Literature DB >> 6345363

Elevated plasma catecholamines in hypertensives with primary glomerular diseases.

M Ishii, T Ikeda, M Takagi, T Sugimoto, K Atarashi, T Igari, Y Uehara, H Matsuoka, Y Hirata, K Kimura, T Takeda, S Murao.   

Abstract

Supine plasma concentration of norepinephrine (PNE), epinephrine (PE), and aldosterone (PA), plasma renin activity (PRA), and blood volume (BV) were measured in 25 normotensive and 11 hypertensive patients with biopsy-proven glomerulonephritis who had serum creatinine concentrations of less than 1.6 mg/dl, and in 20 normotensive control subjects. PNE and PE were measured according to the trihydroxyindol method using high pressure liquid chromatography. Renal clearances of p-aminohippurate (CPAH) and endogenous creatinine (Ccr) were also determined. Age, BV, and 24-hour urinary excretion of sodium were not significantly different in the three groups. Although all the measured variables were comparable between the control subjects and the normotensive nephritic patients, blood pressure, PNE, PE, PRA, and PA were significantly higher and CPAH and Ccr were significantly lower in the hypertensive nephritic patients than in the normotensive nephritic patients or the control subjects. In the pooled nephritic patients, mean blood pressure was significantly correlated with PNE (r = 0.76, p less than 0.001), PE (r = 0.34, p less than 0.05), PRA (r = 0.33, p less than 0.05), PA (r = 0.40, p less than 0.05) and CPAH (r = -0.51, p less than 0.01). Highly significant positive correlation was also observed between PNE and systolic pressure (r = 0.63, p less than 0.001) or diastolic blood pressure (r = 0.78, p less than 0.001). The results suggest that deterioration of renal function is an important factor in the development of hypertension even in non-azotemic patients with glomerulonephritis, and that increased activities of the sympathetic nervous system and the renin-aldosterone system participate, in part, in elevating blood pressure in the hypertensive nephritic patients. Mechanisms involved in the elevation of plasma concentrations of catecholamines and renal effects on the plasma catecholamines remain to be elucidated.

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Year:  1983        PMID: 6345363     DOI: 10.1161/01.hyp.5.4.545

Source DB:  PubMed          Journal:  Hypertension        ISSN: 0194-911X            Impact factor:   10.190


  13 in total

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Authors:  Y Hirata; K Fukui; Y Dan; H Matsuoka; T Sugimoto; M Ishii
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Review 4.  Neurogenic factors in renal hypertension.

Authors:  Vito M Campese; Ewa Krol
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Review 5.  Chronic Kidney Disease and Atrial Fibrillation: A Contemporary Overview.

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6.  Vascular α1-adrenergic sensitivity is enhanced in chronic kidney disease.

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Review 7.  Catheter-based Renal Artery Denervation for Resistant Hypertension: Promise Unfulfilled or Unsettled?

Authors:  Matthew G Denker; Debbie L Cohen; Raymond R Townsend
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8.  Subcutaneous nerve activity and mechanisms of sudden death in a rat model of chronic kidney disease.

Authors:  Ye Zhao; Neal X Chen; Jonathan T Shirazi; Changyu Shen; Shien-Fong Lin; Michael C Fishbein; Sharon M Moe; Peng-Sheng Chen
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Review 9.  The sympathetic nervous system in chronic kidney disease.

Authors:  Sebastian Ewen; Christian Ukena; Dominik Linz; Roland E Schmieder; Michael Böhm; Felix Mahfoud
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10.  High level of adrenal catecholamines in hypertensive subjects with impaired renal function.

Authors:  M Yoshikawa; T Nakada
Journal:  Int Urol Nephrol       Date:  1986       Impact factor: 2.370

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