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)

The effect of a six-week strenuous exercise training programme (modified Bruce protocol, treadmill, three times per week) on resting and exercising blood pressure, heart rate, plasma catecholamines, chromogranin A, renin activity and aldosterone levels was investigated in 15 patients with mild hypertension. An identical exercise test was conducted at baseline and study close (six weeks). At follow-up, seven to ten days after study close, patients completed an exercise test of equivalent intensity to that at baseline, achieving comparable heart rate levels at maximal exercise. On each occasion, blood pressure, heart rate and hormonal variables were measured at rest (supine), maximal exercise and ten minutes after stopping exercise. Resting and exercising blood pressure and heart rate were reduced by the six-week exercise regimen. There was a trend, although not statistically significant, for resting plasma noradrenaline levels to be lower at study close. The reduction in blood pressure and heart rate at maximal exercise was associated with a significant attenuation of the plasma renin response to exercise. Plasma catecholamines also appeared to be lower after exercise training, although this effect was not statistically significant. Plasma levels of chromogranin A and aldosterone measured at rest and maximal exercise were not influenced by the exercise regimen. Further controlled studies are required to corroborate the results of this preliminary study.
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PMID:Short-term strenuous exercise training: effects on blood pressure and hormonal levels in mild hypertension. 136 37

Chromogranin A, co-stored and co-released with catecholamines from adrenal medullary and sympathetic neuronal vesicles, is elevated in the plasma of patients with pheochromocytoma. The usefulness of the hormone in the differential diagnosis of hypertension is examined. An elevated level of chromogranin A had comparable diagnostic sensitivity (83%, 24/29) to, but greater diagnostic specificity (96%, 86/90) than the level of plasma catecholamines when subjects with pheochromocytoma (n = 29) were evaluated in comparison to several reference groups, including normotensive controls (n = 49), subjects with essential hypertension (n = 28), subjects with renovascular hypertension (n = 5), and subjects with primary aldosteronism (n = 3). Subjects with signs or symptoms suggesting pheochromocytoma, but in whom the diagnosis was ultimately ruled out (n = 5) had normal plasma levels of chromogranin A. A modest rise in chromogranin A in those with essential hypertension, and correlation of chromogranin A with diastolic blood pressure in normotensive patients and patients with essential hypertension did not impair the diagnostic usefulness of chromogranin A for pheochromocytoma. Renal failure was associated with an elevated plasma chromogranin A independently of blood pressure. Plasma chromogranin A correlated with tumor mass, tumor chromogranin A content, tumor norepinephrine content, and urinary vanillylmandelic acid excretion; it did not correlate with plasma or urinary catecholamines, nor with blood pressure in patients with pheochromocytoma. Plasma chromogranin A levels did not differ in subjects with pheochromocytoma when stratified by age, sex, tumor location, or tumor pathology. Several drugs used in the diagnosis or treatment of pheochromocytoma (clonidine, metoprolol, phentolamine, and tyramine) had little effect on plasma chromogranin A concentration. Within the pheochromocytoma, chromogranin A was localized along with catecholamines to the soluble core of chromaffin granules, where it accounted for 18 +/- 5% of vesicle soluble protein. We conclude that 1) chromogranin A emerges along with catecholamines from pheochromocytoma chromaffin granules; 2) plasma chromogranin A is a sensitive and specific diagnostic tool in evaluation of actual or suspected pheochromocytoma; 3) plasma chromogranin A predicts pheochromocytoma tumor size and overall catecholamine production; and 4) drugs commonly employed in the diagnosis or treatment of pheochromocytoma have little effect on plasma chromogranin A level, preserving the usefulness of chromogranin A in evaluating pheochromocytoma. Thus, measurement of chromogranin A provides a useful adjunct to the diagnosis of pheochromocytoma.
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PMID:Chromogranin A storage and secretion: sensitivity and specificity for the diagnosis of pheochromocytoma. 198 65

Plasma levels of chromogranin A + B, neuropeptide Y and catecholamines were analysed before, during and after surgery in seven patients with pheochromocytoma. The aim of the study was to determine the diagnostic sensitivity of these plasma amines and peptides, and to investigate their peroperative fluctuations. Chromogranin A + B in plasma was increased preoperatively in all patients, showed no significant increase during surgery, and normalized postoperatively. Neuropeptide Y, which alone can induce hypertension, was present in high levels in plasma from three patients preoperatively, increased further in four patients during surgery, and was postoperatively low in all patients. Fractionated plasma catecholamines were increased in five patients before surgery, increased in all patients during tumour dissection, and normalized postoperatively. It may be concluded that plasma chromogranin A + B exhibited as high a sensitivity for pheochromocytoma as fractionated urinary catecholamines in the patients studied.
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PMID:Plasma chromogranin A + B, neuropeptide Y and catecholamines in pheochromocytoma patients. 204 Aug 71

