Renal and pressor action of angiotensin in the normal dog

1965 ◽  
Vol 208 (6) ◽  
pp. 1093-1099 ◽  
Author(s):  
John K. Healy ◽  
Carlos Barcena ◽  
J. M. Brian O'Connell ◽  
George E. Schreiner
Keyword(s):  
Filtration Rate ◽  
Pressor Response ◽  
Urine Flow ◽  
Sodium Reabsorption ◽  
Potassium Excretion ◽  
Control Blood Pressure ◽  
Electrolyte Excretion ◽  
Initial Depression ◽  
High Doses ◽  
Higher Doses

The renal and pressor actions of angiotensin in relation to dose were studied in unanesthetized dogs. Low doses caused depression of urine flow, electrolyte excretion, glomerular filtration rate (GFR), and Cpah. With higher doses, the initial depression of urine flow, GFR, and Cpah was greater, but subsequently these functions rose toward control values. In fact, diuresis occurred, accompanied by natriuresis, chloruresis, and kaliuresis. The natriuresis occurred at a time when GFR was significantly depressed. In longer experiments at high doses it was found that the natriuresis declined after 50 min despite continued angiotensin infusion; however, potassium excretion gradually increased throughout. These results help clarify the confusing literature regarding the effects of angiotensin on renal function in dogs and also support the hypothesis that angiotensin can block tubular sodium reabsorption. The pressor response was found to be proportional to the logarithm of the dose of angiotensin. It was also inversely related to the control blood pressure of the dog.

Renal responses to graded hemorrhage in conscious pig

1990 ◽  
Vol 259 (1) ◽  
pp. R119-R125 ◽  
Author(s):  
J. L. Sondeen ◽  
G. A. Gonzaludo ◽  
J. A. Loveday ◽  
G. E. Deshon ◽  
C. B. Clifford ◽  
...  
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Arterial Pressure ◽  
Filtration Rate ◽  
Urine Flow ◽  
Electrolyte Excretion ◽  
Flow Probe ◽  
Ureteral Catheter ◽  
Time Points ◽  
Renal Responses

We developed a conscious pig model with a chronically instrumented kidney to measure renal blood flow (RBF), glomerular filtration rate (GFR), and excretory functions during hemorrhage. Seven to 10 days before experimentation, pigs were splenectomized, arterial and venous catheters were implanted, an ultrasonic flow probe was placed on the renal artery, and a pyelostomy was performed for nonocclusively placing a ureteral catheter. Measurements were taken before hemorrhage, and at hemorrhage volumes of 7, 14, 21, and 28 ml/kg (equivalent to 10.5, 21, 31, and 42% of the estimated blood volume), or at corresponding time points for controls. RBF was decreased by 30% when 21% of the blood (14 mg/kg) was removed, before arterial pressure, GFR, or urine flow or excretion was changed. At volumes of hemorrhage greater than 14 ml/kg, there were progressive decreases in RBF, GFR, urine flow rate, osmotic and electrolyte excretion, and arterial pressure. Thus pigs, like humans, respond to hypovolemia with an early redistribution of blood flow away from the kidney.

Renal and vascular responses of the bullfrog (Rana catesbeiana) to mesotocin

1978 ◽  
Vol 235 (2) ◽  
pp. F151-F155 ◽  
Author(s):  
P. K. Pang ◽  
W. H. Sawyer
Keyword(s):  
Filtration Rate ◽  
Rana Catesbeiana ◽  
Urine Flow ◽  
Vascular Responses ◽  
Diuretic Agent ◽  
Diuretic Response ◽  
High Doses ◽  
Blood Pressure Responses ◽  
Renal Responses ◽  
Depressor Effect

Although mesotocin (MT) has long been known to occur in the amphibian neurohypophysis, there have been few reports on its action among amphibians. In the present investigation, renal responses of intact bullfrogs (Rana catesbeiana) and perfused bullfrog kidneys to MT were studied. The blood pressure responses of this amphibian to MT were also analyzed. We found that MT is diuretic at low doses and that the response is dose related. At high doses the diuretic response decreases progressively and, at times, antidiuresis is observed. The changes in urine flow are proportional to the changes in glomerular filtration rate. In addition, there is a dose-related depressor effect. Data from perfused kidney studies suggest that MT may dilate the afferent glomerular vessels. The possible action of MT as a physiologically important diuretic agent is discussed.

