Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously shown that black children have higher blood pressures than white children. In the present study, we examined whether a possible racial difference in adrenal androgen production during adrenarche might contribute to the racial disparity in blood pressure. Adrenal androgen production was estimated from urinary excretion of adrenal androgen metabolites that showed cross-reactivity with antisera to dehydroepiandrosterone sulfate (DHEA-S). Urine samples were collected overnight in 798 children, one third of whom were black. Analyses were performed for two different age groups, less than 10 years and 10 years or more of age. In children less than 10 years of age, adrenal androgen excretion rates were 17% higher in blacks than in whites (p = 0.0099); adrenal androgen excretion rates tended to be higher in older black children as well, but differences here were not statistically significant. Adrenal androgen excretion rates were positively correlated with diastolic blood pressure in the older age group only (p = 0.014). However, when the relation of race to blood pressure was examined along with adrenal androgen excretion adjusted for age, sex, and weight, race remained an independent contributor to the level of blood pressure, suggesting that a difference in adrenal androgens could not explain the racial differences in blood pressure. In summary, black children produced more adrenal androgen, but this did not explain their higher blood pressures. In older children, where adrenal androgen excretion rates were higher, diastolic blood pressure and adrenal androgen excretion were positively related, suggesting that adrenal androgens participate in establishing the level of blood pressure in young people.
Hypertension 1990 Oct
PMID:Adrenal androgen excretion during adrenarche. Relation to race and blood pressure. 214 21

This study was performed to investigate the role of endogenous epinephrine in the regulation of vascular tone in hypertension. The release of endogenous epinephrine and norepinephrine from the vascular adrenergic neurons by periarterial nerve stimulation was examined in spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto rats (WKY). The isolated mesenteric vasculatures were prepared, and the epinephrine and norepinephrine release during electrical nerve stimulation was determined as the increase in epinephrine and norepinephrine contents in the vascular perfusate. Epinephrine and norepinephrine were measured by high performance liquid chromatography with an electrochemical detector. Vasoconstrictor responses and norepinephrine overflow during electrical nerve stimulation were significantly greater in SHR than in WKY. The amount of stimulation-evoked epinephrine overflow into the perfusate was also increased in SHR compared to that in WKY, especially at low frequency stimulation. These results suggest that epinephrine could be released from the vascular adrenergic neurons as a cotransmitter of norepinephrine and contribute to increased vascular tone in hypertension.
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PMID:Enhanced endogenous epinephrine release from the vascular adrenergic neurons in spontaneously hypertensive rats. 215 40

Experiments characterized the dynamics of the pituitary and adrenocortical response to noise in awake dogs to determine if a dissociation exists between changes in plasma bioactive (bio) adrenocorticotropic hormone (ACTH) and immunoreactive (ir) ACTH. In addition, experiments determined the temporal relationship between cardiovascular, adrenomedullary, and adrenocortical responses induced by the acute presentation of noise. Trained dogs were prepared chronically with adrenal venous and femoral arterial cannulas. Experiments were done 48-96 h postsurgery and consisted of presentation of noise (75 dB; 0.25-8 kHz) for 3 min (n = 6) or of blood sampling alone (n = 5). In response to noise, mean arterial pressure and heart rate increased at 30 s and returned to base line at 4 min. Adrenal secretion of epinephrine and norepinephrine increased at 1 min and remained elevated until 4 min. Adrenal blood flow increased from 2 to 4 min as the result of a parallel increase in adrenal vascular conductance. Plasma bioACTH increased from 6 to 15 min in parallel with that of plasma irACTH. Before noise, the ratio of bioACTH to irACTH was 0.2-0.3, but the absolute change in bioACTH and irACTH after noise was not different. The increase in plasma ACTH occurred concomitant with or preceded an increase in cortisol secretion. Blood sampling alone caused no change in any variable. These data show that unexpected noise evokes a sequence of responses with rapid onset that includes tachycardia, hypertension, and increases in adrenomedullary secretion and adrenal vascular conductance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pituitary-adrenal and adrenomedullary responses to noise in awake dogs. 215 60

