Effect of renal vasodilatation on the distribution of cortical blood flow in the kidney of the dog

Stein, Janice Gross; Ferris, Thomas F.; Huprich, James E.; Smith, Timothy C.; Osgood, Richard W.

doi:10.1172/jci106626

Cited by 135 publications

(79 citation statements)

References 23 publications

(24 reference statements)

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“…35 The fall in filtration fraction during infusion of bradykinin may increase sodium excretion by changing renal interstitial pressure or by washout of the medullary solute gradient. 16 ' 33 Our results indicating that captopril increases papillary blood flow and the fractional excretion of sodium and water and reduces urinary osmolality, and that a kinin antagonist blocks these effects, are compatible with this view. There is some evidence indicating that kinins directly inhibit sodium reabsorption in the distal nephron.…”

Section: Discussionsupporting

confidence: 65%

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Effect of an angiotensin II and a kinin receptor antagonist on the renal hemodynamic response to captopril.

et al. 1991

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The role of angiotensin II and kinins on the renal cortical and papillary hemodynamic and on the sodium and water excretory responses to converting enzyme inhibition with captopril was examined in euvolemic Munich-Wistar rats. Cortical and papillary blood flows were measured using a laser Doppler flowmeter. Cortical blood flow increased 28% after blockade of angiotensin II receptors with DuP 753 (2 mg/kg i.v., n=6). Captopril (2 mg/kg i.v., n=6) had no effect on cortical blood flow in rats pretreated with the angiotensin II antagonist DuP 753 had no effect on papillary blood flow, nor did it prevent the rise in papillary blood flow produced by captopril (2 mg/kg, n=6). Infusion of a kinin receptor antagonist, r>Arg,[Hyp 3 ,Thi M , D-Phe 7 ]-bradykinin (2.5 /tg/min i.v.), reduced basal papillary blood flow by 15% and blocked the rise in papillary blood flow produced by captopril. Renal blood flow rose by 11% after DuP 753 (2 mg/kg, n=6), and subsequent administration of captopril and the kinin antagonist had no effect on renal blood flow. Urine flow and sodium excretion increased after DuP 753, but captopril produced additional increases in urine flow and sodium excretion of 68% and 46%, respectively. Fractional sodium excretion rose from 0.85±0.15% to 1.56±0.14% after captopril. Infusion of the kinin antagonist returned sodium and water excretion to control levels, but fractional sodium excretion was not significantly altered.' Giomenilar filtration rate was not altered by DuP 753 or captopril; however, it fell from 1.6±0.1 to 1.2±0.1 ml/min/g kidney wt during infusion of the kinin antagonist This fall in giomenilar filtration rate was associated with a 30% fall in the ultrafiltration coefficient These results indicate that captopril alters renal hemodynamics through mechanisms other than blockade of the renin-angiotensin system. In particular, its effects on papillary blood flow and giomenilar dynamics may be due to alterations in the intrarenal levels of kinins. (Hypertension 1991;17:1038-1044) C onverting enzyme inhibitors (CEIs) are antihypertensive agents that promote sodium excretion at lower levels of arterial pressure. However, the mechanisms underlying the natriuretic and antihypertensive actions of CEIs remain uncertain. It generally is thought that these drugs act by blocking the renin-angiotensin system in the kidney and the peripheral vasculature. However, CEIs lower arterial pressure in nephrectomized animals, as well as in rats pretreated with angiotensin (Ang) II antagonists.

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Section: Discussionsupporting

confidence: 65%

“…Acute administration of CEI has been reported to increase total renal blood flow (RBF) and papillary blood flow. 13 - 16 The increase in RBF induced by CEIs cannot be blocked completely by saralasin. 2 - 17 The rise in papillary blood flow after administration of CEIs can be reversed by a kinin-receptor antagonist.…”

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confidence: 99%

Effect of an angiotensin II and a kinin receptor antagonist on the renal hemodynamic response to captopril.

et al. 1991

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“…A similar pressure-flow relation would have been expected as it would be induced by ACh that dilates both afferent and efferent arterioles (14,16,17). Renal vasodi lation induced by ACh might be a maximum, since other vasodilators such as bradykinin and prostaglandin E2 could not ailate the renal blood vessels to a greater extent than the dilation that would occur with ACh (23)(24)(25). As shown in Table 1, the superimposition of glucagon to adenosine can induce further vasodilation and restore the GFR to the con trol value at normal RPP.…”

