Angll increases total peripheral resistance (TPR) by direct and indirect effects on blood vessels.
Direct Vasoconstriction Angll constricts precapillary arterioles and, to a lesser extent, post-capillary venules by activating AT1 receptors on vascular smooth muscle cells. AngII has differential effects on vascular beds. The kidneys and splanchnic bed constrict markedly, thereby decreasing blood flow. Blood flow to the brain, lung, and skeletal muscle may actually increase in response to AngII because the elevated systemic blood pressure overcomes the relatively weak vasoconstriction. Nevertheless, high circulating concentrations of Angll may decrease cerebral and coronary blood flow.
Enhancement of Peripheral Noradrenergic Neurotransmission Angll augments NE release from sympathetic nerve terminals, inhibits the reuptake of NE into nerve terminals, and enhances the vascular response to NE. Intracoronary AngII potentiates sympathetic nervous system-induced coronary vasoconstriction.
Effects on the CNS Small amounts of Angll infused into the vertebral arteries increases blood pressure. This response—mediated by increased sympathetic outflow—reflects effects of the hormone on circumventricular nuclei that are not protected by the blood-brain barrier. Circulating AngII also attenuates baroreceptor-mediated reductions in sympathetic discharge, thereby increasing arterial pressure. The CNS is affected both by blood-borne AngII and by AngII formed locally. The brain contains all components of a renin-angiotensin system, suggesting that AngII serves as a neurotransmitter or modulator. In addition to increasing sympathetic tone, Angll also causes a centrally mediated dipsogenic effect and enhances the release of vasopressin.
Release of Catecholamines from the Adrenal Medulla AngII stimulates catecholamine release from the adrenal medulla by depolarizing chromaffin cells. Although this response usually is of minimal physiological importance, dangerous reactions have followed Angll administration to individuals with pheochromocytoma.
MECHANISMS BY WHICH AngII ALTERS RENAL FUNCTION AngII has pronounced effects on renal function, reducing urinary excretion of Na+ and water while increasing K+ excretion. The overall effect of Angll on the kidneys is to shift the renal pressure-natriuresis curve to the right (see below).
Direct Effects of AngII on Sodium Reabsorption in the Renal Tubules Very low concentrations of AngII stimulate Na+/H+ exchange in the proximal tubule—an effect that increases Na+, Cl-, and bicarbonate reabsorption. Approximately 25% of the bicarbonate handled by the nephron may be affected by this mechanism. AngII also increases the expression of the Na+-glucose symporter in the proximal tubule. Paradoxically, at high concentrations, AngII may inhibit Na+ transport in the proximal tubule. AngII also directly stimulates the Na+-K+-2Cl- symporter in the thick ascending limb. The proximal tubule secretes angiotensinogen, and the connecting tubule releases renin, so a paracrine tubular renin-angiotensin system may modulate Na+ reabsorption.
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