Occasionally a tumor of the renin-secreting juxta-glomerular cells (the JG cells) occurs and secretes tremendous quantities of renin; in turn, equally large quantities of angiotensin II are formed. In all patients in whom this has occurred, severe hypertension has developed. Also, when large amounts of angiotensin are infused continuously for days or weeks into animals, similar severe long-term hypertension develops.
We have already noted that angiotensin can increase the arterial pressure in two ways:
1.By constricting the arterioles throughout the entire body, thereby increasing the total peripheral resistance and arterial pressure; this effect occurs within seconds after one begins to infuse angiotensin.
2.By causing the kidneys to retain salt and water; over a period of days, this, too, causes hypertension and is the principal cause of the long-term continuation of the elevated pressure.
“One-Kidney” Goldblatt Hypertension. When one kidney isremoved and a constrictor is placed on the renal artery of the remaining kidney, as shown in Figure 19–13, the immediate effect is greatly reduced pressure in the renal artery beyond the constrictor, as demonstrated by the dashed curve in the figure. Then, within seconds or minutes, the systemic arterial pressure begins to rise and continues to rise for several days. The pressure usually rises rapidly for the first hour or so, and this is followed by a slower additional rise during the next several days. When the systemic arterial pressure reaches its new stable pressure level, the renal arterial pressure (the dashed curve in the figure) will have returned almost all the way back to normal.The hyper-tension produced in this way is called “one-kidney”Goldblatt hypertension in honor of Dr. Goldblatt, whofirst studied the important quantitative features of hypertension caused by renal artery constriction.
The early rise in arterial pressure in Goldblatt hypertension is caused by the renin-angiotensin vaso-constrictor mechanism. That is, because of poor blood flow through the kidney after acute constriction of the renal artery, large quantities of renin are secreted by the kidney, as demonstrated by the lowermost curve in Figure 19–13, and this causes increased angiotensin II and aldosterone in the blood. The angiotensin in turn raises the arterial pressure acutely. The secretion of renin rises to a peak in an hour or so but returns nearly to normal in 5 to 7 days because the renal arte-rial pressure by that time has also risen back to normal, so that the kidney is no longer ischemic.
The second rise in arterial pressure is caused by retention of salt and water by the constricted kidney (that is also stimulated by angiotensin II and aldos-terone). In 5 to 7 days, the body fluid volume will have increased enough to raise the arterial pressure to its new sustained level. The quantitative value of this sus-tained pressure level is determined by the degree of constriction of the renal artery. That is, the aortic pres-sure must rise high enough so that renal arterial pres-sure distal to the constrictor is enough to cause normal urine output.
“Two-Kidney” Goldblatt Hypertension. Hypertension alsocan result when the artery to only one kidney is con-stricted while the artery to the other kidney is normal. This hypertension results from the following mecha-nism: The constricted kidney secretes renin and also retains salt and water because of decreased renal arte-rial pressure in this kidney. Then the “normal” oppo-site kidney retains salt and water because of the renin produced by the ischemic kidney. This renin causes formation of angiotension II and aldosterone both of which circulate to the opposite kidney and cause it also to retain salt and water. Thus, both kidneys, but for dif-ferent reasons, become salt and water retainers. Con-sequently, hypertension develops.
Hypertension Caused by Diseased Kidneys That Secrete Renin Chronically. Often, patchy areas of one or both kidneysare diseased and become ischemic because of local vascular constrictions, whereas other areas of the kidneys are normal. When this occurs, almost identical effects occur as in the two-kidney type of Goldblatt hypertension. That is, the patchy ischemic kidney tissue secretes renin, and this in turn, acting through the formation of angiotensin II, causes the remaining kidney mass also to retain salt and water. Indeed, one of the most common causes of renal hypertension, especially in older persons, is such patchy ischemic kidney disease.
Copyright © 2018-2020 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.