Mechanism of the Redistribution of Renal Cortical Blood Flow during Hemorrhagic Hypotension in the Dog

Stein, Janice Gross; Boonjarern, Sampanta; Mauk, Richard C.; Ferris, Thomas F.

doi:10.1172/jci107172

Cited by 58 publications

(24 citation statements)

References 29 publications

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“…. Numerous other laboratories have confirmed the validity of the assessment of canine renal cortical blood flow with radioactive microspheres (McNay and Abe, 1970;Kirschenbaum et al, 1974;Riley et al, 1975;Hardaker et al, 1975;Stein et al, 1973).…”

Section: Effect Of A-blockade On the Distribution Of Renal Blood Flowmentioning

confidence: 88%

Effect of adenosine on the distribution of renal blood flow in dogs.

Spielman

Britton

Fiksen-Olsen

1980

Circulation Research

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SUMMARY Previous reports have shown that the intrarenal infusion of adenosine results in a relatively greater fall in superficial nephron glomerular filtration rate (GFR) than whole kidney GFR. This nonuniform decrease in GFR occurred despite a concomitant increase in total renal blood flow (RBF); thus, the present study was undertaken to assess the effect of intrarenally administered adenosine on the distribution of RBF. RBF distribution was measured with radiolabeled microspheres (15 urn) in anesthetized dogs (n = 8) before and during the intrarenal artery infusion of adenosine (0.3 /imol/min). In dogs with elevated plasma renin activities (PRA), adenosine infusion produced no significant change in outer cortical blood flow (4.36 ± 0.50 vs. 4.41 ± 0.63 ml/min per g), whereas absolute inner cortical blood flow increased by 94% (1.54 ± 0.34 vs. 2.99 ± 0.52 ml/min per g). In dogs with low PRA, outer cortical blood flow was only minimally affected by adenosine infusion (6.39 ± 0.44 vs. 5.88 ± 0.33 ml/min per g), whereas inner cortical blood flow was increased from 4.91 ± 0.43 to 6.06 ± 0.38 ml/min per g. Although adenosine resulted in a deep cortical vasodilation in dogs with both high and low PRA (94% vs. 23%), the relative change was greater in the animals with high PRA. Additional experiments were performed in indomethacin-(or meclofenamate-) treated (n = 14) or phenoxybenzamine-treated (n = 5) dogs to determine whether the deep cortical vasodilation is mediated by increased prostaglandin production or by inhibition of norepinephrine release. The increase in deep cortical flow during adenosine administration was not affected by either the blockade of prostaglandin synthesis or a-adrenergic receptors. We conclude that the effect of adenosine to preferentially dilate vessels of the inner cortex is independent of a prostaglandin-related or sympathetic adrenergic mechanism.Circ Res 46: [449][450][451][452][453][454][455][456] 1980 PREVIOUS reports hypothesize that intrarenal adenosine is a metabolic regulator of renal blood flow and glomerular filtration rate (GFR) Spielman and Osswald, 1978;Miller et al., 1978). Adenosine dilates most vascular beds (Hashimoto and Kumakura, 1965;Haddy and Scott, 1968) and relaxes smooth muscle of the small intestine (Ally and Nakatsu, 1976) and isolated renal artery strips (Walter and Bassenge, 1968); however, it produces vasoconstriction when injected as a bolus directly into the renal artery. On the other hand, the continuous infusion of adenosine into the renal artery results in a transient decrease in renal blood flow which wanes rapidly and returns to or increases above the preinfusion flow rate .Unlike renal blood flow, GFR remains depressed during the infusion of adenosine. This decrease in glomerular filtration is not uniform throughout the kidney, as evidenced by a relatively greater fall in superficial nephron GFR than whole kidney GFR . Additionally, the effect of adenosine to decrease GFR may be related to the Received July.24, 1979; accepted for publication December...

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Section: Effect Of A-blockade On the Distribution Of Renal Blood Flowmentioning

confidence: 88%

Effect of adenosine on the distribution of renal blood flow in dogs.

Spielman

Britton

Fiksen-Olsen

1980

Circulation Research

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“…2). The main common factor for redistribution of RCBF could be identified as decreased renal resistance (Stein et al, 1973) which is caused by vasodilation (Vatner, 1974;Rector et al, 1972;Data et al, 1976) and most likely mediated by a local intrarenal mechanism (Stein et al, 1973). Decreased afferent arteriolar resistance is also considered to contribute to autoregulation of RCBF (Hall, 1977).…”

Section: Discussionmentioning

confidence: 99%

The effect of hemorrhagic hypotension on urinary kallikrein excretion, renin activity, and renal cortical blood flow in the pig.

