Effect of potassium on renal vascular resistance and urine flow rate

1959 ◽  
Vol 197 (2) ◽  
pp. 305-308 ◽  
Author(s):  
Jerry Scott ◽  
Dean Emanuel ◽  
Francis Haddy
Keyword(s):  
Blood Flow ◽  
Potassium Chloride ◽  
Vascular Resistance ◽  
Flow Rate ◽  
Blocking Agent ◽  
Urine Flow ◽  
Renal Vascular Resistance ◽  
Urine Flow Rate ◽  
Before And After ◽  
Renal Vascular

The effect of potassium chloride upon renal vascular resistance and urine flow rate was studied in anesthetized laparotomized dogs. Potassium chloride was infused directly into the renal artery with the rate of blood flow to the kidney held constant and with flow rate not controlled. Resistance progressively decreased when serum potassium level in the kidney was elevated by infusing 0.11–0.69 mEq K+/min. It progressively increased when the infusion rate exceeded 0.69 mEq/min. This relationship was unaltered by the adrenergic blocking agent phentolamine. Urine flow rate increased both before and after denervation of the kidney when potassium was infused at the rate of 0.6 mEq/min. This increase was not apparent when the rate of blood flow was held constant. These findings indicate that a local potassium excess in amounts which might occur naturally leads to dilatation of renal vessels and increase of urine flow rate. The latter probably is related to the former.

Local effect of serotonin on renal vascular resistance and urine flow rate

1959 ◽  
Vol 196 (5) ◽  
pp. 1122-1126 ◽  
Author(s):  
D. A. Emanuel ◽  
J. Scott ◽  
R. Collins ◽  
F. J. Haddy
Keyword(s):  
Renal Artery ◽  
Vascular Resistance ◽  
Flow Rate ◽  
Blood Flow Rate ◽  
Aortic Pressure ◽  
Local Effect ◽  
Urine Flow ◽  
Renal Vascular Resistance ◽  
Urine Flow Rate ◽  
Renal Vascular

The effect of serotonin upon renal vascular resistance and urine flow rate when infused directly into the renal artery was studied in 37 laparotomized anesthetized dogs. Concentrations of 10 and 100 µg/min. were utilized in kidneys that were innervated, denervated and denervated plus infused with a sympatholytic and adrenolytic agent. In one series, blood flow rate was maintained constant with a pump interposed in the renal artery. Pressures were measured in the renal artery and vein. Changes in renal vascular resistance in nerve intact, denervated and denervated phentolaminized kidneys were +0.14 ± 0.14, +0.16 ± 0.11 and +0.09 ± 0.07 mm Hg/ml/min. Urine flow rate did not change. In a second series, urine flow rate and aortic pressure were measured without the blood pump. Urine flow rate changes for intact, denervated and denervated phentolaminized kidneys were –0.30 ± 0.43, –0.06 ± 0.44 and 0.00 ± 0.37 ml/min. Aortic pressure remained constant. These data indicate that the local effect of serotonin in the amount used is to actively increase the geometric component of renal vascular resistance through some mechanism unrelated to extrinsic nerves and circulating or locally released catecholamines. Under the conditions of the study, regular changes in urine flow rate were not observed.

Effect of Change in Renal Venous Pressure Upon Renal Vascular Resistance, Urine and Lymph Flow Rates

1958 ◽  
Vol 195 (1) ◽  
pp. 97-110 ◽  
Author(s):  
F. J. Haddy ◽  
J. Scott ◽  
M. Fleishman ◽  
D. Emanuel
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Flow Rate ◽  
Venous Pressure ◽  
Blood Flow Rate ◽  
Lymph Flow ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Constant Resistance ◽  
Renal Vascular

The usual increase in intrarenal resistance as a function of flow rate was augmented by elevation of venous pressure. The augmentation was more apparent in innervated than denervated kidneys. With blood flow rate held constant, resistance increased as a function of venous pressure in innervated kidneys but decreased slightly in denervated kidneys. The latter response was not different during administration of phentolamine, phentolamine and eserine or during perfusion of live innervated and dead kidneys with dextran. Resistance changes induced by elevation of only arterial pressure were the same in innervated and denervated kidneys. For a given arterial pressure in dead kidneys perfused with dextran, resistance was higher with venous pressure elevated than it was with pressure normal. Lymph flow rate increased as a function of venous pressure. Urine flow rate decreased as a function of venous pressure with blood flow rate uncontrolled but did not change when flow rate was held constant. Therefore, high renal vein pressures increase resistance by reflex active vasoconstriction as well as by passive vasoconstriction. The reduction in urine flow rate is in part related to these resistance controlling mechanisms.

