Are cardiac and vascular "amplifiers" both necessary for the development of hypertension?
The vascular amplifier leads to enhancement of all resistance responses, from full dilatation to maximum constriction. The mechanism of resistance amplification is narrowing of the resistance vasculature, which is approximately constant at all levels of vasomotor tone. From the literature, the site of narrowing is localized to the small arteries and large arterioles. The narrowing at rest leads during constriction, to patchy reduction in blood flow in the microcirculation. The enhanced resistance responses of the vascular amplifier during constriction, increase blood pressure (BP) upstream, which minimizes the hemodynamic effects on the microcirculation and helps to maintain venous return. Concentric left ventricular (LV) hypertrophy is an amplifier of stroke volume and cardiac output. It reinforces the elevation of BP upstream from the site of vascular narrowing. This appears important for the initiation and maintenance of hypertension, in view of findings in SHR showing: (1) that in the course of normal development of hypertension the vascular amplifier properties develop before the onset of hypertension, which occurs in parallel with an increase in rate of LV hypertrophy; (2) after brief periods of enalapril treatment, hypertension redevelops in parallel with the redevelopment of LV hypertrophy, whilst the vascular amplifier properties remain suppressed; (3) treatment with immuno-sympathectomy plus prazosin prevents the development of both LV hypertrophy and hypertension but only produces gradual suppression of the vascular amplifier properties. The role of the sympathetic nervous system on LV-hypertrophy is mediated through alpha 1-adrenoceptors.
Korner
P I
PI
Baker Medical Research Institute, Melbourne, Australia.
Bobik
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A
Angus
J J
JJ
D000818:Animals; D006332:Cardiomegaly / Q000150:complications / Q000503:physiopathology; D006439:Hemodynamics / Q000502:physiology; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D008955:Models, Cardiovascular; D051381:Rats; D011918:Rats, Inbred SHR; D014655:Vascular Resistance / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology