ANATOMY AND PHYSIOLOGY OF THE VASCULAR WALL 



87: 



It may very likely be that in both the carotid sinus 

 and the aortic arch, the neurofibril networks of the 

 pressoreceptors are in one way or another attached 

 to the connective tissue, especially the elastic mem- 

 branes or fibers. Thus the pressoreceptors are assumed 

 to be parallel to the elastic membranes or fibers, an 

 assumption which agrees with the facts now available. 

 They will be stimulated if the smooth muscles increase 

 the tension of the elastic tissue by contraction. But 

 now the stimulated pressoreceptors reflexly lower the 

 blood pressure until the tension of the elastic fibers, 

 and with them that of the pressoreceptors, decreases 

 again to the normal value (equation 1). The tension 

 muscles are thus able to change the blood pressure, 

 as shown in the work of Bader & Kapal (5). The 

 model of Kapal & Bader (43), and the results of 

 Heymans et al. (37-39) agree very well. It also fits very 

 well with the idea that the tension muscles are mul- 

 tiple-unit muscles, since they are a type of control 

 organ which does not depend on the wall tension. 



The model may also explain the higher resistance 

 and blood pressure of older people in contrast to 

 younger people. Smooth muscles degenerate with age 

 and are replaced by collagen fibers [Meyer (58), 

 Kobayashi (46)]. This means that the smooth muscles 

 are no longer able to stretch the elastic tissue as much 

 as in younger individuals. But if the tension of the 

 elastic tissue is lowered by lack of smooth muscle 

 function, the blood pressure will rise until the tension 

 reaches a physiological value for the pressoreceptors. 

 As the muscles continue to degenerate, the pressure 

 needed to stimulate the receptors continues to rise, 

 and this may be one of the various mechanisms which 

 cause essential hypertension. Such a hypertension 

 must be called "essential," since the weakness of the 

 tension muscles cannot be diagnosed and there may 

 be no clearly diagnostic anatomical change of the 

 arterial wall. The only evident sign of such muscle 

 weakness would be the hypertension. 



However, in the aging process degeneration of 

 smooth muscles, fraying of elastic tissue, and increase 

 of the collagen tissue are accompanied by a decrease 

 in the distensibility of the arteries. A 20-year-old 

 aorta can be distended to 300 per cent of its zero- 

 pressure volume, but a go-year-old aorta can be 

 distended only about 25 per cent [Simon & Meyer 

 (86)]. If the inflexion point of the volume pressure is 

 high and the curve reaches its slope of maximum 

 distensibility at about 100 mm Hg (the normal mean 

 blood pressure) (cf the 13-year-old aorta in fig. 8a), 

 the work required of the heart is reduced in maintain- 

 ing a physiological pressure level. If the inflexion 



occurs at a lower pressure level, as after an increase 

 of collagen tissue (older aortas), the mean blood pres- 

 sure falls on a steeper slope of the pressure-volume 

 curve. Under this condition the heart would have to 

 work more were this disadvantage not compensated 

 by enlarging the volume of the aorta. Figure 8a shows 

 a fivefold increase in the volume at 100 mm Hg 

 between the 13-year-old and the 85-year-old aorta. 

 The volume change of the elastic chamber with each 

 heart beat, that is, the volume which can be injected 

 to give the physiological pulse pressure amplitude, 

 remains nearly constant until about the sixth decade 

 of life, as a result of the initial volume increase. This 

 means that the heart work need not increase with the 

 decrease of the wall distensibility [Simon & Meyer 

 (86)]. The aortas over 60 years do not show any 

 inflexion point; they are convex to the abscissa from 

 the very beginning. This signifies that collagen tissue 

 is already stressed near zero pressure. The pulmonary 

 artery shows similar behavior, but the inflexion point 

 occurs at a lower pressure, just as the pulmonary 

 pressure is lower [Meyer & Simon (60), Frasher & 

 Sobin (32)]. 



The ratio of radius to wall thickness, which is im- 

 portant in the relationship of the wall stress to the 

 blood pressure (equation 1 ), is the same at zero 

 pressure in aortas of different ages [Hieronymi 



fig. 8. a: Pressure-volume diagrams of the thoracic aorta of 

 the human at different ages, b: The relationship of radius to 

 wall thickness of the same aortas in relation to the pressure. 

 [Bader (4).] 



