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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adrenaline, noradrenaline and dopamine excretion was investigated in essential hypertension (n = 20), atherosclerotic heart failure (n = 20, NYHA class II and III), chronic angina (n = 10) and in healthy controls, in four time intervals: between 600-1200, 1200-1800, 1800-2400, 2400-600. Fluorimetric method of Anton and Sayre was employed. In patients with essential hypertension the circadian rhythm of adrenaline, noradrenaline and dopamine excretion was maintained but in all time intervals excretion of dopamine was decreased. In individuals with congestive heart failure due to atherosclerosis and in patients with ischemic heart disease, physiological circadian rhythm of adrenaline and noradrenaline excretion was found to be abolished. This was not the case with dopamine excretion which was undisturbed.
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PMID:[Hypertension, heart failure and angina pectoris. Diurnal rhythm of urinary excretion of catecholamines]. 164 Jun 65

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

Hydrodynamics of the eyes was investigated in 57 patients with exophthalmos, with various degree of infiltrative changes. Open angle glaucoma was not found in any case. In 12 eyes (10.5 p.c.) one observed a raised IOP (over 21 mm Hg)--checked by means, of an applanation tonometer with the patient looking straight on; in 24 eyes (18.4 p.c.) the IOP was near the upper limit of the normal pressure. Characteristic for glaucoma pathological changes of the optic disc and the visual field were absent in examined patients. All of them had the filtration angle open. The authors found a statistically significant dependency between the IOP and the degree of changes in the motor muscles, conjunctival tissue and in the lids. The authors suggest that the changes in the intraocular pressure have an external cause and stem from the disturbances of the venous circulation with exclusion of the primary hypertension.
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PMID:[Ocular hydrodynamics in patients with infiltrative-edematous exophthalmos in Graves' disease]. 209 Aug 72

We followed the changes in blood pressure (BP) after discharge from the hospital in 32 patients with essential hypertension whose BP was normalized on a diet containing 7g/day of NaCl during hospitalization. They were divided into two groups on the basis of BP changes: 18 patients whose BP values were elevated by more than 10% after discharge (group I; mean +16.9%, P less than .01) and the remaining 14 patients (group II; -3.6%, P = NS). Urinary Na excretion (UNaV) in Group I patients increased markedly after discharge (83 v 189 mu Eq/min, P less than .001) while it did not change in Group II (122 v 102 mu Eq/min, P = NS), resulting in a greater postdischarge UNaV in group I than in group II (P less than .01). The changes in BP were positively correlated with the overall changes in UNaV (r = 0.45, P less than .01). Plasma epinephrine after discharge was higher in group I than in group II (31 v 18 pg/mL, P less than .05). Thus, increases in NaCl intake seem to play an important role in BP elevation after discharge. Adrenal medullary function may partly contribute also to the BP elevation.
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PMID:Factors participating in blood pressure elevation after discharge from the hospital in patients with essential hypertension. 235 Apr 78

Adrenal venous sampling of blood was performed for nine patients with aldosterone-producing adenoma (APA). Measurement of adrenal venous aldosterone is useful for localization of APA but difficult, because catheterization of the right adrenal vein is not easy, and the blood is diluted by nonadrenal flow. To solve these problems, levels of aldosterone (A; ng/dl) and cortisol (C; micrograms/dl) were measured in samples from the left adrenal vein (LAV) and the inferior vena cava (IVC), and the LAV A/C and (LAV A/C)/(IVC A/C) ratios were calculated. These ratios were also obtained for 16 patients with essential hypertension. The adenoma could be localized in three of the nine cases by the measurement of aldosterone alone, but the use of a LAV A/C ratio greater than 5 x 10(-3) and a (LAV A/C)/(IVA A/C) ratio less than 1.0 as criteria separated the patients into those with a left APA, right APA, or essential hypertension. Consequently, adrenal venous sampling and the calculation of these ratios enables preoperative localization of APA with more accuracy, especially when the tumor is small or the result of CT and adrenal scintigraphy is not consistent.
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PMID:Localization of aldosterone-producing adenoma: venous sampling in primary aldosteronism. 238 50

Administration of 10 micrograms of substance P intrathecally to the spinal T9 level of the adult rat, anaesthetized with urethane, provoked an increase in free catecholamines in plasma taken from the inferior vena cava. Adrenaline levels at 1 min after administration were 154.8 +/- 10.8% (mean +/- SE; n = 11) of preadministration levels and noradrenaline levels were 153.5 +/- 11.8% of preadministration levels. Differences between the values of free catecholamines in animals given substance P vs those given vehicle only were statistically significant at 1 and 10 min postinjection, but not at 30 min. Administration of a substance P analogue with central antagonistic properties 15 min before substance P was given prevented expression of the effects of substance P. These results suggest that substance P may be an excitatory chemical mediator of synaptic transmission in spinal pathways controlling adrenal medullary output. Thus dysfunction of substance P mechanisms may underlie some animal models of hypertension and may be involved in some cases of essential hypertension in man as well as in autonomic dysfunction associated with some neurological entities.
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PMID:Substance P given intrathecally at the spinal T9 level increases adrenal output of adrenaline and noradrenaline in the rat. 241 Aug 14

