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

Epinephrine is routinely used as a marker for intravascular injection during administration of regional anesthesia. The cardiovascular response of patients on beta-blockers to such a test dose has been reported to be unpredictable. We investigated this interaction by administering 15 micrograms of epinephrine intravenously to 6 healthy volunteers 39 to 48 years old before and after beta-blockade, accomplished by intravenous injection of propranolol, 0.04 mg/kg. Epinephrine administration caused a 20 +/- 4% (mean +/- SEM) increase in heart rate before beta-blockade but a 38 +/- 3% reduction after beta-blockade. The lowest heart rate recorded was 28 beats/min. We conclude that, in middle-aged beta-blocked men, intravenous injection of a standard epinephrine-containing test dose will predictably cause significant hypertension followed by marked bradycardia.
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PMID:Epinephrine-containing test dose during beta-blockade. 167 42

Persistent intraocular hypertension followed attack of acute angle-closure glaucoma in 87 eyes of 71 patients. After 1-12 days, averaging 2.1 days, they were treated with sublamellar sclerotomy for initial drainage of aqueous, and then sclerectomy and trabeculectomy were performed for longterm hypotensive effect. No intra- or post-operative serious complications occurred and the anterior chamber reformed within 48 hours, while in all 20 controls the filling of anterior chamber was delayed. This modality of treatment had the advantage of combining immediate relief of critical IOP with permanent aqueous filtration.
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PMID:[Treatment of persistent intraocular hypertension after attack of acute angle-closure glaucoma]. 181 21

Radiotracer methods were used to measure the rates of regional release of adrenaline and noradrenaline into plasma in man. This was done as a partial test of a theory of essential hypertension pathogenesis which envisages an important cotransmitter function for neuronally released adrenaline. In healthy resting men no release of adrenaline could be detected from the heart, lungs or liver. Adrenaline was released into the right renal vein but an adrenal medullary source is suspected. With the relatively limited activation of the cardiac sympathetic outflow which accompanied mental challenge and isometric exercise, cardiac adrenaline release remained undetectable. During supine bicycle exercise, which increased cardiac noradrenaline release 10-30 fold, to a mean value of 197 ng/min, cardiac adrenaline release averaged 2.36 ng/min. In two clinical conditions associated with persistently elevated plasma adrenaline concentrations, cardiac failure and adrenaline-secreting phaeochromocytoma, regional release of adrenaline was clearly evident. Thus, in normal man during exercise, and in patients with cardiac failure at rest, adrenaline is released from non-adrenal sources, and probably from sympathetic nerves. Whether neuronal adrenaline release of the degree found would be sufficient to facilitate noradrenaline release, augment sympathetically-mediated cardiovascular responses and contribute to the development of arterial hypertension remains to be tested.
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PMID:Is adrenaline released by sympathetic nerves in man? 182 56

In 20% of cases, essential hypertension is of high renin pathogenesis which is indifferent of that of renal lesions. In these patients high blood pressure is closely related to high aldosterone generation due to elevated angiotensin II levels. Adrenal blood portalization is a possible way of abolishing secondary aldosteronism and hyperreninemia in this case. With this, 90-98% aldosterone and 20-30% renin are inactivated, which served as the basis for bilateral electrocoagulation of adrenal central veins in 13 patients with permanent and malignant arterial hypertension. The renin-dependent pattern of essential hypertension was confirmed by a positive BP response to a tested captopril dose (25 mg), the vasorenal one was ruled out on the basis of the peripheral captopril test, captopril pharmacorenography. Bilateral electrocoagulation of adrenal central veins was performed during a phlebographic examination. The manipulation proved to be successful on 11 (85%) left and 9 (70%) right adrenals. Blood pressure became lower in the first day and stable on days 4-5. There was a significant decrease in blood pressure at a year follow-up, in increased aldosterone levels, plasma renin activity with unchanged adrenocorticotropic hormone concentrations. After the manipulation, 2 patients refused to take antihypertensive drugs, 11 patients received lower doses of drugs. The method for abolishing secondary aldosteronism is considered to be promising for further clinical studies. A special attention should be given to patients with diseases concomitant with essential hypertension who have no alternative to surgical treatment.
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PMID:[The x-ray endovascular treatment of renin-dependent arterial hypertension with secondary aldosteronism in patients without vasorenal involvement]. 187 22

