Glomerular pressure

Systemic blood pressure correlates with glomerular pressure and elevations in both systemic blood pressure and glomerular pressure contribute to glomerular damage. The rate of GFR decline is related to elevated systolic blood pressure and mean arterial pressure. The decline in GFR is estimated to be 14 mL/minute per year with a systolic blood pressure of 180 mm Hg. Conversely, the decline in GFR decreases to 2 mL/minute per year with a systolic blood pressure of 135 mm Hg.11... 

All hypotensive drugs lower systemic BP but, due to the specific characteristics of the glomerular capillary system, different agents may affect glomerular hemodynamics in different ways. This could be of major importance. During antihyper-tensive therapy, systemic BP may be reduced but glomerular pressure may be elevated. This may explain why the incidence of some cardiovascular complications such as stroke, has decreased, whereas the incidence of hypertensive nephropathy has remained high. 

The glomerular pressure Pg is determined by distributing the arterial to venous pressure drop between the afferent and the efferent arteriolar resistances, i.e., as the solution to the linear equation ... 

Here, Rao denotes the total flow resistance for each of the two nephrons in equilibrium. ri and ri are the normalized radii of the active parts of the afferent arterioles for nephron 1 and nephron 2, respectively, and Pg and Pg2 are the corresponding glomerular pressures. As a base value of the hemodynamic coupling parameter we shall use s = 0.2. This parameter measures the fraction of the arteriolar length that is shared between the two nephrons. 

Because of the implicit manner in which the glomerular pressure is related to the efferent colloid osmotic pressure and the filtration rate [Eqs. (5)—(8)], direct solution of the set of coupled algebraic equations for the two-nephron system becomes... 

Most of the beneficial effects provided by valsartan appear to be related to a complete blockade of the angiotensin ATI receptor. The mechanisms for these beneficial effects of valsartan as an angiotensin II receptor blocker have been studied in model systems and in humans [23]. It was found that valsartan maintains glomerular filtration rate and glomerular pressure and it has been proposed that this might explain the favourable renal outcome with ATI receptor blocker therapy [24]. 

In the kidney, ANG II reduces renal blood flow and constricts preferentially the efferent arteriole of the glomerulus with the result of increased glomerular filtration pressure. ANG II further enhances renal sodium and water reabsorption at the proximal tubulus. ACE inhibitors thus increase renal blood flow and decrease sodium and water retention. Furthermore, ACE inhibitors are nephroprotective, delaying the progression of glomerulosclerosis. This also appears to be a result of reduced ANG II levels and is at least partially independent from pressure reduction. On the other hand, ACE inhibitors decrease glomerular filtration pressure due to the lack of ANG II-mediated constriction of the efferent arterioles. Thus, one important undesired effect of ACE inhibitors is impaired glomerular filtration rate and impaired kidney function. 

Glomerular filtration rate (GFR) is the volume of plasma-like fluid that is filtered per unit time across the glomerular capillary membranes to enter the tubular space. Filtrate formation is driven by the net filtration pressure that is equal to the capillary hydrostatic pressure diminished by the sum of capillary oncotic... 

In addition to excess sodium intake, abnormal renal sodium retention may be the primary event in the development of hypertension, and it includes abnormalities in the pressure-natriuresis mechanism. In hypertensive individuals, this theory proposes a shift in the control mechanism preventing the normalization of blood pressure. The mechanisms behind the resetting of the pressure-natriuresis curve may include afferent arteriolar vasoconstriction, decreased glomerular ultrafiltration, or an increase in tubular sodium reabsorption.4 Other theories supporting abnormal renal sodium retention suggest a congenital reduction in the number of nephrons, enhanced renin secretion from nephrons that are ischemic, or an acquired compensatory mechanism for renal sodium retention.9... 

Glomerulonephritis Glomerular lesions that are characterized by inflammation of the capillary loops of the glomerulus. These lesions are generally caused by immunologic, vascular, or other idiopathic diseases. Glomerulonephritis can lead to high blood pressure and loss of kidney function. 

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). 

Explain how the filtration coefficient and net filtration pressure determine glomerular filtration... 

Glomerular capillary pressure (PGC) is a hydrostatic pressure that pushes blood out of the capillary. The blood pressure in these capillaries is markedly different from that of typical capillaries. In capillaries elsewhere in the body, blood pressure at the arteriolar end is about 30 mmHg and at the venular end is about 10 mmHg (see Chapter 15). These pressures lead to the net filtration of fluid at the inflow end of the capillary and net reabsorption of fluid at the outflow end. 

Glomerular capillary pressure is determined primarily by renal blood flow (RBF). As RBF increases, PGC and therefore GFR increase. On the other hand, as RBF decreases, PGC and GFR decrease. Renal blood flow is determined by mean arterial pressure (MAP) and the resistance of the afferent arteriole (aff art) ... 

Kidneys are exquisitely sensitive to changes in perfusion pressures. Moderate alterations can lead to significant changes in glomerular filtration rate. Oliguria, progressing to anuria, occurs because of vasoconstriction of afferent arterioles. 

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