Renal Circulatory Responses to General Anaesthesia in the Rabbit: Studies Using Radioactive Microspheres

1975 ◽  
Vol 48 (1) ◽  
pp. 61-66 ◽  
Author(s):  
D. J. Warren ◽  
J. G. G. Ledingham
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Control Mechanisms ◽  
Anaesthetic Agents ◽  
Regional Renal Blood Flow ◽  
Urethane Anaesthesia ◽  
Cortical Distribution ◽  
Total Renal Blood Flow

1. Total renal blood flow and its cortical distribution were measured by the radioactive microsphere technique in conscious rabbits and after anaesthesia with pentobarbitone, chloralose-urethane or ether. 2. Pentobarbitone anaesthesia caused a fall of 26% in total renal blood flow, of 26% in superficial cortical flow, and of 24% in deep cortical flow. Sodium excretion rate fell by 33%. 3. Chloralose-urethane anaesthesia caused no change in total or regional renal blood flow, or in sodium excretion. 4. Ether anaesthesia caused an insignificant fall in total renal blood flow, but superficial cortical flow fell by 13 % and deep cortical flow rose by 21 %. Urinary sodium excretion fell by 65%. 5. Possible mechanisms for these changes in response to anaesthesia are discussed. 6. The effects of anaesthetic agents may influence the interpretation of published work on control mechanisms in the renal circulation.

Renal Vascular Response to Haemorrhage in the Rabbit after Pentobarbitone, Chloralose–Urethane and Ether Anaesthesia

1978 ◽  
Vol 54 (5) ◽  
pp. 489-494
Author(s):  
D. J. Warren ◽  
J. G. G. Ledingham
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Cortex ◽  
Ether Anaesthesia ◽  
Before And After ◽  
Conscious Rabbits ◽  
Urethane Anaesthesia ◽  
Renal Vascular ◽  
Cortical Distribution ◽  
Total Renal Blood Flow

1. Total renal blood flow and its cortical distribution were measured by the microsphere technique before and after haemorrhage in conscious rabbits, and after haemorrhage in rabbits anaesthetized with pentobarbitone, chloralose—urethane or ether. 2. The average blood loss necessary to achieve a fall in systolic blood pressure to about 65 mmHg was 101 ml in conscious rabbits and 38, 90 and 118 ml in weight-matched groups of rabbits anaesthetized with pentobarbitone, chloralose—urethane and ether respectively. 3. After haemorrhage in conscious rabbits total renal blood flow fell by 25%, this fall being confined to the superficial renal cortex. 4. In rabbits subject to haemorrhage under pentobarbitone anaesthesia renal blood flow fell by a further 23% when compared with the conscious bled rabbits. This reduction in blood flow was confined to the superficial cortex. 5. Haemorrhage in the rabbits subjected to chloralose—urethane anaesthesia caused no significant change in renal blood flow, as compared with conscious bled rabbits. 6. Haemorrhage under ether anaesthesia was associated with a further 33% fall in total renal blood flow, as compared with conscious bled rabbits. This was associated with a fall of 32% and 34% in superficial and deep cortical blood flow respectively. 7. Animals subjected to general anaesthesia may be particularly susceptible to the renal haemodynamic effects of haemorrhage.

scholarly journals Vascular Type 1A Angiotensin II Receptors Control BP by Regulating Renal Blood Flow and Urinary Sodium Excretion

2015 ◽  
Vol 26 (12) ◽  
pp. 2953-2962 ◽  
Author(s):  
Matthew A. Sparks ◽  
Johannes Stegbauer ◽  
Daian Chen ◽  
Jose A. Gomez ◽  
Robert C. Griffiths ◽  
...  
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Angiotensin Ii Receptors ◽  
Vascular Type

