The determinants of GFR that are most variable and subject to physiological control include the glomerular hydrostatic pressure and the glomerular capillary colloid osmotic pressure. These variables, in turn, are influenced by the sympathetic nervous system, hormones and autacoids (vasoactive substances that are released in the kidneys and act locally), and other feedback controls that are intrinsic to the kidneys.

STRONG SYMPATHETIC NERVOUS SYSTEM ACTIVATION DECREASES GFR

Essentially all the blood vessels of the kidneys, including the afferent and the efferent arterioles, are richly innervated by sympathetic nerve fibers. Strong activation of the renal sympathetic nerves can constrict the renal arterioles and decrease renal blood flow and GFR. Moderate or mild sympathetic stimulation has little influence on renal blood flow and GFR. For example, reflex activation of the sympathetic nervous system resulting from moder ate decreases in pressure at the carotid sinus baroreceptors or cardiopulmonary receptors has little influence on renal blood flow or GFR. However, as discussed in Chapter 28, even mild increases in renal sympathetic activity can cause decreased sodium and water excretion by increasing renal tubular reabsorption.

The renal sympathetic nerves seem to be most important in reducing GFR during severe, acute disturbances lasting for a few minutes to a few hours, such as those elicited by the defense reaction, brain ischemia, or severe hemorrhage. In the healthy resting person, sympathetic tone appears to have little influence on renal blood flow.

HORMONAL AND AUTACOID CONTROL OF RENAL CIRCULATION

Several hormones and autacoids can influence GFR and renal blood flow, as summarized in Table 1.

Table1. Hormones and Autacoids That  Influence GFR

Norepinephrine, Epinephrine, and Endothelin Con strict Renal Blood Vessels and Decrease GFR. Hormones that constrict afferent and efferent arterioles, causing reductions in GFR and renal blood flow, include norepinephrine and epinephrine released from the adrenal medulla. In general, blood levels of these hormones parallel the activity of the sympathetic nervous system; thus, norepinephrine and epinephrine have little influence on renal hemodynamics except under extreme conditions, such as severe hemorrhage.

Another vasoconstrictor, endothelin, is a peptide that can be released by damaged vascular endothelial cells of the kidneys, as well as by other tissues. The physio logical role of this autacoid is not completely understood. However, endothelin may contribute to hemostasis (minimizing blood loss) when a blood vessel is severed, which damages the endothelium and releases this powerful vasoconstrictor. Plasma endothelin levels are also increased in many disease states associated with vascular injury, such as toxemia of pregnancy, acute renal failure, and chronic uremia, and may contribute to renal vasoconstriction and decreased GFR in some of these pathophysiological conditions.

Angiotensin II Preferentially Constricts Efferent Arterioles in Most Physiological Conditions. A powerful renal vasoconstrictor, angiotensin II, can be considered a circulating hormone and a locally produced autacoid because it is formed in the kidneys and in the systemic circulation. Receptors for angiotensin II are present in virtually all blood vessels of the kidneys. However, the preglomerular blood vessels, especially the afferent arterioles, appear to be relatively protected from angiotensin II–mediated constriction in most physiological conditions associated with activation of the renin angiotensin system, such as during a low-sodium diet or reduced renal perfusion pressure due to renal artery stenosis. This protection is due to release of vasodilators, especially nitric oxide and prostaglandins, which counter act the vasoconstrictor effects of angiotensin II in these blood vessels.

The efferent arterioles, however, are highly sensitive to angiotensin II. Because angiotensin II preferentially constricts efferent arterioles in most physiological conditions, increased angiotensin II levels raise glomerular hydro static pressure while reducing renal blood flow. It should be kept in mind that increased angiotensin II formation usually occurs in circumstances associated with decreased arterial pressure or volume depletion, which tend to decrease GFR. In these circumstances, the increased level of angiotensin II, by constricting efferent arterioles, helps prevent decreases in glomerular hydrostatic pressure and GFR; at the same time, though, the reduction in renal blood flow caused by efferent arteriolar constriction con tributes to decreased flow through the peritubular capillaries, which in turn increases reabsorption of sodium and water, as discussed in Chapter 28.

Thus, increased angiotensin II levels that occur with a low-sodium diet or volume depletion help maintain GFR and normal excretion of metabolic waste products such as urea and creatinine that depend on glomerular filtration for their excretion; at the same time, the angiotensin II–induced constriction of efferent arterioles increases tubular reabsorption of sodium and water, which helps restore blood volume and blood pressure. This effect of angiotensin II in helping to “autoregulate” GFR is dis cussed in more detail later in this chapter.

Endothelial-Derived Nitric Oxide Decreases Renal Vascular Resistance and Increases GFR. An autacoid that decreases renal vascular resistance and is released by the vascular endothelium throughout the body is endothelial-derived nitric oxide. A basal level of nitric oxide production appears to be important for maintaining vasodilation of the kidneys because it allows the kidneys to excrete normal amounts of sodium and water. Therefore, administration of drugs that inhibit formation of nitric oxide increases renal vascular resistance and decreases GFR and urinary sodium excretion, eventually causing high blood pressure. In some hypertensive patients or in patients with atherosclerosis, damage of the vascular endothelium and impaired nitric oxide production may contribute to increased renal vasoconstriction and elevated blood pressure.

Prostaglandins and Bradykinin Decrease Renal Vascular Resistance and Tend to Increase GFR. Hormones and autacoids that cause vasodilation and increased renal blood flow and GFR include the prostaglandins (PGE2 and PGI2) and bradykinin. These substances are discussed in Chapter 17. Although these vasodilators do not appear to be of major importance in regulating renal blood flow or GFR in normal conditions, they may dampen the renal vasoconstrictor effects of the sympathetic nerves or angiotensin II, especially their effects to constrict the afferent arterioles.

By opposing vasoconstriction of afferent arterioles, the prostaglandins may help prevent excessive reductions in GFR and renal blood flow. Under stressful conditions, such as volume depletion or after surgery, the administration of nonsteroidal anti-inflammatory agents, such as aspirin, that inhibit prostaglandin synthesis may cause significant reductions in GFR.

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مواضيع ذات صلة

Renal Blood Flow

Determinants of The GFR

Glomerular Filtration—The First Step in Urine Formation

Urine Formation Results From Glomerular Filtration, Tubular Reabsorption, and Tubular Secretion

Multiple Functions of The Kidneys

التنظيم الحمضي – القاعدي في الجسم Acid-Base Balance

حصى الكلية Urinary Caliculi

أمراض الجهاز البولي

آلية التبول

المثانة البولية

طرق قياس وظائف الكلية

هرمون مضاد إدرار البول Anti-diuretic Hormone , ADH