Baumbach G L, Chillon J M
Department of Pathology, University of Iowa College of Medicine & Cardiovascular Center, Iowa City 52242, USA.
J Hypertens Suppl. 2000 May;18(1):S7-11.
Chronic hypertension profoundly alters the function and structure of cerebral blood vessels. Cerebral arterioles undergo remodelling, with a reduction in external diameter and hypertrophy of the vessel wall and a paradoxical increase in distensibility. The primary aim of this review is to consider recent findings in relation to determinants of remodelling, hypertrophy, and altered distensibility and composition of cerebral blood vessels during chronic hypertension, with an emphasis on the renin-angiotensin system. In particular, we highlight studies designed to examine the hypothesis that the effects of angiotensin-converting enzyme (ACE) inhibitors on cerebral vascular structure in stroke-prone spontaneously hypertensive rats (spSHR) may be independent of their effects on reductions in arterial pressure. For example, treatment of spSHR with the ACE inhibitor perindopril attenuates remodelling of cerebral arterioles, even when given in a low dose that only partially normalizes systemic arterial pressure and does not prevent hypertrophy. In contrast, treatment of spSHR with propranolol does not prevent cerebral arteriolar remodelling, even when given in a dose that produces a larger decrease in blood pressure than is achieved with the low dose of perindopril. Results such as these suggest that remodelling of cerebral arterioles during chronic hypertension may be independent of increases in arterial pressure, and instead may depend primarily on increased activity of the renin-angiotensin system. Evidence is also reviewed that suggests that the renin-angiotensin system may not contribute significantly to hypertrophy of cerebral arterioles during chronic hypertension. Rather, hypertrophy appears to depend in large part on increases in arterial pressure and, in particular, its pulsatile component.
慢性高血压会深刻改变脑血管的功能和结构。脑小动脉会发生重塑，其外径减小，血管壁肥厚，而扩张性却反常增加。本综述的主要目的是探讨慢性高血压期间脑血管重塑、肥厚以及扩张性和组成改变的相关决定因素的最新研究发现，重点关注肾素 - 血管紧张素系统。特别是，我们着重介绍旨在检验以下假说的研究：血管紧张素转换酶（ACE）抑制剂对易卒中自发性高血压大鼠（spSHR）脑血管结构的影响可能与其降低动脉压的作用无关。例如，用ACE抑制剂培哚普利治疗spSHR可减轻脑小动脉的重塑，即使给予低剂量，该剂量仅能部分使全身动脉压正常化且不能防止肥厚。相比之下，用普萘洛尔治疗spSHR并不能防止脑小动脉重塑，即使给予的剂量比低剂量培哚普利产生的血压下降幅度更大。诸如此类的结果表明，慢性高血压期间脑小动脉的重塑可能与动脉压升高无关，而可能主要取决于肾素 - 血管紧张素系统活性的增加。本文还综述了证据，表明肾素 - 血管紧张素系统在慢性高血压期间可能对脑小动脉的肥厚贡献不大。相反，肥厚似乎在很大程度上取决于动脉压的升高，尤其是其搏动成分。