Mechanism of natriuresis during intrarenal infusion of prostaglandins

1984 ◽  
Vol 247 (3) ◽  
pp. F475-F479 ◽  
Author(s):  
J. A. Haas ◽  
T. G. Hammond ◽  
J. P. Granger ◽  
E. H. Blaine ◽  
F. G. Knox
Keyword(s):  
Blood Flow ◽  
Hydrostatic Pressure ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Prostaglandin Analogue ◽  
Similar Increase ◽  
Interstitial Pressure

Intrarenal infusion of the natural prostaglandin PGE2 increases renal blood flow, renal interstitial hydrostatic pressure, and urinary sodium excretion. A newly synthesized prostaglandin analogue, 4-3-[3-[2-(1-hydroxycyclohexyl)- ethyl]-4-oxo-2-thiazolidinyl]propyl benzoic acid, increases renal blood flow without increasing sodium excretion. To investigate the role of renal interstitial hydrostatic pressure in this dissociation, comparisons were made between PGE2 and the prostaglandin analogue. Intrarenal infusion of PGE2 increased renal blood flow, renal interstitial hydrostatic pressure, and urinary sodium excretion. Following a similar increase in renal blood flow with intrarenal infusion of prostaglandin analogue, renal interstitial hydrostatic pressure and urinary sodium excretion were not changed. To determine whether increases in urinary sodium excretion due to PGE2 infusion are causally related to the increase in renal interstitial hydrostatic pressure rather than to the increase in renal blood flow, responses to PGE2 were obtained in the absence of increases in interstitial pressure. When renal interstitial hydrostatic pressure was held constant, urinary sodium excretion did not change although there was a marked increase in renal blood flow. We conclude that increased renal interstitial hydrostatic pressure is necessary to produce an increase in urinary sodium excretion with prostaglandin-mediated renal vasodilation.

Effect of a kinin antagonist on renal function and haemodynamics during alterations in sodium balance in conscious normotensive rats

1990 ◽  
Vol 78 (2) ◽  
pp. 165-168 ◽  
Author(s):  
Paolo Madeddu ◽  
Nicola Glorioso ◽  
Aldo Soro ◽  
Paolo Manunta ◽  
Chiara Troffa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Sodium Intake ◽  
Urinary Sodium Excretion

1. To evaluate whether sodium intake can modulate the action of endogenous kinins on renal function and haemodynamics, a receptor antagonist of bradykinin was infused in conscious normotensive rats maintained on either a normal or a low sodium diet. 2. The antagonist inhibited the hypotensive effect of exogenously administered bradykinin. It did not change the vasodepressor effect of acetylcholine, dopamine or prostaglandin E2. 3. The antagonist did not affect mean blood pressure, glomerular filtration rate, renal blood flow or urinary sodium excretion, in rats on sodium restriction. It did not change mean blood pressure, glomerular filtration rate or urinary sodium excretion, but decreased renal blood flow, in rats on a normal sodium intake. 4. The kallikrein–kinin system has a role in the regulation of renal blood flow in rats on a normal sodium diet.

Relaxin-induced changes in renal sodium excretion in the anesthetized male rat

2005 ◽  
Vol 288 (1) ◽  
pp. R322-R328 ◽  
Author(s):  
Alsadek H. Bogzil ◽  
Rachel Eardley ◽  
Nick Ashton
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Plasma Osmolality ◽  
Urinary Sodium Excretion ◽  
Male Rats ◽  
Male Rat ◽  
Short Term ◽  
Induced Changes