Maier¹,

Starlinger²,

Wagner³

et al. 1981

Circulation Research

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SUMMARY We measured urinary kallikrein by its esterolytic and kinin-forming activity in 5-minute urine samples obtained throughout continuous bleeding experiments in pigs to correlate possible changes in urinary kallikrein excretion during hemorrhagic hypotension with renin activity and renal cortical blood flow. Renin activity was determined in venous blood samples and renal cortical blood flow was estimated by the radiolabeled microsphere technique. The rate of urinary kallikrein excretion was increased about 4-fold within an arterial pressure range of 100-70 mm Hg, whereas below 70 mm Hg, arterial pressure urinary kallikrein activity declined to undetectable values. Renin activity was increased only 2-fold in the arterial pressure range between 100 and 70 mm Hg but was increased 4-fold at pressures below 70 mm Hg. The pressure range of 100 to 70 mm Hg corresponded to the autoregulation of renal cortical blood flow and glomerular filtration rate; below that pressure range, renal cortical blood flow dropped to about 10% of the initial value. Therefore, it seems that urinary kallikrein is activated mainly during the period of autoregulation, whereas renin activity is, in the main, increased below the autoregulatory range of pressure. The vasodilatory urinary kallikrein kinin system might be involved in maintaining sufficient local blood flow during autoregulation whereas a decrease in blood pressure below the autoregulatory range leads to a major increase in renin activity, thus illustrating the attempt of the organism to reestablish sufficient blood pressure to maintain autoregulation. Circ Res 48: [386][387][388][389][390][391][392] 1981 Kallikreins, the enzymes that release vasoactive kinin polypeptides from kininogen substrate, are found in plasma and in organs such as pancreas, salivary glands and kidneys. Because urinary kallikrein (Urokallikrein) is functionally and structurally similar to the kallikrein found in the kidney (Nustad and Vaaje, 1975) and kidney cell suspensions (Kaizu and Margolius, 1975), it is thought that urinary kallikrein is synthesized and secreted by the kidney. Urinary kallikrein levels are abnormal in pathological conditions such as essential hypertension (Margolius et al., 1971) and primary aldosteronism (Margolius et al., 1971). The secretion of kallikrein can be altered by changes in perfusion pressure (Bevan et al., 1974;Keiser et al., 1976),

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“…This difference disappeared at PP 8 kPa. Ultrafiltration coefficient (K,) seemed to increase with decreasing PP.Whereas a decrease in renal perfusion pressure (PP) due to aortic or renal artery clamping is accompanied by no change in renal blood flow (RBF) -a phenomenon known as autoregulation of RBF -a similar decrease due to hemorrhagic hypotension (HH) is often followed by a decrease of RBF, 1 With the technical assistance of Jana Hollyovd.especially in long-lasting HH and in general anesthesia with surgery [1,2,28,29], The decrease in RBF is believed to be caused by renal vasoconstriction due to direct nervous stimulation [4,12] and release of vasocon strictor-acting compounds [12,13, 19], Although several studies have been car ried out in the canine kidney at varying PP due to aortic clamp [21, 23], inflatable cuff …”

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confidence: 99%

Kidney Function during Decreased Perfusion Pressure Due to Aortic Clamping and Hemorrhagic Hypotension: A Single Nephron Study in Dog Kidney

Heller¹,

Horáček²

1984

Kidney Blood Press Res

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Whole kidney and single nephron function was compared in dogs during a stepwise lowering of renal perfusion pressure (PP) induced by aortic clamping (C) or hemorrhagic hypotension (HH). In C, renal vascular resistance (RVR) decreased with decreasing PP, the decrease being due to a drop in afferent resistance (R_A) only. HH was associated with a rise in RVR due in the first phase mainly to an increase in R_E, later to both R_A and R_E. There was a decrease in total kidney blood flow (RBF), glomerular filtration rate (GFR), glomerular and peritubular capillary pressure, and proximal tubular pressure. In C, RBF and GFR showed no significant difference at PPs 17 and 13 kPa. However, single nephron pressures were slightly but significantly lowered. In both groups, glomerular capillary hydraulic pressure (GCP) was significantly higher when calculated as SFP + π_A (stop flow pressure + systemic arterial plasma oncotic pressure) than when measured directly by puncturing glomerular capillaries after ablation of a small layer of superficial cortex. This difference disappeared at PP 8 kPa. Ultrafiltration coefficient (K_f) seemed to increase with decreasing PP.

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Mechanism of the Redistribution of Renal Cortical Blood Flow during Hemorrhagic Hypotension in the Dog

Cited by 58 publications

References 29 publications

Effect of adenosine on the distribution of renal blood flow in dogs.

Effect of adenosine on the distribution of renal blood flow in dogs.

The effect of hemorrhagic hypotension on urinary kallikrein excretion, renin activity, and renal cortical blood flow in the pig.

Kidney Function during Decreased Perfusion Pressure Due to Aortic Clamping and Hemorrhagic Hypotension: A Single Nephron Study in Dog Kidney

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