Acute effect of cyclosporin on inner medullary blood flow in normal and postischemic rat kidney

1990 ◽  
Vol 258 (5) ◽  
pp. F1139-F1144
Author(s):  
Y. Yagil
Keyword(s):  
Blood Flow ◽  
Rat Kidney ◽  
Electromagnetic Flowmeter ◽  
Renal Medulla ◽  
Acute Effect ◽  
Acute Administration ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Group 2 ◽  
Group 1

Acute cyclosporin A (CysA) nephrotoxicity has been attributed to intrarenal vasoconstriction. It has been previously demonstrated that CysA decreases whole kidney and cortical blood flow. The effect of CysA on medullary blood flow has not been adequately studied, despite the high susceptibility of structures in the renal medulla to ischemia and the common use of CysA after the kidney is subjected to transient ischemia. To determine its effects on medullary blood flow in the normal and postischemic kidney, CysA was administered acutely in anesthetized Munich-Wistar rats at doses ranging from 4 to 20 mg/kg. Total renal blood flow (TRBF) and glomerular filtration rate (GFR) were determined in normal kidneys (group 1) by standard clearance techniques before and after infusion of CysA. In animals subjected to 40-min unilateral renal ischemia (group 2) TRBF was measured with an electromagnetic flowmeter. Vasa recta blood flow was determined in both groups by fluorescence videomicroscopy. In group 1, infusion with 20 mg/kg CysA, but not with 4 or 8 mg/kg, increased renal vascular resistance (RVR) and decreased TRBF. GFR was not affected and filtration fraction increased. Vasa recta blood flow was not significantly altered. In group 2, 20 mg/kg CysA increased RVR and decreased TRBF. Vasa recta blood flow decreased significantly in the descending but not in the ascending vasa recta. These results suggest that, in the normal kidney, vasa recta blood flow in the renal medulla is not affected by acute administration of CysA, whereas in the postischemic kidney, CysA decreases blood flow preferentially in the descending vasa recta, in proportion to the decline in TRBF.

Renal medullary blood flow: its measurement and physiology

1986 ◽  
Vol 64 (7) ◽  
pp. 873-880 ◽  
Author(s):  
W. A. Cupples
Keyword(s):  
Blood Flow ◽  
Renal Medulla ◽  
Vascular Bundles ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Countercurrent Exchange ◽  
Renal Medullary Blood Flow ◽  
Urinary Concentrating Ability ◽  
Velocity Tracking ◽  
Uptake Method

The vasculature of the mammalian renal medulla is complex, having neither discrete input nor output. There is also efficient countercurrent exchange between ascending and descending vasa recta in the vascular bundles. These considerations have hampered measurement of medullary blood flow since they impose pronounced constraints on methods used to assess flow. Three main strategies have been used: (i) indicator extraction; (ii) erythrocyte velocity tracking; and (iii) indicator dilution. These are discussed with respect to their assumptions, requirements, and limitations. There is a consensus that medullary blood flow is autoregulated, albeit over a narrower pressure range than is total renal blood flow. When normalized to gram tissue weight, medullary blood flow in the dog is similar to that in the rat, on the order of 1 to 1.5 mL∙min−1∙g−1. This is considerably greater than estimated by the radioiodinated albumin uptake method which has severe conceptual and practical problems. From both theoretical and experimental evidence it ssems that urinary concentrating ability is considerably less sensitive to changes in medullary blood flow than is often assumed.

AN EFFECT OF ANTIDIURETIC HORMONE ON THE FLOW OF BLOOD THROUGH THE VASA RECTA OF THE RAT KIDNEY

1966 ◽  
Vol 35 (2) ◽  
pp. 173-NP ◽  
Author(s):  
JULIA FOURMAN ◽  
G. C. KENNEDY
Keyword(s):  
Blood Flow ◽  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Water Conservation ◽  
Rat Kidney ◽  
Renal Medulla ◽  
Countercurrent System ◽  
Vasa Recta ◽  
Collecting Ducts ◽  
Flow Through

SUMMARY The injection of a fluorescent dye which stained the vessel walls showed the pathway taken by the blood in the renal medulla in rats. The vasa recta stained in normal rats given water; they did not stain in dehydrated rats nor did they stain in rats given an antidiuretic dose of vasopressin in addition to water. The vasa recta stained in all rats with diabetes insipidus whether they were given water or dehydrated. These results suggest that antidiuretic hormone increases water conservation in the medulla by reducing blood flow through the countercurrent system as well as by increasing the permeability of the collecting ducts to water.

