMP by 25% in both groups. Plasma glucose and renin activity were unchanged. Plasma noradrenaline and adrenaline were essentially unchanged during stress. 3. There was an insignificant tendency towards higher noradrenaline levels in latent hypertensive subjects and two of these subjects displayed an exaggerated noradrenaline response to standing. 4. Our results indicate that the physiological responses to mental stress are caused by selective neuronal activation, rather than by generalized sympatho-adrenal activation. Latent hypertension does not seem to be associated with adrenergic hyperactivity or receptor supersensitivity, except possibly in individual cases.
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PMID:Sympatho-adrenal and cardiovascular response to mental stress and orthostatic provocation in latent hypertension. 23 22

In various kinds of hypertension clonidine induced a decrease in urinary catecholamines, plasma renin activity and urinary aldosterone, concommitant with a fall in blood pressure and pulse rate in both short term and chronic studies. Furthermore, clonidine lowered the plasma levels of noradrenaline and adrenaline but a postural increase in upright position still occurred. The capacity to increase renin during salt restriction seemed mainatined. When clonidine was withdrawn all parameters returned to pretreatment levels but in some cases a marked rebound increase in catecholamine production was seen. --During clonidine the increase in catecholamines and renin after insulin induced hypoglycemia was largely abolished. Under basal conditions oral penbutolol induced a decrease of pule rate and blood pressure but no change in plasma or urinary catecholamines. During treatment plasma renin was suppressed at rest and after exercise. A work load, which led to only minor changes in blood catecholamines before treatment, was associated with a marked increase during penbutolol. Medication with penbutolol reduced the response in plasma catecholamines after hypoglycemia and renin activity remained low. Clonidine seems to act mainly by central inhibtion of symapthetic tone. Penbutolol probably acts mainly peripherally but may also have a central effect.
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PMID:The effect of clonidine and penbutolol, respectively on catecholamines in blood and urine, plasma renin activity and urinary aldosterone in hypertensive patients. 23 81

1. The concentration of catecholamines was measured in several brain areas of the Hewbrew University Sabra rat (SB rat), and in two substrains selected for their respective sensitivity (H) or immunity (N) to hypertension. 2. Hypertension was induced in SB rats by DOCA-salt, renal artery constriction and NaCl 1.7% drinking. The noradrenaline content was consistently elevated in the medulla oblongata of hypertension animals. In other brain areas the rise in noradrenaline varied in the different types of hypertension. 3. Administration of DOCA-salt to H and N rats, while causing marked hypertension in the former, had no effect on noradrenaline in either strain. 4. Untreated, normotensive N rats had in the medulla oblongata, significantly higher concentrations of noradrenaline than did H rats. 5. Differences in brain noradrenaline may explain the inherited susceptibility or resistance to hypertension in H and N rats.
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PMID:Hypertension and brain catecholamine distribution in the Hebrew University Sabra, H and N rats. 28 36

1. Vascular reactivity was studied in Tyrode solution perfused kidneys from young (7 weeks) and mature (4-6 months) spontaneously hypertensive rats (SH rats). 2. The response to nerve stimulation was greater in the kidneys from young SH rats than in those from young control rats, both in control solution and after inhibition of the disposition of noradrenaline; both groups exhibited the same sensitivity to noradrenaline, angiotensin II and barium chloride. 3. The response to nerve stimulation was normal in kidneys from mature SH rats, but responses to noradrenaline, angiotensin II and barium chloride were greater than the control. 4. Cocaine potentiated the response to nerve stimulation more in the kidneys from mature SH rats than in those from the control rats. 5. The results suggest that renal sympathetic nerves release more noradrenaline than normal in the young SH rats, which could be an important factor in causing hypertension. 6. In the established phase of spontaneous hypertension the vascular reactivity to exogenous agonists is increased, probably as a consequence of high blood pressure; the more efficient neuronal uptake causes normalization of the response to sympathetic nerve stimulation.
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PMID:Neuronal and vascular reactivity in isolated perfused kidneys during the development of spontaneous hypertension. 28 59

