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

Adrenal responsiveness to angiotensin II (AII) and the diastolic blood pressure responses to saralasin were studied in 19 patients with high renin essential hypertension (HREH) on a 10-meq Na(+)/100 meq K(+) diet. The increment in plasma renin activity (PRA) between supine and upright positions was used as an estimate of the acute stimulation of the adrenal gland by endogenous AII; the normal increment in plasma aldosterone divided by the increment in PRA was >3.8. 7 of 19 had abnormal upright posture responses with significantly greater mean PRA increments (24+/-6 ng/ml per h) and significantly smaller plasma aldosterone increments 47 +/- 16 ng/dl) (P < 0.036) compared to the increments observed in HREH patients with normal adrenal responsiveness (PRA = 15 +/- 1 ng/ml per h; plasma aldosterone = 87 +/- 17 ng/dl). When AII was infused at doses of 0.1-3 ng/kg per min, only patients with normal posture responses had normal plasma aldosterone increments; plasma aldosterone levels failed to significantly increase even at the highest infusion rate in the patients with the abnormal upright posture responses. The AII competitive inhibitor, saralasin (0.3-30 mug/kg per min) was then infused to study the occurrence of angiotensinogenic hypertension in both HREH subgroups. The mean decline in diastolic blood pressure to saralasin in the subnormal adrenal responsive patients (-15 +/- 3 mm Hg) was significantly greater than in the normal adrenal responsive group (-3 +/- 2 mm Hg) (P < 0.02).It is concluded that patients with HREH are not a homogeneous population; approximately one-third have AII-dependent hypertension. In these patients, the mechanism responsible for the elevated renin and blood pressure could be a compensatory increase secondary to decreased adrenal responsiveness to AII. In the remainder, the high PRA levels have little, if any, causal role in the pathogenesis of the hypertension but could reflect a marker of other pathophysiologic processes.
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PMID:Abnormal adrenal responsiveness and angiotensin II dependency in high renin essential hypertension. 50 Aug 10

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

3 cases of adrenal cysts are reported. The incidence of cyst originating in the adrenal gland was found to be 0.02-0.06% in autopsies. Adrenal cysts are usually symptomless making the diagnosis difficult. The cases described here were diagnosed and removed at operation. One of them was associated with hypertension, and another with pregnancy, considered to be exceptional. Two of these cysts were calcified. All of them were benign. The definite preoperative diagnosis is difficult and the surgical procedure recommended is resection of the cyst with preservation of as much adrenal tissue as possible if malignancy is excluded by frozen section. Since the number of operated cases diagnosed preoperatively are too small, the possibility of treating adrenal cyst by percutaneous aspiration and injection of opaque material to eventually avoid surgery could not be established.
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PMID:Cysts of the adrenal gland. 63 Nov 62

Adrenal vein catheterizations were done in rats made hypertensive by administration of methylandrostenediol (MAD; 17alpha-methyl-5-androstene-3beta,-17beta-diol), and in control rats at intervals during treatment. All MAD-treated rats were hypertensive by 7 weeks. Secretion of corticosterone was consistently decreased at all times in MAD-treated rats. 18-Hydroxy-11-deoxycorticosterone secretion and 11-deoxycorticosterone (DOC) secretion decreased and increased, respectively, compared to controls at 2, 4, and 6 weeks. Aldosterone secretion was decreased at 2 and 4 weeks. This study shows an in vivo block of adrenal 11- and 18-hydroxylation. Transient DOC accumulation by treatment with MAD produced hypertension, though DOC oversecretion and other changes in steroidogenesis were waning by the time hypertension developed.
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PMID:Adrenal steroidogenesis in methylandrostenediol-induced hypertension. 74 61

The pathogenic role of the sympathetic system in essential hypertension was evaluated by combined analysis of urinary and plasma catecholamine levels and pressor sensitivity to endogenous noradrenaline. The latter was estimated indirectly by the ratio between percentile changes in blood pressure and plasma noradrenaline following adrenergic neuronal blockade with the agent debrisoquine. In normal and mildly hypertensive (141/91 to 160/105 mm Hg) subjects, supine or upright plasma levels and excretion rates of noradrenaline correlated (p less than 0.01) with age and were comparable; no correlation was present in patients with moderate to severe hypertension (greater than 160/105 mm Hg) who tended to have supernormal noradrenaline levels under the age of 40 years. Adrenaline values were normal in essential hypertension. Pressor sensitivity to noradrenaline was comparable in normal and mildly hypertensive subjects (0.03 +/- 0.08 [SE] and 0.17 +/- 0.04, respectively) but increased (p less than 0.001) in moderate to severe hypertension (0.62 +/- 0.11). These findings suggest that moderate to severe essential hypertension may be maintained, at least partly, by the inappropriate association of normal plasma noradrenaline levels with increased noradrenaline pressor sensitivity. This may also provide a rational basis for the use of pharmacologic adrenergic inhibition in the treatment of moderate to severe essential hypertension.
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PMID:[Significance of noradrenaline in the pathogenesis of essential hypertension. Preliminary report]. 74 96