Angiotensin II and prostaglandins in control of vasa recta blood flow

1988 ◽  
Vol 254 (3) ◽  
pp. F417-F424 ◽  
Author(s):  
W. A. Cupples ◽  
T. Sakai ◽  
D. J. Marsh
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Renal Medulla ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Electromagnetic Flow Probe ◽  
Angiotensin Blockade

Angiotensin II has been implicated in the regulation of medullary blood flow and is known to interact with prostaglandins at sites within the kidney. Therefore the role of angiotensin in control of vasa recta blood flow was studied in antidiuretic, Munich-Wistar rats. We also tested the hypothesis that prostaglandins act to modulate the effect of angiotensin. Total renal blood flow was measured by an electromagnetic flow probe, vasa recta blood flow by a dual-slit method. Captopril was used to confirm that angiotensin blockade increased renal blood flow (by 15 +/- 4%). Captopril and saralasin were used to show that angiotensin blockade increased vasa recta blood flow (by 23 +/- 9 and 14 +/- 7%, respectively). The results demonstrate a tonic constrictor effect of angiotensin in the renal medulla. Exogenous angiotensin II, delivered intravenously, failed to mimic the effect of endogenous angiotensin. Indomethacin did not alter blood pressure or renal blood flow but did reduce vasa recta blood flow by 20 +/- 3%, suggesting that prostaglandins act preferentially on the medullary circulation. Nor did it alter the response of blood pressure, of renal blood flow, or of vasa recta blood flow to captopril. Moreover, prior angiotensin blockade with either captopril or saralasin enhanced the medullary vasoconstrictor effect of indomethacin (P less than 0.05). These results are not consistent with the hypothesis that prostaglandins act primarily as angiotensin modulators. They suggest that the medullary interaction between angiotensin and prostaglandins differs from that in the cortex.

Cholinergic regulation of adrenal medullary blood flow

1991 ◽  
Vol 261 (6) ◽  
pp. H1836-H1841 ◽  
Author(s):  
J. G. Kennedy ◽  
M. J. Breslow ◽  
J. R. Tobin ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Splanchnic Nerve ◽  
Catecholamine Secretion ◽  
Relative Role ◽  
Medullary Blood Flow ◽  
Anesthetized Dogs ◽  
Group 2 ◽  
Ganglionic Transmission ◽  
Induced Changes ◽  
Group 1

To determine the relative role of nicotinic and muscarinic mechanisms in splanchnic nerve stimulation (NS)-induced adrenal catecholamine secretion and medullary vasodilation, 12 pentobarbital-anesthetized dogs were subjected to three identical stimulations. The first NS was performed before drug administration and served as a control. The second NS was performed after administration of either the muscarinic antagonist, atropine 0.5 mg/kg (group 1), or the nicotinic antagonist, hexamethonium 20 mg/kg (group 2). The third NS was performed after administration of both drugs. NS in the absence of drug resulted in 4-fold and greater than 200-fold increases in medullary blood flow (Q, measured with radiolabeled microspheres) and catecholamine secretion (assayed by high-pressure liquid chromatography), respectively. Atropine, when administered alone (group 1), had no effect on these responses. Subsequent administration of hexamethonium to group 1 animals resulted in complete blockade of NS-induced changes in medullary Q and secretion. Hexamethonium alone (group 2) reduced the catecholamine response to NS by 95% but had no effect on the medullary Q response. Addition of atropine further attenuated the increase in catecholamine secretion induced by NS and completely blocked the medullary Q increase. These data suggest the presence of redundant mechanisms to increase medullary Q during NS. One mechanism likely involves neurally released acetylcholine-stimulating vascular muscarinic receptors, whereas the second requires either chromaffin cell degranulation or nicotinic ganglionic transmission.

scholarly journals Urine concentrating mechanism: impact of vascular and tubular architecture and a proposed descending limb urea-Na+ cotransporter

2012 ◽  
Vol 302 (5) ◽  
pp. F591-F605 ◽  
Author(s):  
Anita T. Layton ◽  
William H. Dantzler ◽  
Thomas L. Pannabecker
Keyword(s):  
Blood Flow ◽  
Interstitial Fluid ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Renal Medulla ◽  
Fluid Composition ◽  
Vascular Bundles ◽  
Vasa Recta ◽  
Countercurrent Exchange ◽  
Thin Limb