Adrenal imaging using radiopharmaceuticals is a functional test that can contribute significantly to surgical management and follow-up of patients with either benign or malignant conditions of the adrenal cortex and medulla. Imaging of the cortex is achieved by iodine-131-labeled iodomethyl nor-cholesterol (NP-59), while adrenal medulla imaging can be successfully accomplished by 131I-metaiodobenzylguanidine (MIBG), which localizes in the adrenergic nerve terminal with norepinephrine. Both tests carry high sensitivity and specificity for functional tumors and hyperplasia, and often better than CT scanning. This article reviews the current status and clinical utility of nuclear imaging of the adrenal cortex in congenital hyperplasia, low renin hypertension and aldosteronism, and Cushing's syndrome. Adrenal medulla imaging is reviewed in light of our experience at the University of Texas M.D. Anderson Cancer Center in pheochromocytoma, neuroblastoma, and other neuroectodermal tumors. Investigation of 131I-MIBG therapy of metastatic tumors of neuroectodermal origin potentially offers a means of at least controlling symptoms of hormonal secretion in these patients.
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PMID:Role of adrenal imaging in surgical management. 217 29

A 64-year-old female with hypertension, hypokalemia visited our hospital. Endocrinological examinations showed a low level of plasma renin activity and high level of plasma aldosterone. Circadian rhythmicity of plasma aldosterone level was recognized. No change in the plasma level of aldosterone was observed after loading of standing and administration of furosemide. Adrenal scintigraphy, adrenal venous aldosterone assay and CT scan revealed two tumors in the left adrenal. The diagnosis of primary aldosteronism by left adrenal tumors was made from the above findings. A left adrenalectomy was performed and pathological findings showed two adenomas, which had no capsule either and were surrounded by normal adrenocortical tissue. Blood pressure normalized after surgery and the plasma levels of aldosterone and plasma renin activity were normalized.
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PMID:[A case of primary aldosteronism due to unilateral multiple adrenal adenomas]. 223 79

As plasma potassium concentrations, whether normal or elevated, can be reduced by intravenous administration of either epinephrine or ritodrine, the effects of these drugs were examined during acute hyperkalemia. Six anesthetized dogs were studied every 2 wk, on 18 separate occasions. Hyperkalemia was induced by intravenous infusion of potassium chloride, resulting in plasma potassium concentrations of 9.6 +/- 0.3 mEq/L (mean +/- SEM), bradycardia, and idioventricular rhythm. Dogs were then given slow intravenous injections every 30 min of either saline (controls), epinephrine, or ritodrine. Epinephrine doses were 0.01, 0.1, 1.0, 10, or 100 micrograms/kg; ritodrine doses were 0.1, 1.0, 10, 100, or 1000 micrograms/kg. At the highest does, both epinephrine and ritodrine caused clinically important decreases in plasma potassium, reducing concentrations to below 7.0 mEq/L. Ritodrine had a significantly greater effect than epinephrine. Side effects included hypertension and dysrhythmias with epinephrine, serious hypotension with ritodrine, and tachycardia with both drugs. For both drugs, the doses that caused a decrease in plasma potassium also caused an increase in heart rate and there was a correlation between plasma potassium levels and heart rate. Epinephrine and ritodrine may be useful in treating acute hyperkalemia, but cardiovascular side effects may occur. Increased heart rate could be used as an indicator of therapeutic effect and the magnitude of the increase in heart rate may be helpful in predicting the level of response.
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PMID:Effects of epinephrine and ritodrine in dogs with acute hyperkalemia. 231 82

