CHRONIC CAFFEINE INGESTION EXACERBATES 2-KIDNEY, 1-CLIP HYPERTENSION AND AMELIORATES DEOXYCORTICOSTERONE ACETATE-SALT HYPERTENSION IN RATS

被引:10
作者
CHOI, KC [1 ]
LEE, J [1 ]
MOON, KH [1 ]
PARK, KK [1 ]
KIM, SW [1 ]
KIM, NH [1 ]
机构
[1] CHONNAM NATL UNIV, SCH MED, DEPT PHYSIOL, KWANGJU, SOUTH KOREA
关键词
CAFFEINE; RENIN; ATRIAL NATRIURETIC PEPTIDE; RENOVASCULAR HYPERTENSION; DEOXYCORTICOSTERONE ACETATE SALT; HYPERTENSION;
D O I
10.1159/000187574
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
The present study was aimed to determine the effect of caffeine on the development of renal hypertension. Two-kidney, 1-clip (2K1C) hypertension and deoxycorticosterone acetate (DOCA, 200 mg/kg, subcutaneous implantation) - salt (0.9% NaCl drinking) hypertension were instituted in Sprague-Dawley rats. They were then grouped into two groups each: one was supplemented with caffeine (0.1%) in their drinking solution and the other was not. Systolic blood pressure was measured up to 24 days. Caffeine exacerbated the development of 2K1C hypertension in association with a higher plasma renin concentration (PRC). Caffeine ingestion, however, did not exacerbate but ameliorated DOCA-salt hypertension in which PRC was comparable between the caffeine-ingested and control groups. Concentrations of plasma atrial natriuretic peptide (pANP) were significantly different between the caffeine-ingested and control groups neither in 2K1C nor in DOCA-salt rats, suggesting that ANP was not responsible for the modified blood pressure. Acute caffeine infusion (350 mug/min, 30 min) in anesthetized normotensive rats caused increases in urinary excretion (volume and sodium) and in PRC without significantly affecting the blood pressure and pANP. These results suggest that caffeine specifically exacerbates 2K1C hypertension through increasing renin release whereas it ameliorates DOCA-salt hypertension possibly through increasing renal excretion.
引用
收藏
页码:619 / 622
页数:4
相关论文
共 19 条
[1]   ADENOSINE-INDUCED DECREASE IN RENIN RELEASE - DISSOCIATION FROM HEMODYNAMIC-EFFECTS [J].
AREND, LJ ;
HARAMATI, A ;
THOMPSON, CI ;
SPIELMAN, WS .
AMERICAN JOURNAL OF PHYSIOLOGY, 1984, 247 (03) :F447-F452
[2]  
ATARASHI K, 1984, SCIENCE, V224, P992, DOI 10.1126/science.6326267
[3]   INHIBITION OF RENIN RELEASE BY ANALOGS OF ADENOSINE IN RABBIT RENAL CORTICAL SLICES [J].
BARCHOWSKY, A ;
DATA, JL ;
WHORTON, AR .
HYPERTENSION, 1987, 9 (06) :619-623
[4]  
BIAGGIONI I, 1991, J PHARMACOL EXP THER, V258, P588
[5]  
BRAUNMENENDEZ E, 1951, HYPERTENSION, P133
[6]  
BROWNIE AC, 1990, HYPERTENSION PATHOPH, P63
[7]   EFFECTS OF SYNTHETIC ATRIAL NATRIURETIC FACTOR ON RENAL-FUNCTION AND RENIN RELEASE [J].
BURNETT, JC ;
GRANGER, JP ;
OPGENORTH, TJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1984, 247 (05) :F863-F866
[8]   ATRIAL-NATRIURETIC-FACTOR - ITS (PATHO)PHYSIOLOGICAL SIGNIFICANCE IN HUMANS [J].
DEZEEUW, D ;
JANSSEN, WMT ;
DEJONG, PE .
KIDNEY INTERNATIONAL, 1992, 41 (05) :1115-1133
[9]   PHYSIOLOGY AND PATHO-PHYSIOLOGY OF ATRIAL PEPTIDES [J].
GOETZ, KL .
AMERICAN JOURNAL OF PHYSIOLOGY, 1988, 254 (01) :E1-E15
[10]  
JACKSON EK, 1991, ANNU REV PHARMACOL, V31, P1