Neurogenic factors in hypertension
Slonim, Arnold Robert
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The medulla oblongta contains two distinct vasomotor centers, the vasoconstrictor and the vasodilator. Vascular tone is enhanced by vasoconstrictor impulses and relaxed by vaso-dilator impulses. Hooker (1918) and Donegan (1921) reported that venous blood vesselt are under the same tonic influences as the arterial vessels. The capillaries, on the other hand, lack a muscular coat and can not respond to stimulation. However, Fulton and Lutz (1940) directly observed in the frog that precapillaries and capillary origins contain modified smooth muscle cells, which are innervated by a nerve plexus physiologically independent of the supplying arterioles. The sphincter-like capillary origins regulate the capillary blood flow. Dale and Evans (1922) reported that carbon dioxide directly stimulates the vasoconstrictor center. McDowall (1930) showed that oxygen lack also excites the vasoconstrictor center and in later work (1935) reported that the effect of oxygen lack is not as great as that of excess carbon dioxide. Adrenalin and pitressin in moderate doses cause vasoconstriction. Burget and Visscher (1927) reported whether adrenalin constricts or dilates a blood vessel depends on the pH of the blood. Smaller amounts of adrenalin cause vasoconstriction in a more alkaline medium. Lewis and Zotterman (1927) reported that any strong chemical and ultraviolet light produce a flare reaction. Menkin (1936) reported that inflammatory substances cause an immediate local vasodilation and increase the capillary permeability. Temperature changes influence both innervated and denervated vessels. Cold stimuli effect vasoconstriction and warm stimuli cause vasodilatation. Howell, Budgett and Leonard (1894) noticed that the vasoconstrictor nerves are more susceptible to temperature changes than the vasodilators. McDowall (1930) reported that the vasodilator effect lasts longer than the vasoconstrictor effect. Excessive temperature changes produce inconsistent results. Abnormal vasoconstriction causes an increase in the peripheral resistance of the blood vessels. Page (1937) stated that an increased resistance to flow appears to be the major if not sole factor in the production of hypertension. Blood viscosity does not appear to be a factor in increasing the peripheral resistance. That peripheral resistance is of vasomotor origin or due to "intrinsic spasms" of the blood vessels is a very controversial subject (Page, 1937). The main control of peripheral resistance is in the variation of the contraction of the musculature of the vessels, which is normally under nervous and chemical influences. However in the various types of hypertension, several factors may exist which cause an increased peripheral resistance. The cardiac output is usually unchanged in hypertension. Page (1937) reported that only in cases of hyperthyroidism is an increased cardiac output evident. The medullary centers may become hyperactive and cause hypertension. The abnormal vasoconstrictor response following cold stimulation suggests vasomotor instability (Hines, 1940a, and Grimson, 1941). Fulton (1943) stimulated areas 4 and 6 of the cerebral cortex of the cat and produced a marked rise in the systolic pressure. Frontal lobe stimulation also raises the blood pressure (Bailey and Sweet, 1940). An increased intracranial pressure effects marked hypertension (Griffith, Jeffers and Lindauer, 1935). Griffith and Roberts (1938) suggested that hypertension results from the obstruction of the perineural-lymphatic drainage. Grimson, Wilson and Phemister (1937) and Freeman and Jeffers (1940) reported that sympathectomy abolishes this type of hypertension. Alexander (1939) stated that emotional conflicts may either enter into the onset of hypertension or aggravate the existing symptoms. Weiss (1942) reported that emotional tension due to a chronic repressed rage is responsible for increasing both the anxiety state and tha blood pressure. Psychotherapy may dig out the emotional conflict and relieve the anxiety that aggravates the hypertension. The autonomic nervous system with the intrinsic cardiovascular reflexes regulate the blood pressure. The pressor reflex of the heart and large veins shifts the large venous reservoir to the arterial system (Bainbridge, 1915). Nonidez (1937) reported subendothelial pressoreceptors in the intrapericardial portion of all the large veins entering the heart and in the coronary sinus near the right auricle. Nonidez stated that the Bainbridge reflex is due to stimulation of the pressoreceptors of the veins and that auricular