How does acute unilateral renal obstruction predispose people to hypertension?

Acute unilateral renal obstruction can lead to hypertension through several mechanisms:

1. Activation of the renin-angiotensin-aldosterone system (RAAS): Obstruction of the renal artery or ureter causes a decrease in blood flow to the affected kidney. This triggers the release of renin from the juxtaglomerular cells in the kidney. Renin converts angiotensin I to angiotensin II, which is a potent vasoconstrictor. Angiotensin II also stimulates the adrenal glands to release aldosterone, which promotes sodium and water retention. The combination of vasoconstriction and fluid retention leads to an increase in blood pressure.

2. Impaired sodium excretion: The obstructed kidney is unable to properly excrete sodium, which leads to an increase in the circulating blood volume. This increase in blood volume further contributes to hypertension.

3. Sympathetic nervous system activation: Acute unilateral renal obstruction can also lead to activation of the sympathetic nervous system. This causes increased heart rate, increased peripheral vascular resistance, and vasoconstriction, all of which contribute to elevated blood pressure.

4. Increased tubular reabsorption of sodium: The obstruction causes an increase in tubular reabsorption of sodium, which leads to fluid retention and an increase in blood volume, contributing to hypertension.