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.

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.

Potassium and sodium excretion and potassium homeostasis during acute hypokalemia

1965 ◽  
Vol 208 (6) ◽  
pp. 1143-1152 ◽  
Author(s):  
Robert R. Siegel ◽  
William D. Lotspeich
Keyword(s):  
Sodium Excretion ◽  
Extracellular Fluid ◽  
Tubular Secretion ◽  
Urine Flow ◽  
Potassium Excretion ◽  
Distal Nephron ◽  
Close Coupling ◽  
Potassium Homeostasis ◽  
Blood Ph ◽  
Total Body

Decreased potassium and increased sodium excretion were observed in dogs acutely potassium-depleted by hemodialysis. Potassium excretion at constant blood pH varied directly with plasma [K+]. When filtered Na load and urine flow were constant during K+ depletion, increase in Na excretion was equivalent to decrease in K+ excretion, suggesting close coupling between transtubular movements of the two ions. Large changes in plasma [K+] (30%) and K+ excretion (50%) were produced with removal of a relatively small amount (estimated 3%) of total body K+. Plasma [K+] decrease during depletion was rapidly decelerated by movement of intracellular K+ into the extracellular fluid (ECF). When ECF [K+] stabilized, further decrease in K+ excretion ceased despite continued reduction of total body K+. It appears: 1) that tubular secretion of K+ is directly and rapidly responsive to reduction in ECF [K+]; 2) that low ECF [K+] may simultaneously impair contraluminal K+ uptake and Na extrusion, reducing K+ excretion and Na reabsorption during acute hypokalemia. Stoichiometry of changes suggests a 1:1 coupling between K+ secretion and moiety of Na reabsorption in the distal nephron.

DER EINFLUSS HOHER KOCHSALZ-GABEN AUF DIE ALDOSTERON- UND ELEKTROLYTAUSSCHEIDUNG BEI GESUNDEN SCHWANGEREN

1964 ◽  
Vol 47 (3) ◽  
pp. 469-484 ◽  
Author(s):  
G. Stark ◽  
J. Lehmann-Achilles
Keyword(s):  
Blood Pressure ◽  
Water Retention ◽  
Experimental Period ◽  
Test Period ◽  
Potassium Excretion ◽  
Sodium Retention ◽  
Oedema Formation ◽  
Sodium Potassium ◽  
Salt Loading ◽  
Very High

ABSTRACT In order to determine what effect is produced on aldosterone excretion by the sodium retention observed in pre-eclampsia, a large dose of sodium was administered and the following were investigated: excretion of aldosterone, sodium, potassium, water, body weight, blood pressure and oedema formation. This investigation was performed on eleven women between the seventh and tenth months of pregnancy. The experimental period consisted of five (5) pre-test days, ten (10) days of actual testing and two (2) days after the test. During the test-period the patient received 18 g NaCl as a 1.8% i. v. solution daily. All the patients tolerated the infusions well. No definite changes in blood pressure, weight or oedema were noted. By intake and out-put measurements during the test period a sodium and water retention was found, while the potassium excretion remained unchanged. In all cases the values of aldosterone excretion (very high in pregnancy) were reduced as a result of salt-loading to about ⅕ of the pre-test period. In the post-experimental period the values returned to those of the pretest period. It is concluded that the lowered aldosterone excretion values in preeclampsia or eclampsia are caused by increased sodium retention, which also occurs in the sodium loading experiments.

scholarly journals The acute pressure natriuresis response is suppressed by selective ETA receptor blockade

2021 ◽  
Author(s):  
Geoffrey Culshaw ◽  
David Binnie ◽  
Neeraj Dhaun ◽  
Patrick Hadoke ◽  
Matthew Bailey ◽  
...  
Keyword(s):  
Vascular Function ◽  
Water Retention ◽  
Salt Intake ◽  
Separate Experiment ◽  
Receptor Subtypes ◽  
Sodium Retention ◽  
Sprague Dawley ◽  
Water Excretion ◽  
Pressure Natriuresis ◽  
Renal Tubular

