PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10513832-1 1999 The aim of this study was to evaluate plasma levels of ANF in patients with catecholamine-secreting tumors with and without hypertension and to relate ANF secretion to levels of plasma and urinary catecholamines and blood pressure. Catecholamines 76-89 natriuretic peptide A Homo sapiens 55-58 11533551-6 2001 Factors that can determine ANF secretion abnormality in MVP could be: 1) Mitral regurgitation; 2) increased heart rate and the high incidence, in MVP syndrome, of arrhythmias; 3) central nervous system neuroendocrine imbalance; 4) increased catecholamines secretion. Catecholamines 241-255 natriuretic peptide A Homo sapiens 27-30 10513832-12 1999 The significance of the relationships among plasma ANF and urinary and plasma catecholamines requires further investigation. Catecholamines 78-92 natriuretic peptide A Homo sapiens 51-54 7480961-3 1994 Previous studies indicated that plasma ANF provides prognostic information and, ANF levels closely related to both severity of disease and catecholamine levels but, it is still unclear if high circulating levels of ANF, which are present in heart failure constantly, may be to correlate with sympathetic nervous activity in man. Catecholamines 139-152 natriuretic peptide A Homo sapiens 80-83 9280203-12 1997 Several hormones such as angiotensin II, ANP and catecholamines, the levels of which are increased in hypertension, downregulate or upregulate ANP-C receptors and ANP-C receptor-mediated inhibition of adenylyl cyclase. Catecholamines 49-63 natriuretic peptide A Homo sapiens 143-146 7711467-2 1994 ANP levels were compared with blood pressure, heart rate, plasma catecholamines and parameters of renal function. Catecholamines 65-79 natriuretic peptide A Homo sapiens 0-3 7480961-3 1994 Previous studies indicated that plasma ANF provides prognostic information and, ANF levels closely related to both severity of disease and catecholamine levels but, it is still unclear if high circulating levels of ANF, which are present in heart failure constantly, may be to correlate with sympathetic nervous activity in man. Catecholamines 139-152 natriuretic peptide A Homo sapiens 80-83 1676862-2 1991 Previous studies have suggested a stimulating effect of catecholamines on ANF release. Catecholamines 56-70 natriuretic peptide A Homo sapiens 74-77 8356302-6 1993 Previously we have shown that in congestive diseases there is a relation between ANF and catecholamine secretion. Catecholamines 89-102 natriuretic peptide A Homo sapiens 81-84 8469920-9 1993 Humoral factors have been suggested as regulators of ANF release, particularly catecholamines and angiotensin II. Catecholamines 79-93 natriuretic peptide A Homo sapiens 53-56 8469920-11 1993 Circulating catecholamines and angiotensin II stimulate ANF release mainly through their haemodynamic effects. Catecholamines 12-26 natriuretic peptide A Homo sapiens 56-59 1424336-2 1992 Administration of digitalis, catecholamine and angiotensin converting enzyme inhibitor resulted in decrease of ANP levels as well as improvement of clinical symptoms of CHF and cardiomegaly. Catecholamines 29-42 natriuretic peptide A Homo sapiens 111-114 1676862-6 1991 We concluded that chronic elevation of basal catecholamines are without effect on plasma ANF but that manipulation of pheochromocytoma leads to a stimulation of ANF release, possibly mediated by either a direct effect of endogenously released catecholamines and/or an increase in atrial pressure. Catecholamines 243-257 natriuretic peptide A Homo sapiens 161-164 2526581-1 1989 The authors studied the effect of intravenous infusion of atrial natriuretic peptide (ANP) on the plasma catecholamine and forearm vasoconstrictor responses to cardiopulmonary baroreflex deactivation in six normal, male volunteers in order to determine whether ANP influences reflex forearm vasoconstriction in humans. Catecholamines 105-118 natriuretic peptide A Homo sapiens 58-84 1833942-7 1991 That ANF-resistance may be related to the activation of the renin-angiotensin-aldosterone axis, increased circulating catecholamines, renal sympathetic nerve stimulation, changes in renal hemodynamics or increased degradation of ANF. Catecholamines 118-132 natriuretic peptide A Homo sapiens 5-8 2526581-1 1989 The authors studied the effect of intravenous infusion of atrial natriuretic peptide (ANP) on the plasma catecholamine and forearm vasoconstrictor responses to cardiopulmonary baroreflex deactivation in six normal, male volunteers in order to determine whether ANP influences reflex forearm vasoconstriction in humans. Catecholamines 105-118 natriuretic peptide A Homo sapiens 86-89 2537703-4 1989 To investigate the mechanisms of these changes in renal function, nocturnal urinary excretion of catecholamines and guanosine 3":5"-cyclic monophosphate (cyclic GMP), which reflects atrial natriuretic factor (ANF) release, and next-morning plasma active renin concentrations were studied in 21 OSA patients on 2 consecutive nights, either untreated or treated with nasal CPAP. Catecholamines 97-111 natriuretic peptide A Homo sapiens 182-207 2524228-4 1989 The data obtained show that the action of the atriopeptin is mediated by Na+-K+ pump activation of smooth muscle cells and restricts vasoconstriction of catecholamine effect. Catecholamines 153-166 natriuretic peptide A Homo sapiens 46-57 2966690-1 1988 The role of catecholamine in atrial natriuretic peptide (ANP) secretion and its secretory mechanism in normal humans is not well defined; therefore, we studied the relationship among ANP, catecholamine, and atrial pressures in 25 patients