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.

The Patterns of Renal Electrolyte Excretion in the Duck (Anas Platyrhynchos) Maintained on Freshwater and on Hypertonic Saline

1968 ◽  
Vol 48 (3) ◽  
pp. 487-508
Author(s):  
W. N. HOLMES ◽  
G. L. FLETCHER ◽  
D. J. STEWART
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Hypertonic Saline ◽  
Plasma Flow ◽  
Inorganic Phosphate ◽  
Filtration Rate ◽  
Renal Excretion ◽  
Renal Plasma Flow ◽  
Urine Flow ◽  
Electrolyte Excretion

1. The renal excretion of water and electrolytes was examined in starved ducks maintained on fresh water and on hypertonic saline containing 284 mM/1. NaCl and 6.0 mM/l. KCl. 2. No significant differences were observed in the urine flow, glomerular filtration rate, renal plasma flow and the excretory rates of K+, NH4+ and inorganic phosphate between these two groups of birds. 3. The excretory rates of Na+, Cl- and Ca2+ were significantly higher in saline-maintained birds than in the freshwater-maintained birds. 4. NH4+ appeared to be a major cationic component which occupied over half of the available osmotic space in the urine of both the freshwater-maintained and saline-maintained birds. 5. In saline-maintained birds the excretion of K+ and inorganic phosphate appeared to be independent of the available osmotic space in the urine whereas the excretion of Na+ and Cl- appeared to be very dependent upon this factor. 6. These observations suggest that the kidneys of the saline-maintained bird constitute the primary pathway for the excretion of K+, NH4+ and inorganic phosphate, and that with respect to the excretion of Na+ they constitute a relatively minor pathway.

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.

Angiotensin II modulates the intrarenal effects of atrial natriuretic peptide

1988 ◽  
Vol 255 (3) ◽  
pp. F545-F551
Author(s):  
H. M. Siragy ◽  
N. E. Lamb ◽  
C. E. Rose ◽  
M. J. Peach ◽  
R. M. Carey
Keyword(s):  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Systemic Effects ◽  
Ang Ii ◽  
Renal Effects

The mechanism by which atrial natriuretic peptide (ANP) increases renal water and solute excretion is not fully understood. We studied the renal effects of ANP and angiotensin II (ANG II) separately and together in uninephrectomized conscious dogs (n = 7) in sodium metabolic balance (80 meq/day). Exogenous ANG II and ANP were without measurable systemic effects as demonstrated by absence of changes in blood pressure, plasma aldosterone concentration, and plasma renin activity. The quantity of ANG II that had significant renal effects that were without measurable systemic effects was 0.2 pmol.kg-1.min-1. Three infusion rates of ANP had significant renal effects (1, 10, and 20 pmol.kg-1.min-1). These quantities of ANP caused significant diuresis, natriuresis, kaliuresis, and increased glomerular filtration rate without significant changes in renal plasma flow. ANG II alone caused significant antidiuresis, antinatriuresis, and decreased glomerular filtration rate and renal plasma flow. When ANG II and ANP were given together, no change in urinary flow rate, urinary sodium or potassium excretion, or renal plasma flow was observed, whereas glomerular filtration rate increased. Filtration fraction increased significantly with ANG II and ANP separately and together. Intrarenal ANP prevents the ANG II-induced decrement in urinary sodium excretion and urine flow rate. ANP may play an important role in escape from the sodium-retaining action of intrarenal ANG II.

Exogenous cGMP prevents decrease in diuresis and natriuresis induced by inhibition of NO synthesis

1993 ◽  
Vol 264 (2) ◽  
pp. F344-F347 ◽  
Author(s):  
V. Lahera ◽  
J. Navarro ◽  
M. L. Biondi ◽  
L. M. Ruilope ◽  
J. C. Romero
Keyword(s):  
Nitric Oxide ◽  
Intravenous Infusion ◽  
Filtration Rate ◽  
Excretion Rate ◽  
Renal Plasma Flow ◽  
Specific Inhibitor ◽  
Urine Flow ◽  
Dibutyryl Camp ◽  
Excretory Function ◽  
Preventive Effects

We previously demonstrated that the intravenous infusion of the specific inhibitor of nitric oxide (NO) synthesis, NG-nitro-L-arginine methyl ester (L-NAME), over a period of 60 min elevates mean arterial pressure (MAP) and reduces renal hemodynamics and excretory function. The objective of the present study was to determine the ability of a guanosine 3',5'-cyclic monophosphate (cGMP) analogue, 8-bromo-cGMP (8-BrcGMP), in preventing the increase in MAP and the reductions in renal plasma flow (RPF), glomerular filtration rate (GFR), urine flow (UV), and sodium excretion rate (UNaV) induced by intravenous infusion of L-NAME in rats. As expected, the infusion of L-NAME (50 micrograms.kg-1.min-1) increased (P < 0.05) MAP and reduced (P < 0.05) RPF, GFR, UV, and UNaV. The administration of 8-BrcGMP (100 micrograms.kg-1.min-1) and L-NAME resulted in no change in MAP, RPF, and GFR. However, decreased (P < 0.05) UV and UNaV were still observed. When 8-BrcGMP (200 micrograms.kg-1.min-1) and L-NAME were infused together, no significant changes in MAP or in renal function were observed. To prove the specificity of the 8-BrcGMP preventive effects, dibutyryl cAMP (200 micrograms.kg-1.min-1) and L-NAME (50 micrograms.kg-1.min-1) were infused together. Under these conditions, MAP, RPF, GFR, UV, and UNaV were modified in a manner similar to that observed during the infusion of L-NAME.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Mechanism of Early and Chronic Experimental Renal Hypertension as Tested by CCK-179