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

Adrenal regeneration hypertension (ARH) was induced in virgin and breeder, spontaneously hypertensive (SHR) and Sprague-Dawley (SD) rats. The blood pressure of the previously normotensive, virgin, SD rats and the SD breeder rats with preexistent mild hypertension became greatly elevated. ARH caused an increase in the preexisted severe hypertension in SHR virgin and breeder rats. Serum enzymes, e.g., CPK, SGOT and LDH, were greatly elevated concomitant with the finding of old and new foci of myocardial necrosis. ARH produced a dichotomous metabolic effect, i.e., elevated cholesterol, glucose, and corticosterone levels in SD rats but reduced levels in SHR rats. The zonae glomerulosae of the the regenerated adrenal glands of SD rats were devoid of lipid whereas the zonae glomerulosae of SHR rats were full of lipid. Intact SHR breeder rats develop arterial lesions confined to their reproductive organs but after ARH treatment, they were found to have aortic, coronary and renal arterial lesions which were similar to those which occur, spontaneously, in SD breeder rats. It is suggested that changes in the spectrum of adrenal steroids produced during ARH may contribute to the diverse metabolic changes and the alterations in the usual cardiovascular degenerative changes found in these two strains.
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PMID:Comparative effects of adrenal regeneration hypertension on non-arteriosclerotic and arteriosclerotic Sprague-Dawley vs spontaneously hypertensive rats. 83 44

Adrenal responsiveness to angiotensin II was evaluated in patients with "normal-renin" hypertension. Plasma aldosterone, plasma renin activity, and angiotensin II levels were determined, in the supine and, after 21/2 hours in the upright position, in 70 patients with essential hypertension who were on a diet containing 10 meq of sodium and 100 meq of potassium. The increment of plasma aldosterone between supine and upright positions, divided by the increment in plasma renin activity (deltaPA/deltaPRA), was used as an estimate of adrenal sensitivity to angiotensin II. Fifty-seven patients had deltaPa/deltaPRA ratios within the range observed for a normotensive control population; 13 had low ratios. The low ratios suggested subnormal aldosterone responsiveness to angiotensin II. To further test this hypothesis, angiotensin II was infused into 19 of the 70 patients. In those patients with normal deltaPA/deltaPRA ratios, the plasma aldosterone response was similar to that observed in normotensive controls. On the other hand, in those patients with low ratios, a significant increase in plasma aldosterone levels did not occur even with a dose of angiotensin II 10 times higher than that producing an increase in the normally responsive group. In a separate study, the adrenal response to infused angiotensin II was determined in 12 hypertensive patients who were on a sodium intake of 200 meq. These patients were previously known to have normal renin levels after sodium restriction and upright posture. Under these conditions, the hypertensive patients as a group had a significantly greater plasma aldosterone increment to infused angiotensin II than did sodium-loaded normotensive control subjects. Thus, some patients with normal-renin essential hypertension may have either enhanced or reduced adrenal responsiveness to angiotensin II, depending on the conditions of dietary intake of sodium.
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PMID:Aldosterone regulation in essential hypertension: altered adrenal responsiveness to angiotensin II. 87 Jul 73

Healthy virgin and breeder rats (Sprague-Dawley) with naturally occurring hypertension and arteriosclerosis were fed 5% oxonic acid and 1% uric acid added to their regular diet for 30 days. Although rats are able to convert uric acid into excretable allantoin, abnormal urinary and serum urate levels appeared. Males and females, virgins and breeders, differed in the severity of their increased urate levels. Animals with elevated urate levels developed hypertension, hyperglycemia, and hypertriglyceridemia, with only slight changes in cholesterol and free fatty acids. The kidneys were greatly enlarged and manifested medullary streaking indicative of urate deposits but were free of significant damage; BUN levels in these animals were abnormally high. Adrenal glands were reduced in size and depleted of lipid, circulating corticosterone levels were subnormal, and thymi were involuted. Serum enzymes CPK and LDH were greatly increased, whereas SGOT and SGPT levels were not elevated. The abnormal urate levels did not induce de novo arterial disease in the formerly healthy virgin rats and did not cause exacerbation of the pre-existing, naturally occurring arteriosclerosis characteristic of repeatedly bred rats. It is suggested that Sprague-Dawley rats are endowed with an especially efficient hepatic and renal capacity to metabolize uric acid. Increased urate levels in rats may have some direct metabolic relationship to the production of hypertension, hyperglycemia, and hypertriglyceridemia.
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PMID:Effect of increased serum urate levels on virgin rats with no arteriosclerosis versus breeder rats with preexistent arteriosclerosis. 92 65

Female rats of the Wistar-Furth (W/Fu) strain appear to be resistant to the development of adrenal regeneration hypertension. At a time period, after adrenal enucleation, when Holtzman female rats had elevated serum 11-deoxycorticosterone levels and were hypertensive, none of the W/Fu rats became hypertensive. In vitro adrenal studies after quiescent kills of W/Fu rats indicated that cholesterol side chain cleavage activity was greater in mitochondria from regenerating adrenals than from controls. Both serum deoxycorticosterone and corticosterone levels were significantly greater in the adrenal-enucleated group. These studies were repeated in animals which were given a standard ether anesthetic stress. Ether stress increased cholesterol side chain cleavage activity comparably in control and adrenal-enucleated rats and also increased their serum deoxycorticosterone and corticosterone levels. Adrenal-enucleated Wistar-Furth rats had higher serum deoxycorticosterone levels than controls, whereas controls had higher serum corticosterone levels than the adrenal-enucleated group after the ether stress. These results indicate that although the adrenal-enucleated W/Fu rats have increased serum deoxycorticosterone levels, none of these rats develop frank hypertension. This suggests a resistance to deoxycorticosterone-induced hypertension in this strain of rat.
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PMID:Adrenal mitochondrial and serum corticosteroid studies in rats resistant to adrenal-regeneration hypertension (ARH). 97 88


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