without cardiovascular disease and in 35 patients with chronic congestive heart failure (CHF, 20 in mitral valve disease and 15 in dilated cardiomyopathy). Catecholamines 12-25 natriuretic peptide A Homo sapiens 29-55 2473355-3 1989 In these studies and other high dose constant infusion experiments, the response of the renin-angiotension-aldosterone system and plasma catecholamines was varied, either remaining unchanged or showing stimulation when high doses of ANF caused acute and substantial falls in blood pressure. Catecholamines 137-151 natriuretic peptide A Homo sapiens 233-236 2473357-1 1989 The effects of synthetic human atrial natriuretic peptide (ANP) on the release of catecholamines, aldosterone, or cortisol were observed in human adrenal tumors obtained surgically from patients with pheochromocytoma, primary aldosteronism, or Cushing"s syndrome, respectively. Catecholamines 82-96 natriuretic peptide A Homo sapiens 31-57 2473357-1 1989 The effects of synthetic human atrial natriuretic peptide (ANP) on the release of catecholamines, aldosterone, or cortisol were observed in human adrenal tumors obtained surgically from patients with pheochromocytoma, primary aldosteronism, or Cushing"s syndrome, respectively. Catecholamines 82-96 natriuretic peptide A Homo sapiens 59-62 2473357-5 1989 Release of catecholamines from pheochromocytoma tissues was inhibited by ANP, and the presence of the ANP receptor on pheochromocytoma was further demonstrated by both binding assays and affinity labeling; Scatchard analysis revealed a single class of binding sites for ANP with a Kd of 1.0 nM and a Bmax of 0.4 pmol/mg of protein and the molecular size was estimated as 140 and a 70 kDa under nonreducing and reducing conditions, respectively. Catecholamines 11-25 natriuretic peptide A Homo sapiens 73-76 2473357-5 1989 Release of catecholamines from pheochromocytoma tissues was inhibited by ANP, and the presence of the ANP receptor on pheochromocytoma was further demonstrated by both binding assays and affinity labeling; Scatchard analysis revealed a single class of binding sites for ANP with a Kd of 1.0 nM and a Bmax of 0.4 pmol/mg of protein and the molecular size was estimated as 140 and a 70 kDa under nonreducing and reducing conditions, respectively. Catecholamines 11-25 natriuretic peptide A Homo sapiens 102-105 2473357-5 1989 Release of catecholamines from pheochromocytoma tissues was inhibited by ANP, and the presence of the ANP receptor on pheochromocytoma was further demonstrated by both binding assays and affinity labeling; Scatchard analysis revealed a single class of binding sites for ANP with a Kd of 1.0 nM and a Bmax of 0.4 pmol/mg of protein and the molecular size was estimated as 140 and a 70 kDa under nonreducing and reducing conditions, respectively. Catecholamines 11-25 natriuretic peptide A Homo sapiens 102-105 2966690-1 1988 The role of catecholamine in atrial natriuretic peptide (ANP) secretion and its secretory mechanism in normal humans is not well defined; therefore, we studied the relationship among ANP, catecholamine, and atrial pressures in 25 patients without cardiovascular disease and in 35 patients with chronic congestive heart failure (CHF, 20 in mitral valve disease and 15 in dilated cardiomyopathy). Catecholamines 12-25 natriuretic peptide A Homo sapiens 57-60 2967028-5 1988 The augmented ANP levels during exercise after beta-blockade probably reflect catecholamine-stimulated ANP release, whereas the elevated plasma ANP levels after acebutolol at rest might be a beta-adrenoceptor-mediated ANP release due to the intrinsic sympathomimetic effect of acebutolol. Catecholamines 78-91 natriuretic peptide A Homo sapiens 14-17 2967028-5 1988 The augmented ANP levels during exercise after beta-blockade probably reflect catecholamine-stimulated ANP release, whereas the elevated plasma ANP levels after acebutolol at rest might be a beta-adrenoceptor-mediated ANP release due to the intrinsic sympathomimetic effect of acebutolol. Catecholamines 78-91 natriuretic peptide A Homo sapiens 103-106 2967028-5 1988 The augmented ANP levels during exercise after beta-blockade probably reflect catecholamine-stimulated ANP release, whereas the elevated plasma ANP levels after acebutolol at rest might be a beta-adrenoceptor-mediated ANP release due to the intrinsic sympathomimetic effect of acebutolol. Catecholamines 78-91 natriuretic peptide A Homo sapiens 103-106 2967028-5 1988 The augmented ANP levels during exercise after beta-blockade probably reflect catecholamine-stimulated ANP release, whereas the elevated plasma ANP levels after acebutolol at rest might be a beta-adrenoceptor-mediated ANP release due to the intrinsic sympathomimetic effect of acebutolol. Catecholamines 78-91 natriuretic peptide A Homo sapiens 103-106 2887332-7 1987 It is suggested that increased right atrial pressure and/or pulmonary arterial blood pressure and increased plasma levels of catecholamines are important secretory stimuli for ANP during exercise. Catecholamines 125-139 natriuretic peptide A Homo sapiens 176-179 2954451-1 1987 The role of atrial pressure and catecholamines in secreting human atrial natriuretic polypeptides (hANP) were investigated in patients with acute or old myocardial infarction (AMI or OMI). Catecholamines 32-46 natriuretic peptide A Homo sapiens 99-103 2954451-4 1987 In 12 patients with OMI, plasma hANP levels were normal at rest and were significantly increased (p less than 0.01) with bicycle ergometer exercise associated with significant elevations of plasma catecholamine levels, mRA, and PCW. Catecholamines 197-210 natriuretic peptide A Homo sapiens 32-36