Widgren B R
Department of Medicine, Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Hospital. Faculty of Medicine, University of Göteborg, Sweden.
Scand J Urol Nephrol Suppl. 1991;134:1-75.
In an attempt to explore pathophysiological mechanisms relevant for the development for future primary hypertension, we investigated young normotensive men with positive family histories of hypertension (PFH) regarding blood pressure, body weight, systemic and renal haemodynamics as well as cardiovascular hormones and sodium homeostasis. Sixteen subjects with PFH and thirteen controls with negative family histories (NFH), matched for age and body weight were investigated at age 31 and after five years. Blood pressure and heart rate did not differ between the two groups at the first or follow-up examination. At follow-up body weight had increased and a positive correlation between blood pressure and body mass index was found in subjects with PFH, while subjects with NFH had unchanged blood pressure and body weight. Initially, intraerythrocyte sodium content was increased in subjects with PFH, however, at follow-up intraerythrocyte sodium content did not differ between the two groups. At follow-up systemic and renal haemodynamics and sodium homeostasis were investigated in fifteen subjects with PFH and in twenty-nine controls matched for age (36 +/- 5 year) and with NFH. The control group was divided into one group matched for body mass index (n = 15) and one group with normal body mass index (n = 14). Blood pressure and central venous pressure were measured during bolus injections of phenylephrine and during an acute saline/fluid load (1000ml 0.9% NaCl within 10 min). Renal haemodynamics and blood pressure were measured during low doses (0.1 and 0.5 ng/min/kg) continuous infusions of angiotensin II (AII). At baseline blood pressure, body weight and sodium excretion were higher in subjects with PFH and matched controls as compared with lean controls. Calf and forearm haemodynamics (pletysmography), plasma catecholamines, plasma renin activity, angiotensin II, aldosterone, blood volume and erythrocyte sodium efflux rate constant did not differ between the three groups. Circulating atrial natriuretic peptide was higher in subjects with PFH than in the two control groups. In subjects with PFH there was a negative correlation between renal sodium excretion at baseline and the ouabain-sensitive sodium efflux rate constant. During the acute saline/fluid load central venous pressure and systolic blood pressure increased more and venous vascular compliance (ml/mmHg/kg) was reduced in PFH. Atrial natriuretic peptide release and renal sodium excretion were blunted during saline/fluid load in subjects with PFH as compared with the two control groups. Renal blood flow and renal vascular resistance did not differ at baseline. Glomerular filtration rate was somewhat higher in PFH.(ABSTRACT TRUNCATED AT 400 WORDS)
为了探索与未来原发性高血压发生发展相关的病理生理机制,我们对有高血压家族史(PFH)的年轻血压正常男性进行了研究,涉及血压、体重、全身及肾脏血液动力学、心血管激素和钠稳态等方面。选取了16名有PFH的受试者和13名无家族史(NFH)的对照者,两组年龄和体重匹配,在31岁时及5年后进行了调查。首次及随访检查时,两组血压和心率无差异。随访时,有PFH的受试者体重增加,且血压与体重指数呈正相关,而无家族史的受试者血压和体重未变。最初,有PFH的受试者红细胞内钠含量增加,但随访时两组红细胞内钠含量无差异。随访时,对15名有PFH的受试者和29名年龄匹配(36±5岁)且无家族史的对照者进行了全身及肾脏血液动力学和钠稳态研究。对照组分为体重指数匹配组(n = 15)和体重指数正常组(n = 14)。在静脉注射去氧肾上腺素期间及急性盐水/液体负荷(10分钟内输注1000ml 0.9%氯化钠)期间测量血压和中心静脉压。在低剂量(0.1和0.5 ng/min/kg)持续输注血管紧张素II(AII)期间测量肾脏血液动力学和血压。基线时,有PFH的受试者及匹配对照者的血压、体重和钠排泄高于瘦对照者。三组间小腿和前臂血液动力学(体积描记法)、血浆儿茶酚胺、血浆肾素活性、血管紧张素II、醛固酮、血容量和红细胞钠外流速率常数无差异。有PFH的受试者循环心房利钠肽高于两个对照组。有PFH的受试者基线时肾钠排泄与哇巴因敏感的钠外流速率常数呈负相关。急性盐水/液体负荷期间,有PFH者中心静脉压和收缩压升高更多,静脉血管顺应性(ml/mmHg/kg)降低。与两个对照组相比,有PFH的受试者在盐水/液体负荷期间心房利钠肽释放和肾钠排泄减弱。基线时肾血流量和肾血管阻力无差异。有PFH者的肾小球滤过率略高。(摘要截断于400字)