ANATOMY AND PHYSIOLOGY OF THE VASCULAR WALL 



8 7 ■ 



the extremities is reported by Folkow (26). This idea 

 has a long history, beginning with the contribution of 

 Bayliss (9) in 1902. 



It may be assumed that the contraction of smooth 

 muscle is caused by the increase of tension in the 

 vascular wall as a result of the rising blood pressure. 

 There is no adaptation to the tension stimulus, which 

 agrees with the results of Bulbring (17) on the in- 

 testinal smooth muscle. Folkow (28) suggests that the 

 tonus of the resistance vessels is maintained by myo- 

 genic activity of their smooth muscles, which are 

 excited by the tension of the wall (similar to the case 

 for intestinal smooth muscles shown in fig. 4). How- 

 ever, this autoactivity, in both types of smooth 

 muscle, is controlled by the autonomic nervous system. 

 Since the smooth muscles in the peripheral arteries are 

 mostly ring muscles, it may be that the ring muscles 

 can behave like a syncytium. The tension muscles are 

 always interrupted by elastic fibers, and Prosser et al. 

 (69) have found a much larger intercellular distance 

 between the individual muscle cells in vessels of the 

 elastic type than in other organs (1000 nm in the pig 

 carotid artery as against 120 nm in the cat intestine). 

 It is therefore very likely that they form a multiunit 

 system in which the muscle cells receive extensive 

 sympathetic and parasympathetic innervation. This 

 impression is confirmed by Burnstock & Prosser (18), 

 who got no response to stretch from the carotid artery, 

 a vessel of the elastic type, or from the renal vein. 



Over and over the idea appears in the literature that 

 arteries may contract and relax as quickly as the 

 heart and so force the blood to the periphery just as 

 the intestine propels a bolus to the colon. One of its 

 newer proponents, Dickinson (22), shows a contrac- 

 tion curve of a sheep's hepatic artery which develops 

 its peak tension in about 3 sec after an unphysiological 

 stimulus of 120 v. The slowness of contraction and the 

 long latency speak against the possiblity of the propul- 

 sion of blood by arterial contraction. This latter 

 attitude is shared by Fleisch (25) and Wetterer & 

 Kapal (99). 



If smooth muscles are extended slowly they behave 

 like a plastic material. They can maintain a given 

 length, either short or long, for protracted periods 

 with very low metabolism. However, this length 

 maintenance does depend upon repeated stimulations 

 of constant magnitude. If the stimulation is increased, 

 these muscles respond by contracting, regardless of 

 their initial length (except, of course, if already maxi- 

 mally contracted). From this it follows that there must 

 be some mechanism which enables smooth muscle to 

 shift its behavior from plastic when "set" in length to 



visco-elastic, when contracting. Uxkiill (93) has postu- 

 lated for this a "Sperrung" (catch mechanism), 

 signifying that the protein filaments within the muscle 

 fibers "catch" at a certain length so that they cannot 

 slip apart when tension is applied. 



Three possible explanations have been offered for 

 this behavior. The first, suggested by Reichel, is that 

 the smooth muscle consists of two elements in series, 

 an elastic element and a contractile element, where 

 the contractile element can behave with either 

 plasticity or contractility (70). If this is true, the 

 "catch mechanism" could be described as a trans- 

 formation of plasticity to contractility, where the 

 element is "caught" at any length and thus is able to 

 keep a given tension with a low metabolism or to 

 contract. An alternative to this theory, suggested by 

 Lowy & Hanson (56a), is called the sliding filament 

 mechanism. They assume that thin discontinuous 

 actin-containing filaments move relative to thick 

 discontinuous paramyosin-containing filaments, as in 

 striated muscles. Linkages are presumably formed 

 during contraction between both filaments all of one 

 type, with one rate of formation. The rate of breaking 

 can vary from slow (tonic contraction, visco-elastic) 

 to fast (phasic contraction, plastic) depending on the 

 concentration of a relaxant present (i.e., 5-hydrox- 

 ytryptamine). Repeated excitatory stimulation could 

 maintain these linkages, whereas stimulation of 

 inhibitory nerves could increase the rate at which they 

 break [Lowy & Millman (57)]. A second possibility 

 is that the plastic and the contractile elements are in 

 parallel, with an elastic element in series. In such an 

 arrangement the catch mechanism could be in the 

 plastic element, whereas the contractile element 

 could cancel any plastic deformation by contraction. 

 Such a parallel arrangement is postulated by Johnson 

 (41a). He assumes that the contractile system is 

 formed by the actomyosin, and that paramyosin is 

 situated parallel to it as the plastic element. Laszt 

 (54) assumes a similar mechanism in the vascular 

 smoothVmuscle. A third possibility is that the plastic 

 and contractile elements are in series. In such an 

 arrangement the contractile element could work 

 only if the catch mechanism were put in action. 

 But it would then be necessary to have a special 

 mechanism to cancel the plastic deformation, such as 

 the presence of both fast and slow contractile elements 

 within the smooth muscle, the slow elements being 

 virtually "plastic." 



Whether any of these three mechanisms may be 

 the real one is not clear. It is possible, too, that one 

 smooth muscle may work by one mechanism and 