Response of isolated perfused dog kidneys to epinephrine

1962 ◽  
Vol 202 (1) ◽  
pp. 97-102 ◽  
Author(s):  
David M. Worthen ◽  
Quentin N. Anderson ◽  
Lerner B. Hinshaw
Keyword(s):  
Constant Pressure ◽  
Urine Flow ◽  
Low Doses ◽  
Vascular Changes ◽  
Electrolyte Excretion ◽  
Kidney Weight ◽  
Vascular Effect ◽  
Epinephrine Administration ◽  
High Doses ◽  
Renal Vascular

To investigate the renal vascular changes induced by epinephrine, 21 isolated dog kidneys were perfused at constant pressure. Single injections and constant infusions of epinephrine were administered. Changes in blood and urine flow and arterial and intrarenal venous pressures were measured. Changes in renal volume were estimated with a kidney-weighing device, and determinations of cation concentrations were carried out. Data do not support the view that low doses of epinephrine cause diuresis. The previously reported afferent dilation and efferent constriction after epinephrine administration were not found in this investigation. Both increased and decreased urine flows were noted at low doses of epinephrine, whereas a fall in urine flow was consistently seen at high doses. The primary vascular effect of epinephrine is presumably on the afferent arteriole, since there was no consistent diuresis, no increase in kidney weight, a decrease in blood flow, and a decrease in filtration. Electrolyte excretion was not directly influenced by epinephrine. The pressure in the ureter was changed by epinephrine.

Changes in renal hemodynamics and renin release caused by increased plasma oncotic pressure

1976 ◽  
Vol 231 (5) ◽  
pp. 1550-1556 ◽  
Author(s):  
JE Hall ◽  
AC Guyton
Keyword(s):  
Renal Artery ◽  
Filtration Rate ◽  
Colloid Osmotic Pressure ◽  
Urine Flow ◽  
Renin Release ◽  
Sodium Pentobarbital ◽  
Oncotic Pressure ◽  
Electrolyte Excretion ◽  
Afferent Arterioles ◽  
Renal Responses

The effect of increased plasma oncotic pressure on renal blood flow (RBF), glomerular filtration rate (GFR), electrolyte excretion, and renin secretion rate (RSR) was studied in dogs anesthetized with sodium pentobarbital. Renal artery infusions of hyperoncotic dextran or human serum albumin raised renal venous colloid osmotic pressure an average of 7.3 and 10.1 mmHg, respectively, and caused small but consistent increases in RBF, large increases in RSR, marked decreases in urine flow rate and electrolyte excretion, with either no change or small decreases in GFR, and no change in renal artery pressure. Renal vasodilation was confined primarily to afferent arterioles and was not measureable until approximately 45 s after the start of infusions. The renal responses to increased plasma oncotic pressure appeared to be an autoregulatory phenomenon, consistent with a tubular mechanism dependent on an altered distal tubular fluid flow and/or composition. The increased renin release during increased plasma oncotic pressure is not compatible with a renal baroreceptor mechanism that responds to decreases in afferent arteriolar pressure because calculated glomerular pressure increased during albumin and dextran infusions.

Effect of vasopressin on sodium excretion and plasma antinatriferic activity in the dog

1976 ◽  
Vol 231 (1) ◽  
pp. 28-33 ◽  
Author(s):  
VM Buckalew ◽  
KA Dimond
Keyword(s):  
Glomerular Filtration Rate ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Urine Flow ◽  
Potassium Excretion ◽  
State Control ◽  
Sham Control ◽  
Anesthetized Dogs ◽  
Renal Tubular ◽  
Steady State Control

Vasopressin (VP) was administered for 1 h intravenously to hydropenic, anesthetized dogs in doses of 1.0-1.25 mU/kg per min. In 14 experiments, sodium excretion (UNA V) increased from a mean of 13 +/- 5 to a peak of 96 +/- 21 mueq/min 40 min after beginning infusion (P less than .001). Urine flow and potassium excretion increased from 0.18 +/-.04 ml/min and 20 +/- 2 meuq/min to peak values of 0.6 +/- .08 ml/min and 61 +/- 9 mueq/min, respectively (P less than .001), with no significant increase in glomerular filtration rate. No significant changes in UNA V occurred in eight sham control experiments of in six experiments in which VP was given at 75 muU/kf per min. To test the hypothesis that VP might be natriuretic indirectly by releasing a natriuretic substance, plasms ultrafiltrates were tested for toad bladder antinatriferic activity(AA). During steady-state control, AA was -10 +/- 3%. Thirty and sixty minutes after beginning VP, AA increased to -24 +/- 3% (P less than .05) and -26 +/- 2% (P less than .001), respectiviely. No significant change in plasma AA occurred in either sham controls or in animals given the subnatriuretic VP dose. Incubation of plasma with 1,000 muU/ml VP caused no increase in AA. The data show that VP natriuresis is accompanied by an increase in plasms AA. The results suggest that vasopressin natriuresis in hydropenic dogs at least in part to the release of a humoral inhibitor of renal tubular sodium transport.