distention does not actively initiate the reflex cardiac acceleration. The carotid sinus cardiovascular reflex causes a sustained vasodilatation (Winder, 1937). That the carotid sinus cardiac reflex is more poorly maintained than the sinus vasomotor reflex is shown by the fact that there is a larger crossed component of the efferent vasomotor pathway than the efferent cardiac pathway, and that the former shows the process of occlusion, while the latter shows the process of facilitation (Wang and Borison, 1947b). Winder (1937) pointed out that the aortic cardiovascular mechanism has a great buffering effect on the carotid sinus system. The aortic system is concerned more with cardiac control than the vasomotor regulation (Blalock, 1940). The vagi and sympathetics appear to act reciprocally in a certain time sequence in cardiac control via the carotid sinus reflex. Wang and Borison (1947a) showed that the vagi predominate in the first and the sympathetics in the last phase of the sequence in cardiac restraint. Vagal bradycardia is independent, however, of the sympathetic component. Sattler (1940) stated that stimulation of the central end of the cut vagus nerve produces a reflex rise in the blood pressure. Two components exist in the reflex, a sudden rise (sympathetic effect) and a delayed rise (vago-neurohypophysial effect). Schmidt and Comroe (1940) reported that chemical stimulation of the carotid and aortic bodies causes a reflex pressor effect. The chemoreceptors have a lower threshold to anoxia than the vasomotor centers; with carbon dioxide, the opposite is the case. The pH of the blood is more important than excess carbon dioxide in exciting the chemoreceptors. These workers suggested that only in the hypertension of anoxia do the chemoreceptors play an important role. Ranson (1936) postulated that the sympathetic center is located in the posterior region of the hypothalamus and the parasympathetic center in the anterior hypothalamic area. The hypothalamus has direct connections with the brain stem and lower centers as well as indirect connections with the cerebral cortex; during intense emotional excitement, the hypothalamus unifies the activity of the sympathetic nervous system. Removal of this organ prevents the formatlon of a fully developed emotional response. Page (1937) stated that vasoendocrine secretions eithe directly enhance vascular tone and arterial pressure or combine with other secretions to this effect. The adrenal cortical secretions are very important in maintaining vascular tone and may enter into the genesis of renal hypertension. Heymans and Bouckaert (1931) reported that section of the carotid sinus and the aortic depressor nerves produces a sustained neurogenic hypertension. Winder, Bernthal and Weeks (1938) reported that carotid body ischemia greatly excites the chemoreceptors to cause hypertension. Nowak and Walker (1939) and Blalock (1940) reported that cerebral vascular ischemia causes hypertension providing the collateral circulation is also affected. Renal hypertension can be produced by clamping the renal artery (Goldblatt, Lynch, Hanzal and Summerville, 1934) or by a capsule about the kidney (Page, 1939). Braasch, Walters and Hammer (1940) stated that the renal lesion must cause widespread atrophy of the renal tissues and sclerosis of the renal vessels to cause renal hypertension. Foster and Maes (1947) reported that in rabbits neurogenic hypertension caused an increase in the renal plasm flow and glomerular filtration rate. Grimson (1941) and Goldblatt, Kahn and Lewis (1942) reported that neither renal denervation or any type of sympathectomy abolishes renal hypertension. Feet, Woods and Braden (1940) failed to show that the renal vasoconstrictor nerves are hyperactive in renal hypertension. Grollman (1946) reported that chronic renal hypertension is maintained not by a humoral process but by a neurogenic factor; removal of the diseased kidney or all renal tissue does not lower the blood pressure. Grimson (1940) reported that renal denervation, partial and complete sympathectomy all fail to prevent neurogenic hypertension. Grimson (1945) reported that cervical cord section does not permanently reduce the hypertension. Grimson, Wilson and Phemister (1937) reported a new central vasopressor mechanism appears after total sympathectomy which maintains a moderate hypertension. Fishberg (1948) reported that sympathectomy was useful in less than 4 percent of the cases with essential hypertension. If the symptoms of hypertension are severe, sympathectomy may offer some relief.
Thesis (M.A.)--Boston University
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