We extended a region-based mathematical model of the renal medulla of the rat kidney, previously developed by us, to represent new anatomic findings on the vascular architecture in the rat inner medulla (IM). In the outer medulla (OM), tubules and vessels are organized around tightly packed vascular bundles; in the IM, the organization is centered around collecting duct clusters. In particular, the model represents the separation of descending vasa recta from the descending limbs of loops of Henle, and the model represents a papillary segment of the descending thin limb that is water impermeable and highly urea permeable. Model results suggest that, despite the compartmentalization of IM blood flow, IM interstitial fluid composition is substantially more homogeneous compared with OM. We used the model to study medullary blood flow in antidiuresis and the effects of vascular countercurrent exchange. We also hypothesize that the terminal aquaporin-1 null segment of the long descending thin limbs may express a urea-Na+ or urea-Cl− cotransporter. As urea diffuses from the urea-rich papillary interstitium into the descending thin limb luminal fluid, NaCl is secreted via the cotransporter against its concentration gradient. That NaCl is then reabsorbed near the loop bend, raising the interstitial fluid osmolality and promoting water reabsorption from the IM collecting ducts. Indeed, the model predicts that the presence of the urea-Na+ or urea- Cl− cotransporter facilitates the cycling of NaCl within the IM and yields a loop-bend fluid composition consistent with experimental data.

Dopamine-1 receptor stimulation impairs intestinal oxygen utilization during critical hypoperfusion

2003 ◽  
Vol 284 (2) ◽  
pp. H668-H675 ◽  
Author(s):  
Jorge A. Guzman ◽  
Ariosto E. Rosado ◽  
James A. Kruse
Keyword(s):  
Blood Flow ◽  
Mucosal Blood Flow ◽  
Control Group ◽  
Oxygen Utilization ◽  
Hemorrhage Control ◽  
Receptor Stimulation ◽  
Anesthetized Dogs ◽  
Group 2 ◽  
Increased Susceptibility ◽  
Group 1

Effects of a dopamine-1 (DA-1) receptor agonist on systemic and intestinal oxygen delivery (D˙o 2)-uptake relationships were studied in anesthetized dogs during sequential hemorrhage. Control ( group 1) and experimental animals ( group 2) were treated similarly except for the addition of fenoldopam (1.0 μg · kg−1 · min−1) in group 2. Both groups had comparable systemic criticalD˙o 2(D˙o 2crit), but animals in group 2 had a higher gut D˙o 2crit(1.12 ± 1.13 vs. 0.80 ± 0.09 ml · kg−1 · min−1, P < 0.05). At the mucosal level, a clear biphasic delivery-uptake relationship was not observed in group 1; thus oxygen consumption by the mucosa may be supply dependent under physiological conditions. Group 2 demonstrated higher peak mucosal blood flow and lack of supply dependency at higher mucosalD˙o 2 levels. Fenoldopam resulted in a more conspicuous biphasic relationship at the mucosa and a rightward shift of overall splanchnic D˙o 2crit despite increased splanchnic blood flow. These findings suggest that DA-1 receptor stimulation results in increased gut perfusion heterogeneity and maldistribution of perfusion, resulting in increased susceptibility to ischemia.

Bradykinin has no acute effect on the response of forearm blood flow to sympathetic stimulation in man

1990 ◽  
Vol 78 (4) ◽  
pp. 399-401 ◽  
Author(s):  
M. J. Cullen ◽  
J. R. Cockcroft ◽  
D. J. Webb
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Negative Pressure ◽  
Enzyme Inhibitor ◽  
Lower Body Negative Pressure ◽  
Acute Effect ◽  
Acute Administration ◽  
Lower Body ◽  
Resistance Vessels ◽  
Sympathetic Responses

1. Six healthy male subjects received 0.9% (w/v) NaCl (saline) followed by incremental doses of bradykinin (1, 3 and 10 pmol/min), via the left brachial artery. Blood flow and the response of blood flow to lower-body negative pressure were measured in both forearms during infusion of saline and each dose of bradykinin. 2. Bradykinin produced a moderate and dose-dependent increase in blood flow in the infused, but not the non-infused, forearm. Lower-body negative pressure produced an approximately 15–20% reduction in blood flow in both forearms, and this response was unaffected by local infusion of bradykinin. 3. Bradykinin, in contrast to angiotensin II, had no acute effect on peripheral sympathetic responses to lower-body negative pressure. We conclude that, in forearm resistance vessels in man, withdrawal of angiotensin II, rather than accumulation of bradykinin, is likely to account for the attenuation of peripheral sympathetic responses after acute administration of a converting-enzyme inhibitor.