Impaired Autoregulatory Responses in Contralateral Kidneys of Two-Kidney, One-Clip Hypertensive Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 381s-384s ◽  
Author(s):  
D. W. Ploth ◽  
R. N. Roy ◽  
Wann-Chu Huang ◽  
L. G. Navar
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Urine Flow ◽  
Renal Vascular Resistance ◽  
Hypertensive Rats ◽  
Contralateral Kidney ◽  
Arterial Blood ◽  
Renal Vascular

1. Micropuncture and clearance experiments in two-kidney, one-clip renal vascular hypertensive rats examined the ability of the kidney contralateral to renal vascular stenosis to maintain renal function during conditions of reduced renal arterial blood pressure. 2. At their respective spontaneous blood pressures, renal vascular resistance was higher and glomerular filtration rate (GFR) and renal blood flow were not different in the contralateral kidneys of the hypertensive rats (170 ± 5 mmHg) compared with normal animals (129 ± 1 mmHg). Urine flow and absolute and fractional excretion of electrolyte were greater from the kidneys of the hypertensive animals. However, pressures in cortical structures were similar in the two groups. 3. As blood pressure was reduced acutely, the kidney contralateral to the renal artery stenosis achieved only small decreases in renal vascular resistance that failed to allow GFR, renal blood flow or pressures in cortical structures to be maintained. In contrast, normal rats efficiently autoregulated renal vascular resistance to allow GFR, renal blood flow and cortical pressures to be unchanged as blood pressure was altered between 130 and 115 mmHg. Urine flow and electrolyte excretion decreased to a greater extent in the hypertensive kidneys; at comparable blood pressure these indices of excretory function were not different in the two groups. 4. These observations indicate that the contralateral kidney can maintain normal haemodynamic and glomerular function only at elevated blood pressure and suggest the possibility that the impaired capacity to autoregulate renal resistances may contribute to the maintenance of hypertension observed in this model.

Effects of volume expansion on renal nerve activity, renal blood flow, and sodium and water excretion in conscious dogs

1985 ◽  
Vol 249 (5) ◽  
pp. F680-F687 ◽  
Author(s):  
H. Morita ◽  
S. F. Vatner
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Renal Vascular Resistance ◽  
Conscious Dogs ◽  
Renal Nerve ◽  
Water Excretion ◽  
Renal Nerve Activity ◽  
Renal Vascular

Effects of acute volume expansion with isotonic isoncotic 3% dextran in saline were examined on renal nerve activity (RNA), renal blood flow, vascular resistance, and sodium and water excretion in conscious dogs. In intact dogs, acute volume expansion increased mean arterial pressure 15 +/- 3 mmHg, left atrial pressure 5.5 +/- 0.6 mmHg, and decreased RNA 88 +/- 2%, whereas renal blood flow did not change and renal vascular resistance increased slightly. When renal perfusion pressure was maintained at control levels, volume expansion decreased RNA 87 +/- 2% and renal vascular resistance 15 +/- 4%. During the 80-min period after volume expansion, urine flow rate increased 0.66 +/- 0.13 ml/min and sodium excretion rose 3.89 +/- 0.54 mueq X min-1 X kg-1, whereas RNA remained depressed. Arterial baroreceptor denervation (ABD) did not diminish responses of RNA, renal blood flow, renal vascular resistance, or sodium and water excretion to volume expansion. After ABD plus bilateral cervical vagotomy, volume expansion did not decrease RNA, and diuretic and natriuretic responses were significantly attenuated (P less than 0.025). However, responses of renal blood flow to volume expansion were not altered significantly. In conscious dogs with renal denervation, responses of renal blood flow to volume expansion were not impaired, whereas diuretic and natriuretic responses were attenuated (P less than 0.025). Thus, in intact conscious dogs, vagally mediated reflex decreases in RNA induced by acute volume expansion exerted a significant effect on sodium and water excretion but little control of renal blood flow and renal vascular resistance.

