scholarly journals Autoregulation of renal medullary blood flow in rabbits

2003 ◽  
Vol 284 (1) ◽  
pp. R233-R244 ◽  
Author(s):  
Gabriela A. Eppel ◽  
Göran Bergström ◽  
Warwick P. Anderson ◽  
Roger G. Evans

We examined the extent of renal medullary blood flow (MBF) autoregulation in pentobarbital-anesthetized rabbits. Two methods for altering renal arterial pressure (RAP) were compared: the conventional method of graded suprarenal aortic occlusion and an extracorporeal circuit that allows RAP to be increased above systemic arterial pressure. Changes in MBF were estimated by laser-Doppler flowmetry, which appears to predominantly reflect erythrocyte velocity, rather than flow, in the kidney. We compared responses using a dual-fiber needle probe held in place by a micromanipulator, with responses from a single-fiber probe anchored to the renal capsule, to test whether RAP-induced changes in kidney volume confound medullary laser-Doppler flux (MLDF) measurements. MLDF responses were similar for both probe types and both methods for altering RAP. MLDF changed little as RAP was altered from 50 to ≥170 mmHg (24 ± 22% change). Within the same RAP range, RBF increased by 296 ± 48%. Urine flow and sodium excretion also increased with increasing RAP. Thus pressure diuresis/natriuresis proceeds in the absence of measurable increases in medullary erythrocyte velocity estimated by laser-Doppler flowmetry. These data do not, however, exclude the possibility that MBF is increased with increasing RAP in this model, because vasa recta recruitment may occur.

1995 ◽  
Vol 269 (1) ◽  
pp. R193-R200 ◽  
Author(s):  
K. Nakanishi ◽  
D. L. Mattson ◽  
V. Gross ◽  
R. J. Roman ◽  
A. W. Cowley

Experiments were performed in anesthetized renal-denervated rats to determine the contribution of renal medullary vasopressin V1 and V2 receptor stimulation in the regulation of renal medullary blood flow. Renal medullary interstitial infusion of the selective V1 agonist [Phe2,Ile3,Orn8]vasopressin (2 ng.kg-1.min-1) significantly decreased outer medullary blood flow by 15% and inner medullary blood flow by 35%, as measured with implanted optical fibers for laser-Doppler flowmetry. Medullary interstitial infusion of equimolar doses of arginine vasopressin (AVP) also decreased outer medullary blood flow by 15% but decreased inner medullary blood flow by only 17%, a decrease significantly less than that during the infusion of the V1 agonist. These results were confirmed in videomicroscopy experiments on the exposed papilla, which demonstrated that the V1 agonist and AVP decreased descending and ascending vasa recta capillary red blood cell velocity and calculated blood flow, with greater decreases during infusion of the V1 agonist. In further laser-Doppler flowmetry studies, stimulation of V2 receptors by medullary interstitial infusion of 1-desamino-8-D-arginine vasopressin (2 ng.kg-1.min-1) or AVP in rats pretreated with the vasopressin V1 receptor antagonist d(CH2)5[Tyr(Me)2,Ala-NH2]AVP increased renal medullary blood flow by 16 +/- 3 and 27 +/- 8%, respectively. The present experiments indicate that vasopressin V1 receptor stimulation serves to decrease renal medullary blood flow while V2 receptor stimulation appears to increase renal medullary blood flow; however, the net effect of AVP is to decrease renal medullary blood flow.


2019 ◽  
Vol 24 (2) ◽  
pp. 108-119 ◽  
Author(s):  
B. N. Davydov ◽  
D. A. Domenyuk ◽  
S. V. Dmitrienko

Relevance. Morpho-functional changes in peripheral circulation established in type 1 diabetes mellitus correlate with changes in central hemodynamics, allowing the use of microcirculation indicators as diagnostic and prognostic criteria for assessing the degree of functional vascular disorders. Identifcation of microcirculation features of the blood by the method of laser Doppler flowmetry in children with different experience of type 1 diabetes in key age categories.Materials and methods. The study included 67 children with type 1 diabetes mellitus aged 12-15 years with an experience of the disease from six months to ten years. The comparison group consisted of 38 healthy children. The state of the microvasculature was assessed by laser Doppler flowmetry using a laser analyzer for capillary blood flow LAKK-OP.Results. In children with an experience of type 1 diabetes of less than two years, microcirculation disorders in periodontal tissues correspond to the hyperemic form, accompanied by increased perfusion, a decrease in the amplitude of low-frequency oscillations, increased heart rate, high blood flling, and blood flow bypass. For children with an endocrinopathy experience of more than three years, microcirculation disorders correspond to a stagnant form, combined with a decrease in perfusion due to stagnation of blood in the venular link, endothelial domination with suppression of neurogenic and cardiac fluctuations, low efciency and redistribution of blood flow in favor of the nutritive link.Conclusions. With the increase in experience, the degree of compensation of type 1 diabetes, the progression of diabetic microangiopathy, it is advisable to designate two stages of development of microcirculatory disorders. Early – compensatory with active adaptation, including neurogenic and endothelial regulation mechanisms. Late – decompensation with passive adaptation, supporting the effectiveness of microcirculation due to myogenic control of regulation, shunting and increasing the rate of blood outflow.


1991 ◽  
Vol 261 (6) ◽  
pp. F998-F1006 ◽  
Author(s):  
M. S. Nobes ◽  
P. J. Harris ◽  
H. Yamada ◽  
F. A. Mendelsohn

The effects of angiotensin II (ANG II) or angiotensin III (ANG III) on renal cortical blood flow (CBF) or papillary blood flow (PBF) were investigated in Inactin-anesthetized young rats with the use of laser-Doppler flowmetry. Infusion of equimolar pressor doses of ANG II (300 ng.kg-1.min-1 iv) or ANG III (267 ng.kg-1.min-1) decreased CBF by 31 +/- 2.6% (P less than 0.001) and 20.3 +/- 3.2% (P less than 0.01), respectively but increased PBF by 19 +/- 6.1% (P less than 0.05) and 14.6 +/- 4.4% (P less than 0.05). The ANG II-induced increase in PBF was not prevented by aortic clamping to maintain constant renal perfusion pressure or pretreatment with the prostaglandin synthase inhibitor, indomethacin. The nonpeptide ANG II receptor antagonist, DuP 753 completely abolished the systemic and intrarenal effects of ANG II. After pretreatment with a kallikrein inhibitor, aprotinin, ANG II infusion increased mean arterial pressure but did not affect PBF, suggesting that kinins, but not prostaglandins, modulate the action of systemic ANG II on PBF. We conclude that circulating ANG II induces vasoconstriction in the cortex and also promotes the intrarenal production of kinins, which act to enhance papillary blood flow.


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