The chromogranins/secretogranins are a family of acidic, soluble proteins with widespread neuroendocrine distribution in secretory vesicles. Although the precise function of the chromogranins remains elusive, knowledge of their structure, distribution, and potential intracellular and extracellular roles, especially that of chromogranin A, has greatly expanded during recent years. Chromogranin A is coreleased with catecholamines by exocytosis from vesicles in the adrenal medulla and sympathetic nerve endings. Thus, measurement of its circulating concentration by radioimmunoassay may be a useful probe of exocytotic sympathoadrenal activity in humans, under both physiological and pathological conditions. Here, we explore the storage, structure, and function of chromogranin A, and parameters that influence its circulating levels. We have also measured plasma chromogranin A concentrations in different groups of patients with hypertension, including those with pheochromocytoma.
Hypertension 1990 Mar
PMID:Chromogranin A. Storage and release in hypertension. 240 99

Secretory components of the adrenal medulla were compared in normotensive Wistar-Kyoto (WKY) rats and in stroke-prone spontaneously hypertensive rats (SHRSP) at both 4 and 12 months of age. Noradrenaline, adrenaline, dopamine, neuropeptide Y, and chromogranins A and B were significantly higher in adrenal glands of SHRSP than those of WKY rats at 4 months. At 12 months, the levels of these components in SHRSP had increased even more (about 200% in WKY rats). There was no change in the relative composition of the adrenal "secretory cocktail." Neither the chromogranin A/chromogranin B ratio nor their apparent proteolytic processing in chromaffin granules differed between SHRSP or WKY rats. The lack of a significant change in membrane-bound cytochrome b561 and the small increase in dopamine beta-hydroxylase suggest that the higher levels of secretory components in SHRSP are not simply caused by an increase in the number of chromaffin granules, but possibly by a selective increase in the secretory content of these organelles providing a larger package for quantal release by exocytosis. This may be relevant for the elevation of blood pressure in this strain. The immunological methods described in this paper allow for the first time a determination of the secretory quantal levels in catecholamine storage. This should be useful for further studies in hypertensive models.
Hypertension 1989 May
PMID:An increased pool of secretory hormones and peptides in adrenal medulla of stroke-prone spontaneously hypertensive rats. 256 78

Chromogranin A is contained in storage vesicles of chromaffin cells of the adrenal medulla and released with catecholamines when the splanchnic nerve is stimulated. Chromogranin A is similar to secretory protein I (SP-I), a major secreted protein of the parathyroid. Chromogranin A/SP-I immunoreactivity is abundant in endocrine cells that secrete peptide hormones from storage vesicles. Chromogranins may act in neuroendocrine secretion by binding intravesicular calcium. Serum levels of chromogranin are raised in hypertension and endocrine neoplasia. We report here the isolation and sequencing of a cDNA encoding bovine chromogranin A, providing the first complete primary structure of a chromogranin protein. Chromogranin A is a highly acidic protein with an apparent relative molecular mass (Mr) of 75,000 on SDS-PAGE, but an actual Mr of 48,000. Adrenal medulla, brain, pituitary and parathyroid are all sites of synthesis of chromogranin A. The primary structure of chromogranin A, and the presence of chromogranin mRNA in the parathyroid, indicate that chromogranin A and SP-I are identical.
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PMID:Bovine chromogranin A sequence and distribution of its messenger RNA in endocrine tissues. 301 87

Chromogranin A is the major catecholamine storage vesicle soluble protein costored and coreleased by exocytosis with catecholamines. Immunoreactive chromogranin A circulates in human plasma, where it may reflect changes in exocytotic sympathoadrenal activity. We measured plasma chromogranin A concentration in normotensive control subjects as well as in untreated essential (primary) hypertensive subjects and subjects with several varieties of secondary hypertension. Plasma chromogranin A concentration was higher in subjects with essential hypertension (n = 32) than in normal controls (n = 18; 198 +/- 32 versus 129 +/- 12 ng/ml [mean +/- SEM]; p less than 0.05), and was also elevated in subjects with hypertension secondary to renal parenchymal disease (n = 9; 192 +/- 36 ng/ml; 0.05 less than p less than 0.1) and those with pheochromocytoma (n = 11; 1614 +/- 408 ng/ml; p less than 0.01). In essential hypertensive subjects (n = 5), short-term suppression of sympathetic outflow with oral guanabenz (4 mg) reduced plasma chromogranin A concentration within 30 to 60 minutes, while the blood pressure response was more gradual and was maximal at 3 hours. The results suggest that plasma chromogranin A is, at least in part, under neural control and that there may be an excess of exocytotic sympathoadrenal activity in essential hypertension. These initial studies are now being expanded to larger subject groups.
Hypertension
PMID:Plasma chromogranin A. Initial studies in human hypertension. 399 34