Pregnancy is associated with profound changes in renal hemodynamics and electrolyte handling. Relaxin, a hormone secreted by the corpus luteum, has been shown to induce pregnancy-like increases in renal blood flow and glomerular filtration rate (GFR) and alter osmoregulation in nonpregnant female and male rats. However, its effects on renal electrolyte handling are unknown. Accordingly, the influence of short (2 h)- and long-term (7 day) infusion of relaxin on renal function was determined in the male rat. Short term infusion of recombinant human relaxin (rhRLX) at 4 μg·h−1·100 g body wt−1 induced a significant increase in effective renal blood flow (ERBF) within 45 min, which peaked at 2 h of infusion (vehicle, n = 6, 2.1 ± 0.4 vs. rhRLX, n = 7, 8.1 ± 1.1 ml·min−1·100 g body wt−1, P < 0.01). GFR and urinary excretion of electrolytes were unaffected. After a 7-day infusion of rhRLX at 4 μg/h, ERBF (1.4 ± 0.2 vs. 2.5 ± 0.4 ml·min−1·100 g body wt−1, P < 0.05), urine flow rate (3.1 ± 0.3 vs. 4.3 ± 0.4 μl·min−1·100 g body wt−1, P < 0.05) and urinary sodium excretion (0.8 ± 0.1 vs. 1.2 ± 0.1 μmol·min−1·100 g body wt−1, P < 0.05) were significantly higher; plasma osmolality and sodium concentrations were lower in rhRLX-treated rats. These data show that long-term relaxin infusion induces a natriuresis and diuresis in the male rat. The mechanisms involved are unclear, but they do not involve changes in plasma aldosterone or atrial natriuretic peptide concentrations.

Mechanism of dopamine-induced diuresis in the dog

1977 ◽  
Vol 232 (6) ◽  
pp. F524-F528
Author(s):  
P. Cadnapaphornchai ◽  
S. M. Taher ◽  
F. D. McDonald
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Direct Effect ◽  
Sodium Excretion ◽  
Free Water ◽  
Urinary Sodium Excretion ◽  
Antagonistic Effect ◽  
Water Excretion ◽  
Diuretic Response ◽  
Solute Excretion

This study was undertaken to evaluate the effect of dopamine (D) on renal water excretion. Intravenous (i.v.) infusion of D (7.5 microgram/kg per min) was associated with a significant, reversible increase in free water excretion (CH2O) and a decrease in urinary osmolality (Uosmol). These changes, however, were associated with significant increases in renal blood flow (RBF), glomerular filtration rate (GFR), and urinary sodium excretion (UNaV). These increases could have been responsible for the diuretic response to D. To examine whether D has a direct effect on vasopressin (ADH) release, D was infused into one common carotid artery at a dose equal to one-fourth the i.v. dose. No effects on CH2O and Uosmol were observed. To examine whether D might have an antagonistic effect on ADH a single bolus of ADH (100 mU) was given to the same hypophysectomized dogs with and without D infusion. The antidiuretic response to ADH was the same, whether or not D was given concomitantly. The net changes in Uosmol and CH2O in response to ADH were not significantly different. Taken together, the present results provide no evidence for a direct effect of D on ADH release nor do they indicate an interference with the peripheral action of ADH. The dopamine-induced diuresis is probably the result of increased solute excretion. This, in turn, is the result of the combined effects of dopamine on increasing renal blood flow, GFR, and sodium excretion.

Role of renal alpha-adrenoceptors mediating renin secretion

1982 ◽  
Vol 242 (6) ◽  
pp. F620-F626 ◽  
Author(s):  
J. L. Osborn ◽  
G. F. DiBona ◽  
M. D. Thames
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Renin Secretion ◽  
Renal Nerve ◽  
Alpha Adrenoceptors ◽  
Alpha Adrenoceptor