1956 ◽  
Vol 186 (1) ◽  
pp. 161-166 ◽  
Author(s):  
Irene H. Oyen
Keyword(s):  
Blood Pressure ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Renal Hypertension ◽  
Peripheral Resistance ◽  
Repeated Administration ◽  
Maximal Effect ◽  
Renal Effects ◽  
Experimental Renal Hypertension

The effects on blood pressure and renal clearances of a combination of dihydrogenated ergot alkaloids, CCK-179, were studied in normal dogs and dogs with experimental renal (Goldblatt) hypertension. The drug was observed to have a maximal effect at 0.012 mg/kg, about one twelfth to one sixteenth the dose recommended in the literature. In normal dogs the drug causes a slight fall in blood pressure, a moderate decrease in glomerular filtration rate (creatinine clearance) and a pronounced decrease in renal plasma flow (PAH clearance), hemodynamic effects resembling those seen in man. After repeated administration of the drug, the renal effects are of greater magnitude in these dogs. In hypertensive dogs, CCK-179 causes blood pressure to approach normal levels. In the early weeks of hypertension, the renal effects of the drug are similar to those seen in normals but as hypertension increases in duration up to 55 weeks, the decreases in filtration rate and plasma flow become progressively smaller. This could indicate that in chronic experimental renal hypertension the high peripheral resistance is maintained at least in part by increased activity of the sympathetic nervous system rather than by the action of the components of the renal humoral pressor system.

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.

Effects of X-Irradiation on Renal Function of Rats

1957 ◽  
Vol 188 (2) ◽  
pp. 367-370 ◽  
Author(s):  
L. H. Smith ◽  
W. R. Boss
Keyword(s):  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Urine Flow ◽  
Whole Body ◽  
Irradiation Damage ◽  
X Rays

In a study of the direct effects of irradiation on the renal function of rats whose exteriorized kidneys were exposed to massive doses of x-rays, significant augmentation of the urine flow was observed 28 days after 2500 r. On the 7th day after 2500, 3000 and 4000 r the urine flow was slightly above that of control rats. The glomerular filtration rate was enhanced on the 7th day after 2500 and 3000 r. Conversely, 28 days after these x-ray doses the filtration rate was slightly below the control values. In the 4000-r, 28-day group, the glomerular filtration rate was 43% below that of the controls. No significant changes in the renal plasma flow occurred on the 7th day after 2500, 3000 and 4000 r. An insignificant increase in the renal plasma flow was noted 28 days after 2500 and 3000 r. On the 28th day after 4000 r, however, the renal plasma flow was 51% below that of the controls. We concluded that both augmentation and depression of renal function were the result of the direct action of x-rays on the kidneys. The results also suggest that renal failure resulting from direct irradiation damage to the kidneys is not a major factor that contributes to deaths occurring within 7 days after the exposure of rats to 4000 r or less of whole-body x-rays.

The effects of "dead space" and urine flow changes on measurements of glomerular filtration rate by clearance methods

1983 ◽  
Vol 61 (4) ◽  
pp. 435-438 ◽  
Author(s):  
R. Keeler
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Dead Space ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Urine Flow ◽  
Collection Period ◽  
Flow Changes ◽  
Collecting System ◽  
Clearance Methods

The errors inherent in making whole-kidney measurements of glomerular filtration rate or renal plasma flow during periods of changing urine flow are discussed. The quantitative relationships of these errors to the dead space of the collecting system, changes in urine flow, and the duration of the collection period are presented.

DIE RENALE CLEARANCE DES ALDOSTERONS UND SEINER HAUPTMETABOLITE BEIM MENSCHEN

1965 ◽  
Vol 49 (4) ◽  
pp. 510-524 ◽  
Author(s):  
J. Gfeller ◽  
W. Siegenthaler
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Clearance ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Urine Flow ◽  
Order Of Magnitude ◽  
Renale Clearance

ABSTRACT Metabolism and excretion of aldosterone in six normal persons were investigated with the renal clearance method. At normal levels of urine flow (0.5–1.2 ml/min), the reabsorption of free aldosterone in the kidney is 90–95 %, ranging thus in the same order of magnitude as the reabsorption of cortisol. The average clearance of the 3-oxo-conjugate exceeds renal plasma flow by 70 %. Therefore it can be assumed that free aldosterone is converted to the 3-oxo-conjugate by the kidney. The renal clearance of the tetrahydroaldosterone glucuronide was on the average 138 % of the thiosulfate clearance or glomerular filtration rate. The concept of renal clearance properly used cannot be applied to the excretion of the metabolites of aldosterone which apparently are produced to some extent by the kidneys themselves.

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