Part I

The capacity of tissues to regulate their own blood flow is referred to as autoregulation. Most vascular beds have an intrinsic capacity to compensate for moderate changes in perfusion pressure by changes in vascular resistance, so that blood flow remains relative constant. This capacity is well developed in the kidneys (see Part II), but it has also been observed in the mesentery, skeletal muscle, brain, liver, and myocardium.

The intrinsic capacity of autoregulation is probably due to in part to the intrinsic contractile response of smooth muscle to stretch (myogenic theory of autoregulation). As the pressure rises, the blood vessels are distended and the vascular smooth muscle fibres that surround the vessels contract. If it is postulated that the muscle responds to the tension in the vessel wall, this theory could explain the greater degree of contraction at higher pressures; the wall tension is proportional to the distending pressure times the radius of the vessel (law of Laplace), and the maintenance of a given wall tension as the pressure rises would require a decrease in radius.

Second, vasodilator substances tend to accumulate in active tissues, and these “metabolites” also contribute to autoregulation (metabolic theory autoregualtion). When blood flow decreases, they accumulate and the vessels dilate; when blood flow increases, they tend to be washed away.

Figure 1 Law of Laplace

Part II

To understand the autoregulation of renal blood flow, firstly, we need to know the normal blood vessels, the innervation of the renal vessels, and the normal renal circulation.

Renal Blood Vessels and Renal Circulation

Renal blood vessels

The renal circulation is diagrammed in Figure 37-3. The afferent arterioles are short, straight branches of the interlobular arteries. Each divides into multiple capillary branches to form the tuft of vessels in the glomerulus. The capillaries coalesce to form the efferent arteriole, which in turn breaks up into capillaries that supply the tubules (peritubular capillaries) before draining into the interlobular veins. There is relatively little smooth muscle in the efferent arterioles.

PS: the arterial segments between glomeruli and tubules are technically a portal system.

The capillaries draining the tubules of the cortical nephrons form a  peritubular network, whereas the efferent arterioles from the juxtamedullary glomeruli drain not only into peritubular network, but also into vessels that form hairpin loops (the vasa recta). These loops dip into the medullary pyramids alongside the loops of Henle. The descending vasa recta have a nonfenestrated endothelium that contains a facilitated transporter for urea, and the ascending vasa recta have a fenestrated endothelium, consistent with their function in conserving solutes.

The efferent arteriole from each glomerulus breaks up into capillaries that supply a number of different nephrons. Thus, the tubule of each nephron dose not necessarily receive blood solely from the efferent arteriole of the same nephron. In humans, the total surface of the renal capillaries is approximately equal to the total surface area of the tubules, both being about 12 m2. The volume of blood in the renal capillaries at any given time is 30-40 mL.

In normal status, the renal blood flow per minute is approximately 1273 mL/min.

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The macula, the neighbouring lacks cells, and the renin-secreting granular cells in the afferent arteriole form the juxtaglomerular apparatus.

Autoregulation of Renal Blood Flow

Function of the renal nerves

Stimulation of the renal nerves increases renin secretion by a direct action of released norepinephrine on β1-adrenergic receptors on the juxtaglomerular cells and it increases Na+ reabsorption, probably by a direct action of norepinephrine on renal tubular cells. The proximal and distal tubules and the thick ascending limb of the loop of Henle are richly innervated (more accurately, the blood vessels of the proximal and distal tubules). When the renal nerves are stimulated to increasing extents in experimental animals, the first response is an increase in the sensitivity of the granular cells in the juxtaglomerular apparatus, followed by increased renin secretion, then increased Na+ reabsorption, and finally, at the highest threshold, renal vasoconstriction with decreased glomerular filtration and renal blood flow. It is still unsettled whether the effect on Na+ reabsorption is mediated via α- or β-adrenergic receptors, and it may be mediated by both. The physiologic role of the renal nerves in Na+ homeostasis is also unsettled, in part because most renal functions appears to be normal in patients with transplanted kidneys, and it takes some time for transplanted kidneys to acquire a functional innervation.

The factors affecting rennin secretion is at thread here .Generally, the stimulation of the renal nerves causes: 1. increased rennin secretion;2. increased Na+ reabsorption;3. renal vasoconstriction;and 4. decreased renal blood flow and GFR.

Regulation of the renal blood flow

Norepinephrine constricts the renal vessels, with the greatest effect of injected norepinephrine being exerted on the interlobular arteries and the afferent arterioles. Dopamine is made in the kidney and causes renal vasodilation and natriuresis (however, controlled trials of dopamine have failed to show a protective effect on renal function). AngII exerts a constrictor effect on both the afferent and efferent arterioles (AngII can try to maintain GFR by constricting the efferent arterioles [when efferent arteriolar constriction is greater than afferent constriction]). Prostaglandins increase blood flow in the renal cortex and decrease blood flow in the renal medulla. Acetylcholine also produces renal vasodilation. A high-protein diet raises glomerular capillary pressure and increase renal blood flow.

Autoregulation of renal blood flow

When the kidney is perfused at moderate pressures (90-220 mm Hg in the dog), the renal vascular resistance varies with the pressure so that renal blood flow is relatively constant (see figure below).

Autoregulation of this type occurs in other organs, and several factors contribute to it (for detail about autoregulation please see the comment after this post). Renal autoregulation is present in denervated and in isolated, perfused kidneys, but is prevented by the administration of drugs that paralyze vascular smooth muscle. It is probably produced in part by a direct contractile response to stretch of the smooth muscle of the afferent arteriole. NO may also be involved.

The main function of the renal cortex is filtration of large volumes of blood through the glomeruli, so it is not surprising that the renal cortical blood flow is relatively great and little oxygen is extracted from the blood (see Table 3.1 below). However, metabolic work is being done, particularly to reabsorb Na+ in the thick ascending limb of Henle, so relative large amounts of O2 are extracted from the blood in the medulla (The PO2 of the cortex is about 50 mm Hg, whereas in medulla it is about 15 mm Hg). I think the reason for the relative high extracting rate includes both relative low blood flow in the medulla and the load of metabolic work. Thus, this makes the medulla vulnerable to hypoxia if flow is reduced further. NO, prostaglandins, and many cardiovascular peptides in this region function in a paracrine fashion to maintain the balance between low blood flow and metabolic needs.

PS: Oxygen Extracted from Various Organs While The Body is at Rest.

Extracted O2 as Percentage of O2 Available