Angiotensin and electrolyte excretion in renovascular hypertension

1965 ◽  
Vol 208 (6) ◽  
pp. 1087-1092 ◽  
Author(s):  
Abraham J. Borkowski ◽  
Stuart S. Howards ◽  
John H. Laragh
Keyword(s):  
Water Retention ◽  
Tubular Secretion ◽  
Urine Flow ◽  
Left Renal Artery ◽  
Potassium Excretion ◽  
Sodium Retention ◽  
Hypertensive Rats ◽  
Electrolyte Excretion ◽  
Water Excretion ◽  
Ureteral Catheterization

Under conditions of saline, urea, ADH infusion diuresis during anesthesia we observed that in normal rats angiotensin infusion regularly produced natriuresis and diuresis, the degree of which was more closely related to dosage than to increment in blood pressure. Potassium excretion often did not rise appreciably or actually fell during natriuresis, suggesting inhibition of tubular secretion. In animals with a clamp on the left renal artery in which hypertension did not ensue, the renal response to angiotensin was strikingly changed when studied by bilateral ureteral catheterization. Instead of diuresis the peptide produced either no effect or sodium and water retention in both kidneys. In the hypertensive rats, angiotensin consistently produced marked diuresis on the clipped side. Sodium excretion increased much more than urine flow. Simultaneously, in the opposite, unprotected kidney, angiotensin produced quite different effects—sodium and water excretion either did not change or were reduced. Renovascular reflexes and renal renin activity may be involved in determining whether angiotensin induces sodium retention or natriuresis.

Effect of acetylcholine on urinary electrolyte excretion

1964 ◽  
Vol 207 (5) ◽  
pp. 979-982 ◽  
Author(s):  
G. G. Pinter ◽  
C. C. C. O'morchoe ◽  
R. S. Sikand
Keyword(s):  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Urine Flow ◽  
Electrolyte Excretion ◽  
Renal Effects ◽  
Medullary Blood Flow ◽  
Important Mediator ◽  
Separate Control ◽  
Consistent Change ◽  
Excretion Rates

Acetylcholine was infused into the aorta of unanesthetized dogs above the origin of the renal arteries. It produced a statistically significant increase in Na, Cl, and K excretion rates and in renal plasma flow with respect to control values in the same experiments and to results obtained in separate control experiments on the same animals. No consistent change was found in glomerular filtration rate, urine flow, and osmolality. In similar experiments Pitressin was also infused. The renal effects of acetylcholine were slightly enhanced by Pitressin. It was concluded that the antidiuretic hormone was not an important mediator in the production of renal effects during acetylcholine infusion. The possible roles of increased medullary blood flow and of increased angiotensin production are discussed.

Potassium excretion by the isolated perfused kidney from the potassium-adapted rat

1985 ◽  
Vol 248 (4) ◽  
pp. F602-F606
Author(s):  
W. R. Adam ◽  
B. A. Adams
Keyword(s):  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Sodium Reabsorption ◽  
Potassium Excretion ◽  
Free Medium ◽  
High Potassium ◽  
Potassium Intake ◽  
High K ◽  
Renal Adaptation ◽  
A Cell

Adaptation to a high potassium diet leads to an enhanced ability to excrete an acute potassium load. The aim of this study was to examine whether the enhanced kaliuretic ability is an intrinsic renal adaptation or is secondary to extrarenal mediators such as aldosterone. Kidneys from control rats and rats on a high potassium diet were isolated and perfused in a cell-free medium (glomerular filtration rate 0.5 ml/min, fractional sodium reabsorption 95%). Feeding in the 24 h prior to perfusion had a profound effect on fractional K+ excretion in rats on high K+ (fed 1.4 +/- 0.11, fasted 0.70 +/- 0.07) but not in control (fed 0.59 +/- 0.05, fasted 0.64 +/- 0.05) rats. After feeding but not fasting, rats on high K+ had a greater fractional K+ excretion than control K+ rats. Spironolactone inhibited fractional K+ excretion in fed rats on high K+ but not in control rats (high K+ 1.45 +/- 0.18, high K+ + spironolactone 0.95 +/- 0.15; control 0.59 +/- 0.05, control + spironolactone 0.46 +/- 0.02). Although these experiments do not exclude an intrinsic renal adaptation in potassium excretion, a major component of the increased potassium excretion relates to the increased potassium intake, probably mediated via aldosterone.

