Norepinephrine is responsible for the strong constriction of the afferent and efferent glomerular arterioles, resulting in a decrease in both renal blood flow (RBF) and glomerular filtration rate (GFR). This rise in sympathetic activity also leads to the release of epinephrine and angiotensin II, which further constrict the blood vessels and decrease RBF. As a result, the overall resistance in the kidneys and other blood vessels increases, leading to an increase in total peripheral resistance and a tendency for blood pressure to rise. This counteracts the decrease in blood pressure caused by hemorrhage, but at the expense of maintaining normal RBF and GFR.

Prostaglandins do not have a significant role in regulating RBF in healthy individuals at rest. However, during pathophysiological conditions like hemorrhage and reduced extracellular fluid volume (ECFV), prostaglandins are produced locally in the kidneys to increase RBF without affecting GFR. They achieve this by counteracting the vasoconstrictor effects of sympathetic activation and angiotensin II. Prostaglandin synthesis is stimulated by ECFV depletion, stress, angiotensin II, and sympathetic nerves. Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandin synthesis and are contraindicated during renal ischemia and hemorrhagic shock, as they decrease RBF and increase renal ischemia. Prostaglandins become increasingly important in maintaining RBF and GFR as individuals age, and NSAIDs can significantly reduce RBF and GFR in the elderly.

Nitric oxide (NO), which is produced by the endothelium, acts as a vasodilator under normal conditions and counteracts the vasoconstrictive effects of angiotensin II and catecholamines. When blood flow increases, the shear force on endothelial cells in the arterioles triggers an increased production of NO. Additionally, vasoactive hormones like acetylcholine, histamine, bradykinin, and ATP facilitate the release of NO from endothelial cells. The increased production of NO causes dilation of both the afferent and efferent arterioles in the kidneys. Higher levels of NO decrease total peripheral resistance, while inhibiting NO production increases total peripheral resistance.
Fig. 33.22 ). Norepinephrine causes intense vasoconstriction of the afferent and efferent glomerular arterioles and thereby decreases both RBF and GFR. The rise in sympathetic activity also increases release of epinephrine and angiotensin II, which cause further vasoconstriction and a fall in RBF. The rise in vascular resistance of the kidneys and other vascular beds increases total peripheral resistance. The resulting tendency for blood pressure to increase (blood pressure = cardiac output × total peripheral resistance) offsets the tendency of blood pressure to decrease in response to hemorrhage. Hence this system works to preserve arterial pressure at the expense of maintaining normal RBF and GFR.
increase blood pressure and ECFV (e.g., as would occur with hemorrhage).
Prostaglandins do not play a major role in regulating RBF in healthy resting individuals. However, during • Fig. 33.21 Relationship between selective changes in resistance of either the afferent arteriole or the efferent arteriole on RBF and GFR. Constriction of either the afferent or efferent arteriole increases resistance, and according to
Eq. 33.11 (Q =ΔP/R), an increase in resistance (R) decreases flow (Q) (i.e., RBF). Dilation of either the afferent or afferent arteriole increases flow (i.e., RBF). Constriction of the afferent arteriole (A) decreases PGC because less of the arterial pressure is transmitted to the glomerulus, thereby reducing GFR. In contrast, constriction of the efferent arteriole (B) elevates PGC and thus increases GFR. Dilation of the efferent arteriole (C) decreases PGC and thus decreases GFR. Dilation of the afferent arteriole (D) increases PGC because more of the arterial pressure is transmitted to the glomerulus, thereby increasing GFR. (Modified from Rose BD, Rennke KG. Renal Pathophysiology: The Essentials. Baltimore: Williams & Wilkins; 1994.) pathophysiological conditions such as hemorrhage and reduced ECFV, prostaglandins (PGI2, PGE1, and PGE2) are produced locally within the kidneys and serve to increase RBF without changing GFR. Prostaglandins increase RBF by dampening the vasoconstrictor effects of both sympathetic activation and angiotensin II. These effects are important because they prevent severe and potentially harmful vasoconstriction and renal ischemia. Synthesis of prostaglandins is stimulated by ECFV depletion and stress (e.g., surgery, anesthesia), angiotensin II, and sympathetic nerves. Nonsteroidal antiinflammatory drugs (NSAIDs), such as ibuprofen and naproxen, potently inhibit prostaglandin synthesis. Thus administration of these drugs during renal ischemia and hemorrhagic shock is contraindicated because, by blocking the production of prostaglandins, they decrease RBF and increase renal ischemia. Prostaglandins also play an increasingly important role in maintaining RBF and GFR as individuals age. Accordingly, NSAIDs can significantly reduce RBF and GFR in the elderly.
NO, an endothelium-derived relaxing factor, is an important vasodilator under basal conditions, and it counteracts the vasoconstriction produced by angiotensin II and catecholamines. When blood flow increases, greater shear force acts on endothelial cells in the arterioles and increases production of NO. In addition a number of vasoactive hormones, including acetylcholine, histamine, bradykinin, and ATP, facilitate release of NO from endothelial cells. Increased production of NO causes dilation of the afferent and efferent arterioles in the kidneys. Whereas increased levels of NO decrease total peripheral resistance, inhibition of NO production increases total peripheral resistance.