Hypertension is a major risk factor for cardiovascular disease.  In a significant minority of people, it develops when salt intake is increased (salt-sensitivity).  It is not clear whether this represents impaired vascular function or disruption to the relationship between blood pressure (BP) and renal salt-handling (pressure natriuresis, PN).  Endothelin-1 (ET-1) regulates BP via ETA and ETB receptor subtypes.  Blockade of ETA receptors reduces BP, but promotes sodium retention by an unknown mechanism.  ETB blockade increases both BP and sodium retention.  We hypothesised that ETA blockade promotes sodium and water retention by suppressing PN.  We also investigated whether suppression of PN might reflect off-target ETB blockade.  Acute PN was induced by sequential arterial ligation in male Sprague Dawley rats.  Intravenous atrasentan (ETA antagonist, 5mg/kg) halved the normal increase in medullary perfusion and reduced sodium and water excretion by >60%.  This was not due to off-target ETB blockade because intravenous A-192621 (ETB antagonist, 10mg/kg) increased natriuresis by 50% without modifying medullary perfusion.  In a separate experiment in salt-loaded rats monitored by radiotelemetry, oral atrasentan reduced systolic and diastolic BP by ~10mmHg, but additional oral A-192621 reversed these effects.  Endogenous ETA stimulation has natriuretic effects mediated by renal vascular dilation while endogenous ETB stimulation in the kidney has antinatriuretic effects via renal tubular mechanisms.  Pharmacological manipulation of vascular function with ET antagonists modifies the BP set-point, but even highly selective ETA antagonists attenuate PN, which may be associated with salt and water retention.

scholarly journals Open-loop analysis on sympathetically mediated arterial pressure and urine output responses in spontaneously hypertensive rats: effect of renal denervation

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Toru Kawada ◽  
Takuya Nishikawa ◽  
Satoru Suehara ◽  
Satoshi Sawada ◽  
Tetsuo Tanaka ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Urine Output ◽  
Spontaneously Hypertensive Rats ◽  
Renal Denervation ◽  
Sympathetic Innervation ◽  
Urine Flow ◽  
Hypertensive Rats ◽  
Loop Analysis ◽  
Intact Side ◽  
Spontaneously Hypertensive

AbstractPrimary acute sympathetic activation (PASA) causes a subsequent arterial pressure (AP) elevation. In this case, an antidiuretic effect via the renal innervation and pressure diuresis can act antagonistically on the kidneys. We examined the effect of PASA on urine output in spontaneously hypertensive rats (SHR) 4–7 days after unilateral renal denervation (RDN) (n = 9). The slope of the plot of urine flow versus AP was positive (0.120 ± 0.031 μL min−1 kg−1 mmHg−1) on the intact side, but it was less than 1/3 of the slope observed previously in normotensive Wistar–Kyoto rats (WKY). RDN did not normalize the slope of urine flow versus AP (0.179 ± 0.025 μL min−1 kg−1 mmHg−1, P = 0.098 versus the intact side). The urine flow at the operating point of the AP tended to be greater on the denervated than the intact side (29.0 ± 1.8 vs. 25.3 ± 1.9 μL min−1 kg−1, P = 0.055). The percent increase (17.2 ± 7.2%) was not different from that observed previously in WKY. Although high-resting sympathetic nerve activity is prerequisite for maintaining hypertension in SHR, the effect of sympathetic innervation on the urine output function was not greater than that in WKY.

Abstract P489: Effect of Continuous Intake of Hesperidin on Blood Pressure in 2-kidney, 1-clip Renovasucular Hypertensive Rats

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Ayuna Yamaoka ◽  
Yukiko Segawa ◽  
Saki Maruyama ◽  
Natsumi Saito ◽  
Hiroko Hashimoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mrna Expression ◽  
Control Diet ◽  
Left Renal Artery ◽  
Sham Operation ◽  
Hypertensive Rats ◽  
Fruit Peel ◽  
Arterial Blood ◽  
Significant Difference ◽  
Enos Mrna

Objective: Hesperidin (HES) is a flavonoid which is contained in citrus fruit peel. It has physiological effects on blood vessels such as strengthening capillary vessels. Thus, it is known to be one of the effective ingredients of herbal medicine. Some studies have shown that the intake of HES decreases blood pressure (BP) in spontaneously hypertensive rats. The antihypertensive effect of HES is suggested to be due to vasodilation by nitric oxide (NO). However, its mechanism has not been clarified in detail. In this study, we observed whether HES intake decreases BP in 2-kidney, 1-clip renovasucular hypertensive rats (2K1C) and evaluated endothelial NO synthase (eNOS) mRNA to investigate its role in the mechanism. Methods: Male Sprague-Dawley rats (6 weeks old) were treated with sham operation (SHAM) or clipping the left renal artery (2K1C). After surgery, the rats started receiving continuously a control diet (C) or a diet containing 0.1% (w/w) HES for 6 weeks. The systolic BP (SBP) was measured by a tail-cuff method every week. At the end of the protocol, mean arterial blood pressure (MAP) was measured in each rat under anesthesia. Then, the aortas were removed for extracting mRNA. eNOS mRNA expression was evaluated using real-time RT-PCR. Results: At the end of the protocol, SBP in 2K1C-C was significantly higher than in SHAM-C (170±6 vs 117±6 mmHg, p <0.001). On the other hand, 2K1C-HES was lower in SBP (141±4 mmHg) than 2K1C-C ( p <0.01). There were no significant differences between SHAM-HES (122±7 mmHg) and SHAM-C. MAP at the end of the protocol were similar to in SBP. ANOVA revealed mRNA expression of eNOS was significantly higher in 2K1C than in SHAM ( p <0.05), and showed no significant difference between C and HES, nor a significant interaction. Conclusion: Continuous intake of HES may suppress BP increase in 2K1C. The role of eNOS mRNA expression may not be involved in the mechanism.

