In this type of hypertension, increased blood pressure is caused by sodium and water retention with increased blood volume or excessive renal excretion of vasoactive substances with general or local vasoconstrictive effects.
Professional literature differentiates renovascular hypertension from hypertension caused by kidney diseases.
Renovascular hypertension appears when the renin-angiotensin system (RAS) is activated due to renal ischemia caused by stenosis of renal artery or its branches. Angiotensin II increases blood pressure in several ways. It has a direct vasoconstricting effect by stimulating aldosterone synthesis (leading to sodium retention) and increasing sympathetic tone. Absolute activity values of plasma renin exceed the upper normal limit in only half of the patients with renovascular hypertension. But more often, it appears to be related to the sodium level.
There is much evidence that increased blood pressure secondary to renal disease is caused by the inflammation and sclerosis of the small vessels in the renal parenchyma, as well as the activation of RAS.
CIt is thought that in patients with renal diseases increased blood pressure may be caused through specific damage mechanisms:
Production of unknown vasoconstrictor substances.
Lack of vasodilator production (prostaglandins or bradykinin).
Decreased breakdown of vasoconstrictor substances.
Problems with sodium excretion.
All the above-mentioned mechanisms for pathogenesis, including the activation of RAS, are very evident in some cases, but the most reliable assumption is that of sodium retention. As proof of this, arterial hypertension is not characteristic in patients with polycystic kidney disease or chronic pyelonephritis who have an increased sodium excretion, and the removal of fluid and electrolytes using hemodialysis or diuretics allows the return of normal blood pressure in those patients.
Hypertension is rarely caused by renin-secreting tumors, or nephroblastoma, which have similar symptoms to hyperaldosteronism: increased blood pressure, hypokalemia, and aldosterone hypersecretion has been reported.
Distinguishing renin-secreting tumors from primary hyperaldosteronism is possible due to increased renin activity, and from secondary hyperaldosteronism, due to normal renal function and increased renin activity in one of the renal veins and absence of stenosis in the corresponding artery.
The cause of increased blood pressure increase is rarely found; only 5% have diagnosed cause, but it must be found out. First of all, the elimination of the cause can sometimes can lead to curing the disease. Secondly, research on symptomatic hypertension gives us new information on its etiology. In the vast majority of cases, the determined cause is associated with either endocrine or renal pathologies.
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