Plasma concentrations of atrial natriuretic factor and some vasoactive substances were determined in 8 patients with aldosterone-producing adenoma, 10 with idiopathic adrenal hyperplasia, 10 normotensive subjects and 12 patients with essential hypertension. Plasma atrial natriuretic factor concentration in patients with aldosterone-producing adenoma was the highest among the examined groups. Adrenal surgery reduced plasma concentrations of atrial natriuretic factor and aldosterone concomitant with the elevation in urinary sodium excretion, plasma renin activity and urinary sodium-to-potassium ratio. Withdrawal of trilostane (3 beta-hydroxysteroid dehydrogenase inhibitor) in patients with idiopathic adrenal hyperplasia increased plasma concentrations of atrial natriuretic factor and aldosterone, and decreased the urinary sodium-to-potassium ratio, plasma renin activity and urinary sodium excretion. However, reduced urinary sodium excretion following trilostane treatment returned to the control level successively despite the high levels of plasma atrial natriuretic factor and aldosterone. Acute infusion of saline remarkably increased plasma atrial natriuretic factor concentration in patients with idiopathic adrenal hyperplasia and aldosterone-producing adenoma. These results suggest that a high level of atrial natriuretic factor is a characteristic feature in patients with aldosterone-producing adenoma caused chiefly by the expansion of extracellular fluid volume, and circulating atrial natriuretic factor may contribute to regulation of the sodium escape phenomenon in patients with aldosterone-producing adenoma or idiopathic adrenal hyperplasia.
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PMID:The effect of adrenal surgery on plasma atrial natriuretic factor and sodium escape phenomenon in patients with primary aldosteronism. 252 99

Patients with normal- or high-renin non-modulating essential hypertension fail to shift their adrenal sensitivity on a low sodium diet in response to an infusion of angiotensin II (Ang II). In a prior study, 72 hours of converting enzyme inhibition (CEI) partially corrected this subnormal aldosterone response to Ang II in patients with non-modulating hypertension. Since it was uncertain whether the failure to restore normal adrenal responsiveness reflected a continued abnormality or an insufficient duration of CEI, the present study was performed wherein subjects were studied before CEI and then 72 hours and 6 weeks after CEI. Adrenal and renovascular responses were assessed in 13 subjects with normal- or high-renin hypertension in response to an infusion of Ang II (0.3, 1.0, and 3.0 ng/kg/min) in balance on a 10 meq Na+/100 meq K+ diet. Eight of 13 had a normal plasma aldosterone increment above control levels (greater than or equal to 15 ng/dl) and were classified as modulators; the remaining subjects (five of 13) were classified as non-modulators. Enalapril was then administered for 72 hours and 6 weeks, and the assessment of the Ang II dose-response relations was repeated. In the modulators, there was no change compared with levels before CEI in the aldosterone dose-response curve or threshold sensitivity to infused Ang II at either 3 days or 6 weeks after CEI administration. In the non-modulators, CEI for 72 hours partially restored aldosterone responsiveness, but more prolonged CEI for 6 weeks completely corrected the defect, restoring aldosterone responsiveness on a sodium-restricted diet to that seen in modulators and in normotensive control subjects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Prolonged converting enzyme inhibition in non-modulating hypertension. 253 93

The existence of facilitatory presynaptic beta-adrenoceptors has been shown in approximately 30 tissues of 6 different species including human. A positive feed back loop for further release of the transmitter appears to be activated by an endogenous agonist, epinephrine, taken up and released as a cotransmitter with norepinephrine rather than norepinephrine itself released from peripheral noradrenergic nerve terminals. Presynaptic beta-adrenoceptors are mainly of a beta 2-subtype. Some beta 1-subtype receptors are also suggested. There coexist presynaptic beta 1- and beta 2-adrenoceptors in cat and rat hypothalamus. Higher sensitivity of peripheral presynaptic beta-adrenoceptors to isoproterenol may be implicated in the early development of hypertension in SHR. Epinephrine taken up and released initiates the development of hypertension in rats via activation of these receptors. Increased activation of these receptors by epinephrine may play a role in the development of essential hypertension. The antihypertensive action of beta-antagonists may be in part due to blockade of these facilitatory presynaptic beta-adrenoceptors.
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PMID:Presynaptic beta-adrenoceptors. 287 88


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