Chromogranin A is the quantitatively major soluble protein in catecholamine storage vesicles of the adrenal medulla and sympathetic nerve, and has been a useful index of exocytosis during sympathoadrenal neurosecretion. To probe human catecholamine storage and release, we isolated chromogranin A from chromaffin tissue in human pheochromocytoma, and compared it to chromogranin A isolated from chromaffin tissue in bovine adrenal medulla. The preparation included catecholamine storage vesicle isolation by sucrose gradient centrifugation, removal of dopamine-beta-hydroxylase by affinity chromatography on Concanavalin A-Sepharose, and preparative polyacrylamide gel electrophoresis. Human and bovine chromogranin A displayed considerable interspecies homology. Human chromogranin A is a 68,000 dalton monomeric protein with an unusual amino acid composition (31.53 weight % glutamic acid); an acidic, microheterogeneous isoelectric point (4.57-4.68); a characteristic tryptic digest peptide map; and marked dissimilarity to dopamine-beta-hydroxylase in all properties studied. A new probe of human sympathoadrenal function is available in chromogranin A.
Hypertension
PMID:Human chromogranin A. Purification and characterization from catecholamine storage vesicles of human pheochromocytoma. 669 45

We have evaluated a new commercially available ELISA kit for determination of plasma chromogranin A with respect to its usefulness in the diagnosis of neuroendocrine tumors, mainly pheochromocytoma. Serum and differently anticoagulated plasmas gave different chromogranin A concentrations. Control values (n = 21) were 18.9 +/- 5.8 units/l. Chromogranin A values > 30.4 units/l (mean + 2 S.D.) were considered elevated. In 22 patients suspected of (but found not to have) pheochromocytoma and in 24 patients with renovascular hypertension, 18% were found to have elevated chromogranin A concentrations. In renovascular hypertension chromogranin A correlated positively with serum creatinine; chromogranin A was strongly elevated especially in chronic renal failure. In 45 patients with pheochromocytoma, 13 (29%) had chromogranin A concentrations within the normal range, as had 3 out of 11 patients with neuroblastoma (27%). In 13 pheochromocytoma patients with elevated chromogranin A, measurements were repeated after surgical removal of the tumor; values then all fell within the normal range. We conclude that measurement of chromogranin A adds little to already existing methods for the diagnosis of pheochromocytoma.
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PMID:Sensitivity and specificity of a new ELISA method for determination of chromogranin A in the diagnosis of pheochromocytoma and neuroblastoma. 758 87

Multiple heritable traits are associated with essential (genetic) hypertension in humans. Because chromogranin A is increased in both human and rodent genetic hypertension, we examined the influence of heredity and blood pressure on chromogranin A in humans. In estimates derived from among- and within-pair variance in monozygotic versus dizygotic twins, plasma chromogranin A displayed significant (F15,18 = 2.93, P = .016) genetic variance (sigma 2 g), and its broad-sense heritability was high (h2B = 0.983). Plasma chromogranin A was increased in essential hypertension (99.9 +/- 6.7 versus 62.8 +/- 4.7 ng/mL, P < .001) but was influenced little by genetic risk for (family history of) hypertension (in normotensive or hypertensive subjects), by race, or by several antihypertensive therapies (angiotensin-converting enzyme inhibitor, diuretic, or beta-adrenergic antagonist). In normotensive subjects at genetic risk for essential hypertension, neither basal nor sympathoadrenal stress-evoked chromogranin A differed from values found in subjects not at risk. In established essential hypertension, plasma chromogranin A responses to adrenal medullary (insulin-evoked hypoglycemia) or sympathetic neuronal (dynamic exercise) activation were exaggerated, whereas responses to sympathoadrenal suppression (ganglionic blockade) were diminished, suggesting increased vesicular stores of chromogranin A and an adrenergic origin of the augmented chromogranin A expression in this disorder. We conclude that plasma chromogranin A displays substantial heritability and is increased in established essential hypertension. Its elevation in established hypertension is associated with evidence of increased vesicular stores of the protein and with adrenergic hyperactivity but is influenced little by customary antihypertensive therapies. However, the chromogranin A elevation is not evident early in the course of genetic hypertension.
Hypertension 1995 Jul
PMID:Chromogranin A in human hypertension. Influence of heredity. 760 27


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