Angiotensin-involved hypertension: caused by renin-secreting tumour or renal ischemia

2021-05-26 04:02 PM

A tumour of renin-secreting para-glomerular cells emerges and secretes large quantities of renin, followed by a corresponding amount of angiotensin II.

In addition to the kidney's ability to control blood pressure through changes in extracellular fluid volume, the kidney also has a powerful mechanism for blood pressure control: the renin-angiotensin system.

Renin is a protein enzyme released by the kidneys when arterial blood pressure falls too low. In turn, it increases arterial blood pressure in several ways, thereby helping to correct the drop in blood pressure.

Occasionally a tumour of renin-secreting para-glomerular cells is present and large quantities of renin are produced, followed by a corresponding amount of angiotensin II. In all patients in whom this phenomenon has occurred, severe hypertension has developed. In addition, when large amounts of angiotensin II are infused continuously over days or weeks into animals, similarly severe long-term hypertension develops.

We have noted that angiotensin II can increase arterial blood pressure in two ways:

1. By constricting arterioles throughout the body, increasing total peripheral resistance and arterial blood pressure; This effect occurs within seconds of starting angiotensin infusion.

2. By causing the kidneys to retain salt and water; causes hypertension and is a major cause of continued long-term hypertension.

One kidney: Goldblatt hypertension (compression or obstruction of the renal artery)

When one kidney is excised and the renal artery clamped in the other kidney, as shown in the figure, the direct effect will be to significantly reduce the pressure in the renal artery posterior to the clamping site, as demonstrated by the sharp curves. broken in the picture. Then, within seconds or minutes, systemic arterial blood pressure begins to rise and continues to rise for several days. Blood pressure usually rises rapidly during the first hours or so, and this effect is slowed by a slower rise over the next few days. When the systemic arterial pressure reaches a new steady level, the renal artery blood pressure (dashed line in the figure) will return to nearly normal. Hypertension produced in this way is known as Goldblatt mono real hypertension (renal artery compression or occlusion) - by Harry Goldblatt, who was the first to study hypertension due to renal artery spasm.

Premature elevation of blood pressure in Goldblatt hypertension is induced by a renin-angiotensin vasoconstrictor mechanism. That is, because renal blood flow is poor after abrupt ligation of the renal artery, large amounts of renin are secreted by the kidneys, as demonstrated by the lowest curve in the figure, and this increases angiotensin II and aldosterone in blood. The angiotensin in turn increases the arterial blood pressure sharply. Renin secretion increases to a peak in an hour or so but returns to near normal in 5-7 days because the renal artery blood pressure has now returned to normal, so the kidneys are no longer ischemic. .

Figure. Effect of placing a constrictor clamp into the renal artery of one kidney after the other kidney has been removed. Note changes in systemic arterial pressure, renal artery pressure distal to renin excretion rate.

The secondary increase in arterial blood pressure is due to salt and water retention by the clamped kidney (which is also stimulated by angiotensin II and aldosterone). In 5-7 days, body fluid volume increases enough to raise arterial blood pressure to its new sustained level. The price of this blood pressure level is related to the degree of renal artery clamping. That is, arterial blood pressure must rise high enough to produce normal urine output.

A similar scenario occurs in patients with renal artery stenosis with a single remaining kidney, sometimes occurring after a kidney transplant. In addition, increased functional or pathological resistance in the renal arterioles, due to atherosclerosis or excessive vasoconstriction, may cause hypertension through a mechanism similar to that of major renal artery ligation.

Goldblatt "Two Kidneys" Hypertension

Hypertension can also occur when the arteries of one kidney are constricted while the other is normal. The kidney is clamped to secrete renin and also retain salt and water due to a decrease in renal artery blood pressure in this kidney. Then the normal side retains salt and water due to renin produced by the anaemic kidney. Thus, both kidneys—but for different reasons—retain salt and water. As a result, develop hypertension.

The clinical analogy of Goldblatt bilateral hypertension occurs when there is unilateral renal artery stenosis, for example, due to atherosclerosis, in a person with two kidneys.

Hypertension caused by chronic renin-secreting kidney disease

Usually, localized areas of one or both kidneys are diseased and ischemic because of ischemic vasoconstriction or infarction, while other areas of the kidney are normal. When this occurs, the effect is almost the same as in Goldblatt's birenal hypertension. That is, ischemic renal tissues secrete renin, followed by the formation of angiotensin II which causes the remaining renal mass to retain salt and water. Indeed, one of the most common causes of renal hypertension, especially in the elderly, is ischemic nephropathy.