Figure 212

Major candidate mechanisms that may elevate peripheral vascular resistance in renal parenchymal disease. Some data support each of these pathways, although rarely does one mechanism predominate. Experimental studies suggest that endothelin-1 may magnify interstitial fibrosis and contribute to hypertension in some models; however, rarely is the effect major [8,9]. Most levels of vasodilators, including nitric oxide, prostacyclin, and atrial natriuretic peptide, are normal or elevated in patients with renal disease. The vasodilators appear to buffer the vasoconstrictive actions of angiotensin II, which may be increased abruptly if the vasodilator is removed, as occurs with inhibition of cyclo-oxygenase with the use of nonsteroidal anti-inflammatory drugs.

Increased vasoconstrictors

Impaired or relatively inadequate vasodilators

Renin-angiotensin system

Nitric oxide: inadequate compensation

Endothelin

Vasodilator prostaglandins: prostacyclin 2

Prostanoids: thromboxane

Natriuretic peptides: atrial natriuretic peptide

Arginine vasopressin

Kallikrein-kinin system

Endogenous digitalis-like

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