Mechanisms for the diuresis of acute cold exposure: role for vasopressin?

1993 ◽  
Vol 264 (3) ◽  
pp. R524-R532 ◽  
Author(s):  
D. E. Allen ◽  
M. Gellai
Keyword(s):  
Cold Exposure ◽  
Filtration Rate ◽  
Pressor Response ◽  
Urine Flow ◽  
Prolonged Infusion ◽  
Treatment Groups ◽  
Acute Cold Exposure ◽  
Diuretic Response ◽  
Long Evans ◽  
All Treatment

The hypothesis that inhibition of vasopressin (VP) secretion initiates cold-induced diuresis was tested in six Brattleboro homozygous (diabetes insipidus, DI) rats exposed to 60 min at 5 degrees C. For 9-14 days before cold exposure (CE) the rats were treated with VP (750 pg.kg-1.min-1) subcutaneously via osmotic minipumps. Eight vehicle-treated Long-Evans (LE) rats characterized the response to acute exposure at 5 degrees C. Additional groups of six to eight LE and six DI rats were infused with VP (30-90 pg.kg-1.min-1 iv) on the day of CE. The DI rats receiving chronic VP replacement and untreated LE rats exhibited cold-induced diuresis, with peak increases in urine flow (V) of 63 +/- 12 (DIs) and 29 +/- 4 (LEs) microliters.min-1 x 100 g body wt-1. LE rats acutely infused with VP exhibited a diuresis at the two lower doses (peak V was 18 +/- 3 at the 30 and 18 +/- 4 microliters.min-1 x 100 g body wt-1 at the 60 pg.kg-1.min-1 dose), but the diuretic response was completely blunted at the uppermost dose of VP. Cold-induced diuresis was absent at the lowest VP dose in the acutely infused DI rats. A pressor response (30-36 mmHg) to CE was noted with all treatment groups, including those that did not exhibit a diuresis. No changes in glomerular filtration rate (GFR) with CE were observed. These data suggest that when plasma VP levels are controlled by prolonged infusion of VP in the DI rats, other mechanisms can operate to initiate cold-induced diuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

Neutral endopeptidase inhibition potentiates the natriuretic actions of adrenomedullin

1998 ◽  
Vol 275 (3) ◽  
pp. F410-F414 ◽  
Author(s):  
Ondrej Lisy ◽  
Michihisa Jougasaki ◽  
John A. Schirger ◽  
Horng H. Chen ◽  
Paul T. Barclay ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Filtration Rate ◽  
Urinary Sodium Excretion ◽  
Neutral Endopeptidase ◽  
Urine Flow ◽  
Sodium Reabsorption ◽  
Contralateral Kidney ◽  
Endogenous Peptides ◽  
Anesthetized Dogs ◽  
Nep Inhibition

Adrenomedullin (ADM) is a potent renal vasodilating and natriuretic peptide possessing a six amino acid disulfide ring. Neutral endopeptidase 24.11 (NEP) is localized in greatest abundance in the kidney and cleaves endogenous peptides like atrial natriuretic peptide, which also possesses a disulfide ring. We hypothesized that NEP inhibition potentiates the natriuretic actions of exogenous ADM in anesthetized dogs ( n = 6). We therefore investigated renal function in which one kidney received intrarenal infusion of ADM (1 ng ⋅ kg−1 ⋅ min−1) while the contralateral kidney served as control before and during the systemic infusion of a NEP inhibitor (Candoxatrilat, 8 μg ⋅ kg−1 ⋅ min−1; Pfizer). In response to ADM, glomerular filtration rate (GFR) in the ADM kidney did not change, whereas renal blood flow, urine flow (UV), and urinary sodium excretion (UNaV) increased from baseline. Proximal and distal fractional reabsorption of sodium decreased in the ADM-infused kidney. In response to systemic NEP inhibition, UNaV and UV increased further in the ADM kidney. Indeed, ΔUNaV and ΔUV were markedly greater in the ADM kidney compared with the control kidney. Plasma ADM was unchanged during ADM infusion but increased during NEP inhibition. In conclusion, the present investigation is the first to demonstrate that NEP inhibition potentiates the natriuretic and diuretic responses to intrarenal ADM. This potentiation occurs secondary to a decrease in tubular sodium reabsorption. Lastly, the increase in plasma ADM during systemic NEP inhibition supports the conclusion that ADM is a substrate for NEP.

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