Active reactions of the rabbit ear artery to distension.

Abstract

SUMMARY1. Changes in the external diameter of active arteries, excised from the rabbit ear, were recorded following jumps in pressure within the arteries. The arteries were either spontaneously active or were constricted with noradrenaline.2. Active arteries dilated when the transmural pressure was jumped from 60 to 100 mmHg, but the dilatation was largely, sometimes completely, overcome by compensatory constriction within 1-2 min. Varying the constriction from 15 to 80 % of the maximal constriction had no effect on the ability of the arteries to counteract distension. An average of 90 ± 2 % of the distension was overcome in 2 min and this was achieved against increases in stress (force/wall cross-sectional area) on the muscle of not less than 74 %. Jumps in pressure rarely enhanced constriction and then only when constriction was slight (< 15 % of maximal).3. Restoring the transmural pressure to 60 from 100 mmHg produced a transient constriction when the initial constriction was less than 50 % of the maximal constriction. The sequence of counteraction of distension and transient constriction on reversing the pressure jump was reproducible for many hours.4. Increasing constriction of the arteries first decreased and then, at maximal constriction, suppressed all transient changes in diameter. Smaller jumps in pressure produced less dilatation which was more readily prevented by increasing constriction.5. These results show that the wall of the ear artery possesses a pressure-sensitive, negative feed-back mechanism which minimized changes in diameter following jumps in pressure.

The interaction between noradrenaline activation and distension activation of the rabbit ear artery.

“…2, 3 and 4). Changing the contribution of the active and passive stresses to the total wall stress by varying constriction from 20 to 70 % of maximal had, as reported previously (Speden, 1984a), no significant effect on the counteraction of distension.…”

“…The compliance of the series elastic component (Dobrin, 1983) must also make some as yet undefined contribution to the reaction to distension. Despite this complexity, the counteraction of the distension achieved in 2 min was in these, as in previous experiments (Speden, 1984a), remarkably constant at all examined constrictions which went up to 75 % of the maximal constriction. This counteraction of distension was achieved primarily through enhanced activation of the muscle.…”

“…Constriction of blood vessels is a complex interaction between the distending force, the opposing passive recoil and active forces, and the contractile capacity which all change when constriction alters (Dobrin, 1978(Dobrin, , 1983. It was also necessary to suppress a tendency towards instability and spontaneity of constriction (Speden, 1984a) before the interaction between noradrenaline activation and distension activation could be assessed. This was achieved by lowering the organ bath temperature to 32-33 'C.…”

“…Despite this early recognition, the physiological significance of these local reactions of blood vessels, which are often referred to as myogenic responses, remains poorly understood (Bouskela & Wiederhielm, 1979;Johnson, 1980, Borgstrom, Griinde & Mellander, 1982 Burrows & Johnson, 1983). The ability of pressurized segments of the rabbit ear artery to react reproducibly to jumps in transmural pressure (Speden, 1984a) provides an opportunity to evaluate the physiological role of these myogenic responses. The geometry of tubes does impose special functional requirements upon vascular smooth muscle (Burton, 1951) and a myogenic control system could help the muscle to fulfil these requirements.…”

Evidence that the contraction-induced rapid hyperemia in rabbit masseter muscle is based on a mechanosensitive mechanism, not shared by cutaneous vascular beds

“…In this respect, a prominent myogenic reactivity is described for arterial and arteriolar segments of brain, skeletal muscle (5), and kidney while no explicit reference is usually made to skin blood vessels (30,39,40). To our knowledge, only few studies described the occurrence of a slow myogenic response in cutaneous vascular beds (13,20,42) developing in 1-2 min upon sustained changes in transmural pressure, while the rapid component has never been investigated.…”