Section: Discussionmentioning

confidence: 79%

Intrarenal Vascular Sites of Action of Adenosine and Glucagon

Aki

Shoji

Hasui

et al. 1990

Japanese Journal of Pharmacology

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Abstract-Our purpose was to localize the intrarenal vascular sites of action of adenosine and glucagon. Renal blood flow (RBF) and glomerular filtration rate (GFR) were measured in anesthetized dogs, and renal perfusion pressure (RPP) was varied by an adjustable aortic clamp. At normal RPP, RBF was increased by all agents. In contrast, GFR was increased by glucagon, decreased by adenosine and unchanged by acetylcholine (ACh) or adenosine plus glucagon. The increases in RBF by glucagon occurred only at RPPs within the autoregulatory pressure range, and renal autoregulatory capability was attenuated during the infusion of glucagon. In contrast, adenosine increased RBF at RPPs both within and below the autoregulatory pressure range, and the autoregulatory capability was not perceptibly impaired. Superimposition of glucagon to adenosine caused further vasodilation, and the autoregulatory efficiency was completely attenuated. There was no difference between the RPP-RBF or RPP-GFR relations obtained during infusion of adenosine plus glucagon and ACh, which dilates both the afferent and efferent arterioles. It is generally accepted that afferent arteriolar resistance attains a minimum value at RPP near the lower limit of the autoregulatory range. Thus, our data indicate that glucagon and adenosine preferentially dilate the afferent arteriole and the efferent arteriole, respectively.

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“…In the present study, GPR was determined using radioactive microspheres with an average diameter of approximately 15 p. The microsphere method to be accepted as a reliable measure of glomerular perfusion rate must comply to certain criteria (25,27). We previously demonstrated that sequential infusion of microspheres into the fetal circulation does not modify the fetal renal function and that 15 p diameter spheres are most suitable to study blood flow distribution in fetal lambs because spheres of smaller diameter (9 p) recirculate (23).…”

Section: Developmental Aspects O F Gprmentioning

confidence: 99%

Ontogeny of Single Glomerular Perfusion Rate in Fetal and Newborn Lambs

et al. 1981

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Pediatr. Res. 15: 1248Res. 15: -1255 one can speculate that a decrease in glomerular vascular resistcatheterized fetal lambs between 106 and 140 days of gestation ance is a major determinant in the postnatal increase in glomerular (term, 145 days) and in six newborn lambs between 3 and 19 days perfusion rate and GFR. of age. The present study demonstrates for the first time in lambs that the nephrogenic zone disappears around 130 days of gestation and that the total glomerular counts per kidney in fetuses over Previous studies (5,13,14,16) have demonstrated that the 130 days (4682% + 41173 glomeruli per kidney) is not significantly cortical blood flow is distributed preferentially to the juxtameduldifferent than in newborn lambs (433704 + 21553). Glomerular lary area of the cortex during early postnatal life, and with density, determined in four cortical zones (zone I being the out-maturation, the development of cortical flow follows a centrifugal ermost portion of the cortex) did not show any significant changes pattern. Spitzer and Brandis (26) also demonstrated that the during fetal life; however, significant decreases in glomerular maturation of glomerular filtration rate (GFR) closely follows the density were observed in each cortical zone after birth. The relative developmental pattern of cortical blood flow, M~~~ recently, distribution of glomeruli during fetal life decreased in the outer ~~~~i~ and ~~~i~ (31, studying factors modulating the changes in portion (zones I and 11) and increased in the inner Portion (zones GFR during maturation, have suggested that glomerular perfusion 111 and IV) of the cortex as fetuses matured and approached term. rate (GPR) is an important determinant of the increase in GFR After birth, this difference became even more prominent; the outer during postnatal life, cortical fraction (zone I) decreased from 49.6 + 2.9% in fetuses of studies from our laboratory have demonstrated that during less than 120 days 37-8 * (P < Oeo5) in lambs, fetal life G F R increases at the same rate as the fetal body weight whereas the fraction found in zone 111 increased from 14.9 + 1.3% and kidney weight (18, 21). ~h~~~ observations are contrary to to 20.8 + 0.7% ( P < 0.05). Small but significant increases in what occurs after birth, where the increase in G F R is disproporglomerular filtration rate (GFR) ( P < 0.01) and total renal blood tionately higher than the concomitant rise in body weight and flow (P < 0.05) were observed during fetal life: GFR and total kidney weight (1 1, 20). Factors responsible for the difference in renal blood flow increased, respectively, from 1.84 2 0.11 and 37 the developmental patterns of fetal and newborn G F R have not f 2 ml/min in fetuses I30 days gestation. During the same period, filtration important factor responsible for the development of GFR in fraction (FF) did not increase significantly whereas a significant newborn rats (31, the pre...

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Effect of renal vasodilatation on the distribution of cortical blood flow in the kidney of the dog

Cited by 135 publications

References 23 publications

Effect of an angiotensin II and a kinin receptor antagonist on the renal hemodynamic response to captopril.

Effect of an angiotensin II and a kinin receptor antagonist on the renal hemodynamic response to captopril.

Intrarenal Vascular Sites of Action of Adenosine and Glucagon

Ontogeny of Single Glomerular Perfusion Rate in Fetal and Newborn Lambs

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