This in turn depending upon the VMC activity

ty and the end diastolic volume (i. e venous return to the heart), affect the BP. Peripheral resistance. Recall, the peripheral resistance. R= 8 rl. From this, we have 1. If the viscosity rises (i.e. in polytythemia) the BP rises, and vice versa. 2 But the most important factor is the radius of the blood vessel 'r' as BP varies inversely as r4. The radius in turn, varies according to the tone of the vascular smooth muscles. Greater the tone smaller the lumen of the vessel and greater is the resistance. As described in chapter 8 of see. V, the tone of the smooth muscle depends'upon the following: 1. Sympathetic discharge. This in turn depending upon the VMC activity. [The VMC activity, in turn, is influenced by, - (a) raflexes from the periphery (e. g. baroreceptors from the arterial tree) ,(b) impulses from higher center (e.g. emotion) and (c) PaO2 etc. (see fig. 5.8.1 for de-tails)]. In short, the sympathetic stimulation causes vasoconstriction, which leads to increased resistance and thus the BP rises. 2. Chemicals, like the angiotensm, adrenalin etc. (chap. 8 sec. V, for details), which act directly on the smooth mus-cles. The actual process of regulation (that is, maintenance of BP homeostasis) is usually divided into two groups viz (A) short term and (B) long term controls. A Short term control is achieved via neural mechanism. It includes the sinu aortic reflex (for details, see chaps. 4 & 8. sec V) principally and some other reflexes like reflexes from atrial receptors, stretch reflexes from left ventricle etc. (fig. 5.8.1). In short, baroreteptors of the heart and artenal tree are the kingpin of the homeo static mechanism of short term reflex. The sinu aortic mechanism is the principal short term reflex in maintaining the BP homeostasis. In abnormal circumstances, like, a sharp fall of BP (say due to massive hemorrhage or severe diarrhoea) or a sharp rise of BP (say due to uncontrolled anger causing severe sympathetic stimulation) it begins to act immediately, and tries to bring back the BP to the normal value ("buffer nerves"). The other reflexes also maintain the BP homaostasis to some extent. Thus, hypervolemia causing elevation of BP stimulation of atrial volume receptors suppression of ADH loss of extracellular fluid via urine restoration of blood volume and thus of BP. Some other reflexes like the J receptors from lung affect the BP and work towards the benefit of the body. But they are not called into action in day to day life. [The VMC is also stimulated when the limbic system is stimulated (fig. 5.8.1.) as in rage. But this is not aimad towards the maintenance of BP homeostasis. Rather, the elevation of BP is an associated feature of the emotions like rage. The hypothalamus is stimulated during exposure to cold (chap 1, Sec. XD); this too is an associated feature. Motor and premoter cortex are stimulated during exercise, causing tremendous redistribution of blood (by dilatation of skeletal muscle vessels and constriction of splanchnic and cutaneous vessels) but this is to meet the demands arising, out of a particular situation and not aimed towards achieving BP homeostasis)] B. Long term control. This is achieve a through the renin-angiotensin - aldosterone axis as well as via ANP and work through adjustment of blood volume as described below. Blood volume and BP. In the foregoing discussion (neural control) it has bean assumed that the volume of blood has been kept constant throughout. Blood pressure homeostasis however, can be achieved by adjusting the blood volume also. Thus, fall of blood volume release of renin from the kidneys production of angiotensin production of aldosterone sodium retention retention of body fluid so that blood volume expands restoration of BP. In short, fall of BP due to hemorrhage can be tackled by increasing the blood volume, via renin angiotensin axis. This mechanism is however slow to appear and of prolonged duration. Conversely, if there is hypervolemia of blood. the atria are distended ANP (atrial natriuretic peptide. for details, see chap 2 sec VIII) secreted from atrium — diuresis hypervolemia corrected hypertension corrected. Elasticity of blood vessel and BP. The Windkessel vessels are elastic vessels. As already stated (chap. 7, sec. V) if they lose their elasticity, systole hypertension develops, where the SBP is raised but not the DBP. In systolic hypertension the mean BP does not change so much [Compare Ihe effects of systolic and diastolic hypertension on the mean BP. from a pressure of 120/3C mm Hg, let the BP rises to 170/80 mm Hg in one person or to 140/110 mm Hg in a second person. In the first instance, the mean BP is 110 bul in the second it becomes 120 mm Hg although the rise of SBP + DBP together, is 50 mm in both the cases ). A predominant rise in DBP indicates rise m penpheral resistance and is characteristic of essential hypertension whereas a systolic hypertension indicates atherosclerotic degeneration of Windkessel vessels. In the past, rise of DBP used to be regarded as more ominus of the two types (systolic versus diastolic) of hypertension but the leaching was not wholly correct. Effect of velocity on BP If the velocity of blood is very high, the BP determined by sphygmomanometer (henceforth to be mentioned at BP) will give a low value. Thus, (i) in aortic stenosis, the BP is very low. (ii) LowBP is also found in cases of coarciation of aorta, beyond the narrowing. In both the instances, the narrowing increased the velocity of the blood as explained earlier (fig. 5.7.1) and this partly explains the sharp fall of BP. Conditions affecting BP A. Physiological 1. The effect of age on BP has already been