Acute renal denervation produces a diuresis and natriuresis in young SHR but not WKY rats

1986 ◽  
Vol 251 (4) ◽  
pp. F655-F661 ◽  
Author(s):  
M. A. Rudd ◽  
R. S. Grippo ◽  
W. J. Arendshorst
Keyword(s):  
Sodium Excretion ◽  
Renal Denervation ◽  
Strain Differences ◽  
Urine Flow ◽  
Sprague Dawley ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Water Excretion ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Clearance experiments were conducted to determine the effect of acute unilateral renal denervation (DNX) on renal hemodynamics and salt and water excretion in anesthetized 6-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto genetic control rats (WKY). Before DNX, SHR had higher mean arterial pressure (33%) and renal vascular resistance (RVR) (57%) and lower glomerular filtration rate (GFR) (10%); urine flow and sodium excretion were similar. Following DNX in SHR, sodium and water excretion increased by 138 and 62%, respectively (P less than 0.001); GFR and RVR were unchanged. In contrast, DNX in WKY did not affect urine flow (0%) or sodium excretion (-21%). These strain differences were observed in Okamoto-Aoki rats from two sources. Effective DNX was indicated by 95% reduction of norepinephrine content 3 days after DNX in both strains. Six-week-old Sprague-Dawley and Munich-Wistar rats, in contrast to WKY, responded to DNX with a natriuresis (+182%) and diuresis (+95%) (P less than 0.001). Renal function was unaffected by sham DNX in SHR. Our results indicate that efferent renal nerve activity has little tonic influence on the renal vasculature in these young rats. Augmented neurotransmitter release and/or tubular responsiveness may be involved in fluid and electrolyte retention and the pathogenesis of hypertension in SHR. Conversely, blunted renal neuroeffector responses may prevent WKY from developing hypertension.

Homeostatic potassium excretion in fed and fasted sheep

1988 ◽  
Vol 254 (2) ◽  
pp. R357-R380 ◽  
Author(s):  
L. Rabinowitz ◽  
D. M. Green ◽  
R. L. Sarason ◽  
H. Yamauchi
Keyword(s):  
Flow Rate ◽  
Urine Flow ◽  
Plasma Aldosterone ◽  
Urine Flow Rate ◽  
Potassium Excretion ◽  
Adult Sheep ◽  
Blood Ph ◽  
Low Levels ◽  
K Concentration ◽  
Filtered Load

In unanesthetized adult sheep, following intake of a daily meal, there was a peak in K excretion. The maximum and minimum rates of K excretion following meals were directly related to meal K content. On days without meals, no peak in K excretion occurred. Changes in K excretion on fed and fast days occurred without changes in the low levels of plasma aldosterone and were poorly correlated with urine or blood pH, urine flow rate, Na excretion, or the filtered load of K, but they correlated well with fractional K excretion. Plasma K did not change on fast days. Plasma K increased on some, but not all, fed days. Increases in plasma K that occurred on fed days were insufficient to account for the concurrent kaliuresis. Infusion of aldosterone or isotonic NaCl failed to alter K excretion in fed or fasted sheep. Infusion of isotonic NaCl + aldosterone hypertonic Na2SO4 + aldosterone increased K excretion in fasted but not fed sheep. Infusion of K in the rumen of fed and fasted sheep elevated rumen K concentration and led to increases in K excretion that could not be explained by increases in plasma K. The mechanisms responsible for the homeostatic changes in K excretion on fed and fast days were not ascertained but may importantly depend on sensors of enteric K content.

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.

Sign in / Sign up

Export Citation Format

Share Document