The increase in renin secretion resulting from low-frequency renal nerve stimulation (0.5 Hz) occurs in the absence of changes in urinary sodium excretion or renal blood flow and is apparently derived from a direct effect of renal sympathetic nerves on juxtaglomerular granular cells. We sought to determine the role of renal alpha-adrenoceptors in this neurally evoked renin secretion. The neurally evoked renin secretion was unaffected by renal alpha-adrenoceptor blockade with phentolamine or prazosin; however, two dose levels of phenoxybenzamine equally inhibited the renin secretion. The renal vasoconstrictor response to graded renal nerve stimulation was similarly diminished by phentolamine, prazosin, and the higher phenoxybenzamine dose, whereas the lower phenoxybenzamine dose was significantly less effective. Renal alpha-adrenoceptor stimulation with methoxamine infusion at doses that were just subthreshold for altering renal blood flow and urinary sodium excretion or at doses that just reduced urinary sodium excretion also did not change renin secretion. Higher doses of methoxamine that decreased both renal blood flow and sodium excretion increased renin secretion. Based on the inability of phentolamine and prazosin to prevent neurally mediated renin secretion and on the dose-response relationship between methoxamine and changes in renin secretion, renal blood flow, and urinary sodium excretion, we conclude that renal alpha-adrenoceptors do not mediate renin secretion elicited by direct neural activation of the juxtaglomerular granular cells. The data suggest that phenoxybenzamine inhibits neurally mediated renin secretion by a mechanism other than renal alpha-adrenoceptor blockade.

Renorenal reflex responses to mechano- and chemoreceptor stimulation in the dog and rat

1984 ◽  
Vol 246 (1) ◽  
pp. F67-F77 ◽  
Author(s):  
U. C. Kopp ◽  
L. A. Olson ◽  
G. F. DiBona
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
Renal Blood Flow ◽  
Flow Rate ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Urine Flow Rate

The renal functional effects of renal mechano- (MR) and chemoreceptor (CR) stimulation were examined in dogs and rats. In dogs increasing ureteral pressure (increases UP) increased ipsilateral (ipsi) renal blood flow and renin secretion rate, decreased contralateral (contra) renal blood flow, but did not affect contra renal excretion or renin secretion rate. Increasing renal venous pressure (increases RVP) increased ipsi renin secretion rate but did not affect contra renal function. Retrograde ureteropelvic perfusion with 0.9 M NaCl at unchanged UP did not affect either ipsi or contra renal function. In rats,increases UP and retrograde ureteropelvic perfusion with 0.9 M NaCl at unchanged UP did not affect mean arterial pressure, heart rate, contra renal blood flow, or glomerular filtration rate but increased contra urine flow rate and urinary sodium excretion. Increasing ureteral pressure with 0.1 M NaCl increased contra urine flow rate and urinary sodium excretion, whereas retrograde ureteropelvic perfusion with 0.1 M NaCl was without effect. Thus increases UP and retrograde ureteropelvic perfusion with 0.9 M NaCl stimulated renal MR and CR, respectively. The contra diuretic and natriuretic responses to renal MR and CR stimulation were abolished by either ipsi or contra renal denervation. Renal MR and CR stimulation increased ipsi afferent renal nerve activity (RNA) and decreased contra efferent RNA. These results indicate that in dogs renal MR stimulation results in a modest contralateral excitatory renorenal reflex, whereas in rats renal MR and CR stimulation produce a contralateral inhibitory renorenal reflex.

Effect of General Anaesthesia on Renal Haemodynamics in the Rat

1979 ◽  
Vol 57 (5) ◽  
pp. 469-471 ◽  
Author(s):  
B. M. Koeppen ◽  
A. I. Katz ◽  
M. D. Lindheimer
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
Renal Blood Flow ◽  
General Anaesthesia ◽  
Renal Haemodynamics ◽  
Sodium Pentobarbital ◽  
Radioactive Microspheres ◽  
Anaesthetic Agents ◽  
Total Renal Blood Flow

1. The effect of sodium pentobarbital and Inactin anaesthesia on renal haemodynamics in the rat was evaluated with radioactive microspheres 15 μm in diameter. 2. Both anaesthetic agents caused substantial decrements in total renal blood flow (sodium pentobarbital, −34%; Inactin, −24%) compared with unanaesthetized animals. 3. Measurements of renal function obtained in rats anaesthetized with either of these anaesthetic agents should be interpreted with caution.

Sign in / Sign up

Export Citation Format

Share Document