Role of renal medullary adenosine in the control of blood flow and sodium excretion

1999 ◽  
Vol 276 (3) ◽  
pp. R790-R798 ◽  
Author(s):  
Ai-Ping Zou ◽  
Kasem Nithipatikom ◽  
Pin-Lan Li ◽  
Allen W. Cowley
Keyword(s):  
Blood Flow ◽  
Sodium Excretion ◽  
Renal Medulla ◽  
Urine Flow ◽  
Doppler Flowmetry ◽  
Blood Flows ◽  
Medullary Blood Flow ◽  
Adenosine Concentration ◽  
Interstitial Infusion

This study determined the levels of adenosine in the renal medullary interstitium using microdialysis and fluorescence HPLC techniques and examined the role of endogenous adenosine in the control of medullary blood flow and sodium excretion by infusing the specific adenosine receptor antagonists or agonists into the renal medulla of anesthetized Sprague-Dawley rats. Renal cortical and medullary blood flows were measured using laser-Doppler flowmetry. Analysis of microdialyzed samples showed that the adenosine concentration in the renal medullary interstitial dialysate averaged 212 ± 5.2 nM, which was significantly higher than 55.6 ± 5.3 nM in the renal cortex ( n = 9). Renal medullary interstitial infusion of a selective A1antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 300 pmol ⋅ kg−1 ⋅ min−1, n = 8), did not alter renal blood flows, but increased urine flow by 37% and sodium excretion by 42%. In contrast, renal medullary infusion of the selective A2 receptor blocker 3,7-dimethyl-1-propargylxanthine (DMPX; 150 pmol ⋅ kg−1 ⋅ min−1, n = 9) decreased outer medullary blood flow (OMBF) by 28%, inner medullary blood flows (IMBF) by 21%, and sodium excretion by 35%. Renal medullary interstitial infusion of adenosine produced a dose-dependent increase in OMBF, IMBF, urine flow, and sodium excretion at doses from 3 to 300 pmol ⋅ kg−1 ⋅ min−1( n = 7). These effects of adenosine were markedly attenuated by the pretreatment of DMPX, but unaltered by DPCPX. Infusion of a selective A3receptor agonist, N 6-benzyl-5′-( N-ethylcarbonxamido)adenosine (300 pmol ⋅ kg−1 ⋅ min−1, n = 6) into the renal medulla had no effect on medullary blood flows or renal function. Glomerular filtration rate and arterial pressure were not changed by medullary infusion of any drugs. Our results indicate that endogenous medullary adenosine at physiological concentrations serves to dilate medullary vessels via A2 receptors, resulting in a natriuretic response that overrides the tubular A1 receptor-mediated antinatriuretic effects.

Acute effect of salmon calcitonin on renal magnesium transport in the magnesium-loaded rat

1986 ◽  
Vol 64 (1) ◽  
pp. 66-71 ◽  
Author(s):  
Denis R. Roy
Keyword(s):  
Significant Relationship ◽  
Salmon Calcitonin ◽  
Acute Effect ◽  
Magnesium Concentration ◽  
Thick Ascending Limb ◽  
Group 3 ◽  
Group 2 ◽  
Magnesium Excretion ◽  
Tubule Fluid ◽  
Group 1

The present studies were undertaken to examine whether salmon calcitonin, by increasing magnesium reabsorption in the thick ascending limb, and presumably the tubulointerstitial magnesium concentration gradient, would lead to an increase in fractional magnesium delivery to the end-descending limb (magnesium secretion) in magnesium-loaded rats. Thyroparathyroidectomized, postprandial Munich–Wistar rats were prepared for micropuncture of papillary end-descending limbs and of superficial end-accessible proximal tubules. Group 1 served as clonidine–water diuresis time controls; group 2 was treated as group 1 but also received synthetic salmon calcitonin (10 mU/min); and group 3 was treated as group 2 but also received calcium chloride intravenously. Calcitonin, alone or with calcium, produced a significant fall in fractional magnesium excretion. A significant relationship was also observed between fractional magnesium excretion and urine flow rate (r = 0.56, p < 0.01). Calcitonin did not modify fractional magnesium delivery to the end-descending limb. A highly significant relationship was observed between tubule fluid-to-ultrafiltrate magnesium ratio and tubule fluid-to-plasma inulin ratio (r = 0.88, p < 0.001). Within each group, fractional magnesium delivery to the end-descending limb was similar to the corresponding value in the superficial end-accessible proximal tubule. Our results suggest that despite intense magnesium reabsorption, presumably in the thick ascending limb, magnesium secretion does not occur in the juxtameduilary pars recta and (or) thin descending limb.

Sign in / Sign up

Export Citation Format

Share Document