1. Average supine circulating total catecholamine concentrations were found to be higher than the normal range in about 50% of patients with labile hypertension and in about 30% of patients with sustained essential hypertension. 2. These higher resting concentrations were mainly due to an increase in adrenaline in labile hypertension and to an increase in noradrenaline in sustained hypertension. 3. Patients with elevated catecholamine concentrations were also characterized by a higher heart rate, by an increased myocardial contractility and by greater hypotensive response after treatment with beta-adrenoreceptor blocking agents. 4. These studies suggest the existence of sub-groups of hypertensive patients with increased sympathetic tone.
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PMID:Circulating catecholamines and systolic time intervals in labile and sustained hypertension. 28

1. Noradrenaline and adrenaline in the adrenal vein of essential hypertensive patients are almost exclusively (99%) unconjugated or free. However only 17% of dopamine is free, the rest is conjugated. The further the site of sampling from the adrenal vein the closer come the free catecholamines to their normal peripheral venous proportion (noradrenaline + adrenaline 20%, dopamine less than 1% of total catecholamines). Deviations from these patterns help to detect the site and type of secretion of phaeochromocytoma. 2. Essential hypertensive patients have, compared with control subjects, higher conjugated plasma dopamine, less urinary free and conjugated dopamine with blunted urinary free dopamine and sodium responsiveness to frusemide. Conjugated noradrenaline + adrenaline, mean arterial pressure and age are positively interrelated. 3. Patients with primary aldosteronism have elevated plasma and urinary total dopamine. After removal of the adenoma urinary dopamine excretion decreases to normal. 4. Elevated conjugated dopamine appears to reflect a compensatory activation of the dopaminergic vasodilator pathway in hypertension, the total urinary dopamine excretion an intrinsic deficiency or compensatory increase of a dopamine-modulated natriuretic mechanism.
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PMID:Free and conjugated catecholamines in human hypertension. 28 3

Changes in the axial position of the left upper incisor in response to loading by 5-20 g were measured with ultrasonic technique in anesthetized rabbits. The time-response of the load-induced intrusion described a biphasic curve, with a steep initial part followed by a slower part. Maximum amplitudes after 20 s increased with increasing loads. A rise in arterial blood pressure (aortic balloon inflation) resulted in extrusion, while i.v. injection of noradrenaline or papaverine caused intrusion and extrusion, respectively. The responses to loading and changes in blood pressure were largely unaffected by transection of the root, but the effects of pressure changes were severely diminished by local infiltration of the periodontium with noradrenaline. Participation of periodontal blood vessels in the damping of load-induced intrusion was excluded by the finding of roughly equal intrusion curves at low, normal and high blood pressure and up to 38 h after death. We conclude that the resting position of the rabbit's incisor is greatly influenced by arterial blood pressure, via the periodontal vessels. The intrusion in response to loading by up to 20 g is resisted by periodontal fibers only, the blood vessels or the pulpal and periapical tissues and pressure taking no part.
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PMID:Influences of axial load and blood pressure on the position of the rabbit's incisor tooth. 29 Jan 25

The influence of intravenous injection of Prostacyclin (PGI2) on systemic blood pressure was investigated in conscious and anaesthetized hypertensive rats. PGI2 in doses of 1.0, 5.0 and 10.0 micrograms/kg showed a dose dependent antihypertensive effect in conscious rats with spontaneous and chronic renal hypertension. A similar response could be demonstrated in conscious rats with normal blood pressure with doses of 1.0, 10.0 and 100.0 micrograms/kg. In anaesthetized rats with acute renal hypertension or blood pressure increase, induced by continous infusion of Angiotensin II or Norepinephrine, PGI2 caused a marked decrease of blood pressure. PGI2 induced an increase of plasma renin activity in anaesthetized rats with doses of 0.1, 1.0 and 10.0 micrograms/kg. These findings support the suggestion of an antihypertensive role for PGI2 in experimental hypertension.
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PMID:Antihypertensive effect of prostacyclin (PGI2) in experimental hypertension and its influence on plasma renin activity in rats. 36 7


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