The paraventricular hypothalamus regulates autonomic nerve outflow and is innervated with beta-endorphin-immunoreactive nerve terminals. This study examined the effects of beta-endorphin microinjected into the paraventricular hypothalamus on blood pressure, heart rate, and plasma catecholamine and glucose concentrations in conscious, unrestrained spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats at the age of about 9 weeks. Thirty minutes after paraventricular hypothalamic injection of [125I] beta-endorphin (3.5 micrograms), most of the recovered radioactivity was detectable within +/- 0.5 mm from the injection site in the coronal, sagittal, and horizontal planes. Unilateral paraventricular hypothalamic injections of beta-endorphin (1 and 0.1 microgram/0.1 microliter) increased blood pressure and heart rate in both strains in a dose-independent manner with significantly greater increases in SHR. Plasma catecholamine and glucose concentrations were measured 15, 30, and 60 minutes after beta-endorphin injection. Norepinephrine concentrations were not significantly altered in WKY rats but increased in SHR. Epinephrine concentrations increased in both strains with significantly greater increases in SHR. Increases in catecholamine concentrations were not dose-related. Glucose concentrations also increased in both strains with significantly greater increases in SHR only at the lower dose. Ganglionic blockade with pentolinium significantly reduced beta-endorphin-induced pressor and tachycardiac responses in SHR. Pretreatment of the paraventricular hypothalamus with naltrexone (1.1 micrograms) in SHR blocked the initial pressor and tachycardiac responses to beta-endorphin (0.1 microgram) and blunted increases in epinephrine and glucose levels. When the animals were anesthetized with alpha-chloralose 2-5 days after the study in conscious animals, there were no differences in blood pressure or heart rate between strains after beta-endorphin (0.1 microgram) injection. The results indicate that conscious SHR show enhanced cardiovascular and sympathoadrenal responses to beta-endorphin injected into the paraventricular hypothalamus, suggesting that alterations in the activity of the paraventricular hypothalamic beta-endorphin system can modulate the development of hypertension in SHR.
Hypertension 1991 Oct
PMID:Sympathoadrenal control by paraventricular hypothalamic beta-endorphin in hypertension. 191 93

The potential role of adrenaline, both circulating and in the central nervous system, in the maintenance of high blood pressure was examined in stroke-prone spontaneously hypertensive rats (SHRSP). alpha-Monofluoromethyldopa, a long-lasting inhibitor of dopa decarboxylase, was used to induce rapid depletion of central and peripheral catecholamine stores. Subsequent inhibition of phenylethanolamine-N-methyltransferase (PNMT) allowed the gradual restoration of dopamine and noradrenaline but not adrenaline, resulting in a greater relative depletion of adrenaline. Adrenaline was almost totally depleted in the circulation and peripheral tissues. The resting level of blood pressure, however, was unaffected, excepting after administration of a vasopressin (AVP) antagonist. Moreover, there was no reduction in the magnitude of acute pressor responses to electrical stimulation of the rostral ventrolateral medulla oblongata (C1 area), despite extensive loss of adrenaline from the brainstem and spinal cord. The results suggest that adrenaline contributes to the resting level of blood pressure but that its loss can be offset by the pressor activity of AVP. Thus neither central nor peripheral adrenaline stores appear to be essential for the maintenance of hypertension or for centrally-evoked vasoconstriction in adult SHRSP.
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PMID:Effects of depleting central and peripheral adrenaline stores on blood pressure in stroke-prone spontaneously hypertensive rats. 194 21