Trout vascular and renal responses to atrial natriuretic factor and heart extracts

1986 ◽  
Vol 251 (3) ◽  
pp. R639-R642 ◽  
Author(s):  
D. W. Duff ◽  
K. R. Olson
Keyword(s):  
Flow Rate ◽  
Atrial Natriuretic Factor ◽  
Pressor Response ◽  
Aortic Pressure ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Natriuretic Factor ◽  
Long Duration ◽  
Before And After ◽  
Atrial Natriuretic

Dorsal aortic pressure (DAP), urine flow rate, and urinary K+, Na+, and Cl- were monitored in chronically catheterized unanesthetized rainbow trout before and after injection of saline, tissue extracts, or synthetic (rat, Ile-26) atrial natriuretic factor (ANF). Synthetic ANF (1.0 and 10.0 micrograms/kg body wt) and extracts from trout atria and ventricles increased DAP, urine flow rate, and electrolyte excretion. Saline, skeletal muscle extracts, and 0.1 microgram/kg body wt synthetic ANF had no effect on DAP and only minor effects on renal water and ion excretion. The slow-onset long-duration pressor response to ANF and heart extracts contrasted with a rapid short-acting pressor effect of epinephrine. Synthetic ANF (10 micrograms/kg body wt) and ventricular extracts produced marked increases in Na+ and Cl- excretion but only a mild diuresis. Much of the increase in urine flow rate appears to be due to solvent injection. These results show that trout hearts contain an ANF-like material and that mammalian and piscine ANF produce hemodynamic and renal effects upon intra-arterial injection.

Renal vasodilatation after inhibition of renin or converting enzyme in marmoset

1986 ◽  
Vol 251 (5) ◽  
pp. H897-H902
Author(s):  
D. Neisius ◽  
J. M. Wood ◽  
K. G. Hofbauer
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Enzyme Inhibitor ◽  
Renal Vascular Resistance ◽  
Converting Enzyme ◽  
Renin Inhibition ◽  
Renal Vascular

The relative importance of angiotensin II for the renal vasodilatory response after converting-enzyme inhibition was evaluated by a comparison of the effects of converting-enzyme and renin inhibition on renal vascular resistance. Renal, mesenteric, and hindquarter blood flows were measured with chronically implanted ultrasonic-pulsed Doppler flow probes in conscious, mildly volume-depleted marmosets after administration of a converting-enzyme inhibitor (enalaprilat, 2 mg/kg iv), a synthetic renin inhibitor (CGP 29,287, 1 mg/kg iv), or a renin-inhibitory monoclonal antibody (R-3-36-16, 0.1 mg/kg iv). Enalaprilat reduced blood pressure (-16 +/- 4 mmHg, n = 6) and induced a selective increase in renal blood flow (27 +/- 8%, n = 6). CGP 29,287 and R-3-36-16 induced comparable reductions in blood pressure (-16 +/- 4 mmHg, n = 6 and -20 +/- 4 mmHg, n = 5, respectively) and selective increases in renal blood flow (36 +/- 12%, n = 6 and 34 +/- 16%, n = 4, respectively). The decrease in renal vascular resistance was of similar magnitude for all of the inhibitors (enalaprilat -28 +/- 3%, CGP 29,287 -32 +/- 6%; and R-3-36-16 -33 +/- 7%). These results indicate that the renal vasodilatation induced after converting-enzyme or renin inhibition is mainly due to decreased formation of angiotensin II.

