HYDROCORTISONE-INDUCED HYPERTENSION IN MEN - THE ROLE OF CARDIAC-OUTPUT

被引：37

作者：

PIRPIRIS, M ^{[1
]}

YEUNG, S ^{[1
]}

DEWAR, E ^{[1
]}

JENNINGS, GL ^{[1
]}

WHITWORTH, JA ^{[1
]}

机构：

[1] ROYAL MELBOURNE HOSP,DEPT NEPHROL,PARKVILLE,VIC 3050,AUSTRALIA

来源：

AMERICAN JOURNAL OF HYPERTENSION | 1993年 / 6卷 / 04期

基金：

英国医学研究理事会;

关键词：

BETA-BLOCKADE; BLOOD PRESSURE; CARDIAC OUTPUT; PERIPHERAL RESISTANCE; STEROIDS;

D O I：

10.1093/ajh/6.4.287

中图分类号：

R6 [外科学];

学科分类号：

1002 ; 100210 ;

摘要：

In previous studies we have shown that administration of 200 mg/day hydrocortisone (cortisol) to normal subjects raises blood pressure and cardiac output, with no change in total peripheral resistance or resting forearm vascular resistance. We have tested the hypothesis that this rise in cardiac output is essential for the rise in blood pressure (BP). Six normal volunteer men, aged 22 to 34 years, took part in two studies of 10 days, in random order, at least 4 weeks apart. Placebo (Study A) or 50 mg atenolol orally, 12 hourly (Study B), was given on days 1 to 10 and 50 mg cortisol orally, 6 hourly, on days 5 to 10. Blood pressure and cardiac output (Fick technique, alternative Doppler) were measured on days 4 and 10. In Study A (placebo and cortisol) systolic BP rose from 116 to 125 mm Hg (standard error of the difference, SED 1.5), P < .01, and in Study B (atenolol and cortisol) from 109 to 120 mm Hg (SED 1.5), P < .01. Cardiac output (indirect Fick) rose from 4.8 +/- 0.01 to 5.9 +/- 0.2 L/min, P < .01, in A, and was unchanged in Study B, 4.4 +/- 0.1 to 4.4 +/- 0.2 L/min. Cardiac output measured by Doppler method was similar in pattern, 5.1 +/- 0.2 to 6.7 +/- 0.2 L/min (P < .01) in A and 5.7 +/- 0.2 to 5.8 +/- 0.2 in B. Calculated peripheral resistance fell in Study A and increased in Study B. These data are consistent with the notion that the rise in blood pressure produced by cortisol administration in humans is not dependent on increase in cardiac output.

引用

页码：287 / 294

页数：8

共 49 条

[1]

Whitworth J.A., Saines D., Scoggins B.A., Blood pressure and metabolic effects of cortisol and DOC in man, Clin Exp Hypertens, 6, pp. 795-809, (1984)

[2]

Connell J., Fisher B.M., Davidson G., Fraser R., Whitworth J.A., Effect of sodium depletion on pressor responsiveness in ACTH-induced hypertension in man, Clin Exp Pharmacol Physiol, 14, pp. 237-242, (1987)

[3]

Sudhr K., Jennings G.L., Esler M.D., Hydrocortisone-iiiuulcu iiypciiciiöiuii ui liuuiciiid. I ic&sui icajpuiiaivc-ness and sympathetic function, Hypertension, 13, pp. 416-421, (1989)

[4]

Hargreaves M., Jennings G., Evaluation of the C02 rebreathing method for the non-invasive measurement of resting cardiac output in man, Clin Exp Pharm Physiol, 10, pp. 609-614, (1983)

[5]

Snedecor G.W., Cochran W.G., Two Way Classifications, in Statistical Methods. Iowa, pp. 299-338, (1967)

[6]

Whitworth J.A., Mechanisms of glucocorticoid-induced hypertension, Kidney Int, 31, pp. 1213-1224, (1987)

[7]

Vanhees L., Aubert, Fagard A.R., Hespel P., Amery A., Influence of /^-versus ^-adrenoreceptor blockade on left ventricular function in humans, J Cardiovasc Pharmacol, 8, pp. 1086-1091, (1986)

[8]

Kupari M., Heikkila J., Tolppaner E.-M., Nieminen, Ylikahri M.SR., Acute effects of alcohol, beta blockade and their combination on left ventricular function and haemodynamics in normal man, Eur Heart J, 4, (1983)

[9]

Reeves R.A., Smith D.L., Leenen F., Hemodynamic interaction of nonselective vs beta-1-selective beta blockade with hydralazine in normal humans, Clin Pharmacol Ther, 41, pp. 326-335, (1987)

[10]

Gisvold S.E., Brubakk A.O., Transcutaneous measurement of blood flow velocity in the human aorta using pulsed ultrasound, Cardiovasc Res, 16, pp. 26-33, (1982)

← 1 2 3 4 5 →