Hypertension in the Upper Part of the Body Caused by Coarctation of the Aorta. One out of every few thousand babies is born with pathological constriction or blockage of the aorta at a point beyond the aortic arterial branches to the head and arms but proximal to the renal arteries, a condition called coarctation of the aorta. When this occurs, blood flow to the lower body is carried by multiple, small collateral arteries in the body wall, with much vascular resistance between the upper aorta and the lower aorta. As a consequence, the arterial pressure in the upper part of the may be 40-50 per cent higher than that in the lower body.
The mechanism of this upper-body hypertension is almost identical to that of one-kidney Goldblatt hypertension. That is, when a constrictor is placed on the aorta above the renal arteries, the blood pressure in both kidneys at first falls, renin is secreted, angiotensin and aldosterone are formed, and hypertension occurs in the upper body. The arterial pressure in the lower body at the level of the kidneys rises approximately to normal, but high pressure persists in the upper body. The kidneys are no longer ischemic, so that secretion of renin and formation of angiotensin and aldosterone return to normal. Likewise, in coarctation of the aorta, the arterial pressure in the lower body is usually almost normal, whereas the pressure in the upper body is far higher than normal.
Role of Autoregulation in the Hypertension Caused by Aortic Coarctation. A significant feature of hypertension caused by aortic coarctation is that blood flow in the arms, where the pressure may be 40 to 60 per cent above normal, is almost exactly normal. Also, blood flow in the legs, where the pressure is not elevated, is almost exactly normal. How could this be, with the pressure in the upper body 40 to 60 per cent greater than in the lower body? The answer is not that there are differences in vasoconstrictor substances in the blood of the upper and lower body, because the same blood flows to both areas. Likewise, the nervous system innervates both areas of the circulation similarly, so that there is no reason to believe that there is a difference in nervous control of the blood vessels. The only reasonable answer is that long-term autoregulation develops so nearly completely that the local blood flow control mechanisms have compensated almost 100 per cent for the differences in pressure. The result is that, in both the high-pressure area and the low-pressure area, the local blood flow is controlled almost exactly in accord with the needs of the tissue and not in accord with the level of the pressure. One of the reasons these observations are so important is that they demonstrate how nearly complete the long-term autoregulation process can be.
Hypertension in Preeclampsia (Toxemia of Pregnancy). Approximately 5 to 10 per cent of expectant mothers develop a syndrome called preeclampsia (also called toxemia of pregnancy). One of the manifestations of preeclampsia is hypertension that usually subsides after delivery of the baby. Although the precise causes of preeclampsia are not completely understood, ischemia of the placenta and subsequent release by the placenta of toxic factors are believed to play a role in causing many of the man ifestations of this disorder, including hypertension in the mother. Substances released by the ischemic placenta, in turn, cause dysfunction of vascular endothelial cells throughout the body, including the blood vessels of the kidneys.This endothelial dysfunction decreases release of nitric oxide and other vasodilator substances, causing vasoconstriction, decreased rate of fluid filtration from the glomeruli into the renal tubules, impaired renal-pressure natriuresis, and development of hypertension.
Another pathological abnormality that may contribute to hypertension in preeclampsia is thickening of the kidney glomerular membranes (perhaps caused by an autoimmune process), which also reduces the rate of glomerular fluid filtration. For obvious reasons, the arterial pressure level required to cause normal formation of urine becomes elevated, and the long-term level of arterial pressure becomes correspondingly elevated. These patients are especially prone to extra degrees of hypertension when they have excess salt intake.
Neurogenic Hypertension. Acute neurogenic hypertension can be caused by strong stimulation of the sympathetic nervous system. For instance, when a person becomes excited for any reason or at times during states of anxiety, the sympathetic system becomes excessively stimulated, peripheral vasoconstriction occurs everywhere in the body, and acute hypertension ensues.
Acute Neurogenic Hypertension Caused by Sectioning the Barore-ceptor Nerves. Another type of acute neurogenic hypertension occurs when the nerves leading from the baroreceptors are cut or when the tractus solitarius is destroyed in each side of the medulla oblongata (these are the areas where the nerves from the carotid and aortic baroreceptors connect in the brain stem). The sudden cessation of normal nerve signals from the baroreceptors has the same effect on the nervous pressure control mechanisms as a sudden reduction of the arterial pressure in the aorta and carotid arteries. That is, loss of the normal inhibitory effect on the vasomotor center caused by normal baroreceptor nervous signals allows the vasomotor center suddenly to become extremely active and the mean arterial pressure to increase from 100 mm Hg to as high as 160 mm Hg. The pressure returns to nearly normal within about 2 days because the response of the vasomotor center to the absent baroreceptor signal fades away, which is called central "resetting" of the baroreceptor pressure control mechanism. Therefore, the neurogenic hypertension caused by sectioning the baroreceptor nerves is mainly an acute type of hypertension, not a chronic type.
Spontaneous Hereditary Hypertension in Lower Animals. Spontaneous hereditary hypertension has been observed in a number of strains of lower animals, including several different strains of rats, at least one strain of rabbits, and at least one strain of dogs. In the strain of rats that has been studied to the greatest extent, the Okamoto strain, there is evidence that in early development of the hypertension, the sympathetic nervous system is considerably more active than in normal rats. However, in the late stages of this type of hypertension, two structural changes have been observed in the nephrons of the kidneys: (1) increased preglomerular renal arterial resistance and (2) decreased permeability of the glomerular membranes. These structural changes could easily be the basis for the long-term continuance of the hypertension. In other strains of hypertensive rats, impaired renal function also has been observed.
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