To assess the rate of activation of the renin-angiotensin-aldosterone axis and enhancement of adrenal responsiveness to angiotensin II (Ang II) with restriction of sodium intake, 16 healthy male subjects were placed initially on a 200 meq daily sodium intake; adrenal responsiveness to Ang II was assessed, and then daily sodium intake was reduced abruptly to 10 meq. Adrenal responses to Ang II were assessed again during the non-steady state interval 24 and 48 hours later, and after balance was achieved in 5-7 days. Renin-angiotensin system activation was evident within 24 hours after sodium intake was restricted. The increase in basal plasma aldosterone concentration and enhancement of the adrenal response to Ang II, on the other hand, tended to lag. Within 24 hours of restricting sodium intake, despite a significant increase in both plasma renin activity (1.0 +/- 0.2 vs. 2.4 +/- 0.7 ng/ml/hr, p less than 0.01) and Ang II concentration (22.0 +/- 1.9 vs. 29.5 +/- 1.3 pg/ml, p less than 0.05), there was no increase in basal plasma aldosterone concentration (10.4 +/- 1.3 vs. 11.7 +/- 1.2 ng/dl). At 48 hours, despite little further change in plasma renin activity or plasma Ang II concentration, there was a sharp increase in basal plasma aldosterone concentration (22.5 +/- 3.6 ng/dl, p less than 0.01). The adrenal response to Ang II was increased significantly at 24 hours, evident at only a 10 ng/kg/min dose, but showed progressive further enhancement with time.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1990 Apr
PMID:Time course of enhanced adrenal responsiveness to angiotensin on a low salt diet. 231 19

Clinical features of epinephrine release led to the finding of spontaneously elevated plasma epinephrine concentrations in five patients, in four of whom plasma norepinephrine concentrations were normal. Adrenal medullary hyperplasia was suspected in one patient, whose first cousin had multiple endocrine neoplasia type IIa, and in two others, all of whom have experienced relief from symptoms during propranolol or atenolol administration. The other two patients had unilateral adrenal cysts, with negative metaiodobenzylguanidine scans and no histological evidence of pheochromocytoma, but complete relief of symptoms by excision of the cysts. In one patient, Cushing's syndrome and associated hypertension, diabetes, and ischemic finger-tip ulceration all disappeared after surgery. It is concluded that spontaneous hyperepinephrinemic manifestations can be received by beta-blockers or, when an adrenal mass is present, by unilateral adrenalectomy even when the metalodobenzylguanidine test result is negative.
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PMID:Primary hyperepinephrinemia in patients without pheochromocytoma. 236 52

The startle response, consisting of behavioral and cardiovascular components, was used to study the reaction of the cardiovascular system to a mild environmental stressor. We used tactile air puff startle to study responses in adult Wistar-Kyoto and spontaneously hypertensive rats. In both strains, air puff elicits a transient motor response with rapid habituation over the test session of 30 trials. Spontaneously hypertensive rats exhibit exaggerated motor responses compared with Wistar-Kyoto rats. Similarly, a 2-3-second duration pressor response was significantly greater in spontaneously hypertensive rats than in Wistar-Kyoto rats (47.7 +/- 2.0 versus 37.1 +/- 1.5 mm Hg, respectively). However, spontaneously hypertensive rats and Wistar-Kyoto rats exhibited strikingly dissimilar heart rate responses. Wistar-Kyoto rats exhibited a transient bradycardia (-42 +/- 7 beats/min) on early trials yielding to tachycardia on later trials (35 +/- 11 beats/min). In contrast, spontaneously hypertensive rats exhibited only tachycardia to all stimuli with an absence of bradycardia. Adrenal medullary secretions chronically modulate cardiac responses in both strains. Sinoaortic denervation did not alter the magnitude or profile of the heart rate responses. Spontaneously hypertensive--Wistar-Kyoto rat differences were not secondary to hypertension because renovascular hypertensive Wistar-Kyoto rats show normal responses to air puff. Four-week-old spontaneously hypertensive rats exhibit enhanced pressor and suppressed bradycardia responses relative to age-matched Wistar-Kyoto rats, indicating chronotropic differences precede development of established hypertension. Our results indicate parasympathetic activation by the mild startle stimuli rather than sympathetic withdrawal allows bradycardia to mask a latent tachycardia in Wistar-Kyoto rats. Spontaneously hypertensive rats exhibit a parasympathetic insufficiency in the startle response to novel alerting stimuli. Thus, mild air puff startle identifies a unique and discriminatory phenotypic difference between inbred normotensive and hypertensive rats.
Hypertension 1990 Sep
PMID:Exaggerated response to alerting stimuli in spontaneously hypertensive rats. 239 88

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


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