Cardiovascular hypertrophy and hypertension: causes and consequences.
In chronic hypertension, vascular resistance is raised and there is concentric left ventricular (LV) hypertrophy, at least in animal models. Together these changes enhance hemodynamic performance ("amplifier" properties) and help maintain elevated blood pressure (BP) and net microcirculatory exchange. Sometimes there is vascular "remodelling", with only luminal narrowing, but no net increase in medial mass. This can be related to non-uniform distribution of wall stress: when the amount of hypertrophy normalizes average wall stress, that on luminal side tends to be undercorrected accounting for preferential growth in that direction, whilst stress on the adventitial side is overcorrected, which results in a tendency to reabsorb material. In Goldblatt hypertension, about 20% of the rise in BP is due to the renal artery stenosis resistance, with the rest differing during the early and late phases: the early contribution is due to angiotensin II (AngII)-mediated systemic constriction and subtle fluid volume changes, whilst later on the cardiovascular amplifiers take over many of the actions of AngII. In SHR, trophic sympathetic nervous system actions are crucial for the rise in BP and development of structural changes and both contribute to the elevation of BP. Neonatal sympathectomy + prazosin treatment prevents hypertension and structural changes in SHR. Angiotensin converting enzyme (ACE) plays a similar role in cardiovascular development in SHR and Wistar Kyoto (WKY) rats. Prolonged administration of ACE inhibitors to SHR produces long term attenuation of hypertension because of an impaired capacity for cardiovascular development in adult animals. In human hypertension, long term treatment with common antihypertensive drugs is required to produce substantial regression of cardiovascular hypertrophy. Since it imposes marked non-uniformity on the distribution of capillary blood flow, with the potential for rarefaction and organ damage, therapy aimed at regression of hypertrophy is a worthwhile target.
Korner
P I
PI
Baker Medical Research Institute, Melbourne, Victoria, Australia.
D000818:Animals; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000150:complications* / Q000503:physiopathology; D014655:Vascular Resistance / Q000502:physiology