Biomechanical and Electrical Responses of Normal and Hypertensive Veins to Short-Term Pressure Increases

Abstract

Observation of elevated central venous pressure or systemic filling pressure in various forms of arterial hypertension strongly suggests that systemic veins may participate in inducing and/or maintaining the hypertensive state [1,12]. However, sufficient information is not available to identify the mechanism(s) by which veins could contribute to the development and/or maintenance of chronic arterial pressure elevation [6]. It is plausible to hypothesize that some basic properties of the smooth muscle — such as intrinsic myogenic reactivity — in the systemic veins are altered in the hypertensive state, for then even a relatively small enhancement of stretch-induced intrinsic tone of the vessel wall could contribute significantly to the hemodynamic changes observed in arterial hypertension. Augmentation of this response may lead to the increase of central cardiopulmonary blood volume, postcapillary resistance, and the reduction of the pressure-buffer capacity of the venous system. This hypothesis is encouraged by our recent data demonstrating that there is an enhanced pressure-induced myogenic tone in isolated, small (100–150 μm internal diameter) gracilis arteries from reduced renal mass (RRM) rats — a model of volume-expanded hypertension — relative to non-RRM controls [13]. In accordance with these data, results recently published by Mulvany [10] suggest that increased intrinsic oscillatory activity of the mesenteric resistance vessels of spontaneous hypertensive rats plays a part in the development of high blood pressure.

This work was supported by National Heart, Lung, and Blood Institute Research Grant HL-29587, by National Science Foundation Grant INT-8908904 (USA), and by OTKA1/1314/1988 (Hungary).