Effects of a new dihydropyridine derivative, S12968 (pranedipine), and its stereoisomer, S12967, on renal effects of endothelin-1

1994 ◽  
Vol 72 (11) ◽  
pp. 1294-1298 ◽  
Author(s):  
Immaculada Montañés ◽  
Olga Flores ◽  
Nélida Eleno ◽  
José M. López-Novoa
Keyword(s):  
Renal Function ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Fold Increase ◽  
Urine Flow ◽  
Renal Vascular Resistance ◽  
Potassium Excretion ◽  
Endothelin 1 ◽  
Dihydropyridine Derivative ◽  
Renal Vascular

The purpose of the present study was to assess in rats the prevention by two enantiomers of a new dihydropyridine derivative (pranedipine) (called S12967 for the dextrogyre(+) and S12968 for the levogyre (−) molecules) of the renal and cardiovascular effects induced by endothelin-1. The injection of endothelin-1 (1 nmol/kg body weight) induced a sharp and transient decrease in urine flow, sodium and potassium excretion, glomerular filtration rate, renal plasma flow, and renal blood flow, a significant increase in renal vascular resistance, and a small but significant increase in arterial pressure. Treatment with S12968 alone (0.3 mg/kg) induced a 2.5-fold increase in urine flow and potassium excretion and a 4.5-fold increase in sodium excretion. Pretreatment with S12968 completely blocked the endothelin-1 induced increase in arterial pressure, did not affect the acute effect of endothelin-1 on urine flow, sodium and potassium excretion, filtration rate, and renal blood flow, but blunted the effect on renal vascular resistance. Administration of S12967 alone (1 mg/kg) did not induce changes in either renal function or arterial pressure. In S12967-treated animals, endothelin-1 also induced a transient increase in arterial pressure and renal vascular resistance but failed to change renal function in a significant manner. In summary, the above reported experiments show that at the higher, nonhypotensive doses, the levogyre enantiomer (S12968) of a new dihydropyridine derivative (pranedipine) completely prevented the hypertensive effect of endothelin 1, and partially prevented the effect of endothelin-1 on renal vascular resistance. The dextrogyre enantiomer (S12967) had almost no effect on either mean arterial pressure or renal vascular resistance but completely blocked the endothelin-1-induced decrease in urine flow and urinary sodium excretion.Key words: calcium antagonists, endothelin, dihydropyridines, kidney, renal function (rat).

Differences in ouabain-induced natriuresis between isolated kidneys of Milan hypertensive and normotensive rats

1992 ◽  
Vol 82 (2) ◽  
pp. 185-190 ◽  
Author(s):  
Roland Foulkes ◽  
Romana G. Ferrario ◽  
Patricia Salvati ◽  
Giuseppe Bianchi
Keyword(s):  
Vascular Resistance ◽  
Receptor Occupancy ◽  
Renal Vascular Resistance ◽  
The Other ◽  
Hypertensive Rats ◽  
Other Hand ◽  
Before And After ◽  
Renal Vascular ◽  
Isolated Kidneys

1. Several observations support the hypothesis that in rats of the Milan hypertensive strain elevated levels of a circulating ouabain-like factor might normalize the elevated Na+ reabsorption, but, on the other hand, might contribute to the development of hypertension. 2. As the receptor occupancy of this endogenous factor seems to be reversible, the aim of our study was to test, in vitro, the hypothesis of its presence in isolated kidneys from Milan hypertensive rats by studying the response to exogenous ouabain before and after prolonged washing. 3. The kidneys were isolated from adult Milan hypertensive rats and from age-matched normotensive controls and ouabain was given at two different experimental time intervals: shortly (15 min) after washout or after a further 60 min of washout (75 min in total). Comparative experiments with the diuretic hydrochlorothiazide were performed using the same protocol. 4. Ouabain given after 15 min of perfusion caused an increase in renal vascular resistance, diuresis and natriuresis; these haemodynamic and tubular responses were similar in kidneys from both Milan hypertensive and Milan normotensive rats. If given after the washout period, ouabain caused a comparable increase in renal vascular resistance, but a significantly greater natriuresis in kidneys from Milan hypertensive rats as compared with kidneys from Milan normotensive rats. On the other hand, hydrochlorothiazide caused similar natriuresis in kidneys from both strains after washout. 5. These results support the hypothesis that a factor, capable of interacting with the ouabain receptor on the Na+/K+−ATPase of tubular cells, is present in the kidney of adult Milan hypertensive rats and that it can be removed by prolonged washout.

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