1. The effects of adrenal demedullation and subcutaneous depots of adrenaline, on hypertension development and vascular reactivity, were determined in young spontaneously hypertensive rats (SHRs). 2. Plasma adrenaline, but not noradrenaline, was significantly lower in all 16-week-old demedullated SHRs, irrespective of the time of demedullation. However, hypertension development was attenuated only in SHRs demedullated at 6 weeks of age or younger. 3. Adrenaline depots restored hypertension development in SHRs demedullated at 4 weeks, irrespective of the time of depot implantation, but were without effect in sham-operated rats. 4. Pressor responses to exogenous noradrenaline, in isolated perfused mesenteric arteries from 16-week-old demedullated and sham-operated SHRs and those treated with adrenaline depots, did not differ significantly. Maximal neurogenic pressor responses were, however, reduced in mesenteries from all demedullated rats, including those treated with depot adrenaline. Adding adrenaline to the perfusate facilitated neurogenic responses only. 5. Thus, the adrenal medulla appears to be involved in modulating sympathetic neurogenic vasoconstriction. The nature of this sympathoadrenal interaction and its role in the early development of hypertension in the SHR is unclear and is not explicable simply in terms of a facilitation of sympathetic neurogenic responses by adrenaline.
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PMID:Effect of adrenal demedullation and adrenaline on hypertension development and vascular reactivity in young spontaneously hypertensive rats. 203 Jan 6

We report a case of adrenal myelolipoma with multiple calcification and hypertension. A 69-year-old woman visited our hospital with a complaint of right flank pain. Computed tomography demonstrated a right adrenal tumor which was a spherical mass with fat density and multiple calcification. Adrenal scintigraphy of I-131 adosterol demonstrated predominant accumulation of the right adrenal gland. Selective venous sampling disclosed a high aldosterone level (303.7 ng/dl) from the affected side. Right adrenalectomy was performed. Pathological diagnosis revealed adrenal myelolipoma with calcification. After the operation the patient became normotensive. The characteristics of the 12 cases of myelolipoma with calcification we found in the Japanese literature are also briefly reviewed.
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PMID:[Multiple calcified adrenal myelolipoma suggestive of association of primary aldosteronism: report of a case]. 204 94

Among 436 patients with hypertension unrelated to any renal lesion, renovascular damage, pheochromocytoma, Cushing's syndrome or hyperthyroidism, 15 patients had low plasma renin activity (PRA) and elevated plasma aldosterone concentrations in the upright position and resultant high aldosterone/PRA ratios: 8 with aldosterone-producing adenoma (APA; group 1) and 7 with idiopathic hyperaldosteronism (IHA; group 2). Thirty-nine patients had suppressed PRA in the presence of normal plasma aldosterone levels and moderately elevated aldosterone/PRA ratios (group 3). Thirty of them had elevated plasma 11-deoxycorticosterone (DOC) and 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) concentrations (group 3a) and 9 of them had normal levels of those mineralocorticoids (group 3b). The rest of them (382 patients) had low aldosterone/PRA ratios (group 4). Adrenal scintigraphy with dexamethasone pretreatment revealed [13I]-cholesterol accumulation not only in patients with APA (unilateral) or IHA (bilateral), but also in patients of group 3a (bilateral). In patients in groups 3a and 3b adrenal size (especially thickness), as measured by computed tomography (CT scan), was enlarged, as in patients with IHA (group 2), and was significantly greater than in patients of group 4 (p less than 0.001). Spironolactone reduced blood pressure in all tested patients of group 3a, and the removal of adrenal tumor or hyperplastic tissue normalized blood pressure in patients of groups 1, 2 and 3a. Excised adrenal glands exhibited cortical hyperplasia with or without nodular hyperplasia in patients of group 3a. Good agreement was found between the actual size of the excised tissue and the measurement obtained by CT scan. Since beta-endorphin and beta-lipotropin were depressed in patients of group 3a, it is suggested that an unknown pituitary substance stimulates the adrenal cortex to release too large amounts of DOC and 18-OH-DOC and inappropriate secretion of aldosterone.
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PMID:Inappropriate elevation of the aldosterone/plasma renin activity ratio in hypertensive patients with increases of 11-deoxycorticosterone and 18-hydroxy-11-deoxycorticosterone: a subtype of essential hypertension? 207 Mar 75

Adrenal lymphangiectatic cyst is a very rare pathological and clinical disease entity, and its clinical silence and lack of characteristic symptoms and signs makes it difficult to diagnose preoperatively. We experienced a case of adrenal lymphangiectatic cyst, accompanied by severe refractory hypertension, which was corrected by surgical removal of the cyst. We report it with a review of the literature.
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PMID:A case of adrenal lymphangiectatic cyst associated with severe hypertension. 209 94


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