Effect of propranolol on renin release in the dog

1977 ◽  
Vol 55 (4) ◽  
pp. 747-754 ◽  
Author(s):  
John C. H. Yun ◽  
Gerald D. Kelly ◽  
Frederic C. Bartter
Keyword(s):  
Plasma Renin ◽  
Plasma Potassium ◽  
Sodium Concentration ◽  
Plasma Aldosterone ◽  
Renin Release ◽  
Plasma Sodium ◽  
Renin Substrate ◽  
Arterial Blood ◽  
Consistent Change ◽  
Change In Mean

Infusion of d,l-propranolol in both anesthetized and conscious dogs caused decreases in heart rate (HR), plasma renin activity (PRA), and plasma aldosterone. There was no consistent change in mean arterial blood pressure, plasma renin substrate concentration, packed cell volume, plasma potassium, or plasma sodium concentration following the infusion of propranolol. In five conscious animals, infusion of propranolol (1 mg/kg followed by 0.47–0.65 mg kg−1 h−1) reduced HR from 117.6 ± 4.0 beats per minute (mean ± SE) during control periods to 73.2 ± 2.0 beats per minute (P < 0.005) 90 min after the start of infusion. PRA decreased from 9.97 ± 1.79 ng ml−1 h−1 during control periods to reach 1.50 ± 0.42 ng ml−1 h−1 (P < 0.005) at the end of the 90-min infusions. Plasma aldosterone also decreased during this time from 17.60 ± 1.93 ng% during control periods to reach 6.64 ± 0.98 ng% (P < 0.005). The data suggest that propranolol at the dose administered suppresses renin and aldosterone secretion in unstimulated dogs. They suggest also that β-receptor activity contributes to basal renin release.

Response of the renin-aldosterone system in the camel to acute dehydration

1978 ◽  
Vol 44 (6) ◽  
pp. 926-930 ◽  
Author(s):  
J. P. Finberg ◽  
R. Yagil ◽  
G. M. Berlyne
Keyword(s):  
Plasma Renin Activity ◽  
Potassium Concentration ◽  
Plasma Renin ◽  
Plasma Potassium ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Hormonal Changes ◽  
Water Reabsorption ◽  
Renin Substrate ◽  
Plasma Sodium Concentration

Plasma renin activity (PRA), renin substrate concentration (PRS), aldosterone concentration (PA), and cortisol levels were determined in five camels during dehydration (8–10 days complete denial of water) and at timed intervals after rapid rehydration in cool spring and hot summer weather. Plasma sodium concentration increased from 138 +/- 3.7 to 147 +/- 2.5 (mean +/- SE) meq/l during spring dehydration, and from 146 +/- 1.3 to 157 +/- 1.14 meq/l during dehydration in the summer. Plasma sodium concentration returned to control levels over the course of several hours following rapid rehydration. Only minor changes in plasma potassium concentration occurred. The hormonal changes were accentuated in the summer dehydration. PRA increased slightly on dehydration, and returned to control levels over the course of several hours following rehydration. PA increased slightly on dehydration but was markedly elevated 24 h after rehydration. PRS showed a slight increase following rehydration in the spring experiment, but no significant change in the summer experiment. Changes in cortisol were insignificant. The results are consistent with a role for angiotensin and aldosterone in enhancing sodium and water reabsorption from kidney and large intestine on dehydration in this species.

Sodium balance and aldosterone during dehydration and rehydration in the dog

1984 ◽  
Vol 247 (1) ◽  
pp. R76-R83 ◽  
Author(s):  
T. N. Thrasher ◽  
C. E. Wade ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Sodium Intake ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Plasma Potassium ◽  
Urinary Sodium Excretion ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Sodium Retention

The regulation of sodium metabolism and the renin-angiotensin-aldosterone system was evaluated during 24 h of water, but not food, deprivation and during rehydration in the dog. Dehydration caused increases in plasma concentrations of sodium (6.0 +/- 0.7 meq/l), protein (0.8 +/- 0.1 g/dl), vasopressin (5.3 +/- 0.9 pg/ml), and renin activity (3.5 +/- 1.1 ng AI X ml-1 X 3 h-1). Plasma aldosterone was unchanged and plasma potassium fell slightly (0.2 +/- 0.1 meq/l). During dehydration, food, and thus sodium intake fell by more than 10% in 12 of 19 dogs, but urinary sodium excretion increased significantly, leading to a negative sodium balance (1.9 +/- 0.2 meq/kg). Sodium retention was observed after rehydration and sodium balance; plasma electrolytes, vasopressin, and plasma renin activity (PRA) returned turned to control levels after the 1st day of recovery. However, plasma aldosterone was slightly elevated at this time, returning to control after the 2nd day of recovery. The dehydration-induced natriuresis could not be accounted for by a fall in plasma aldosterone. However, sodium retention following rehydration could be aldosterone dependent, because additional studies showed a threefold rise in plasma levels of the hormone 1 h after drinking. The acute rise in aldosterone correlated closely (r = 0.82) with the fall in plasma sodium after drinking but not with changes in adrenocorticotrophic hormone, PRA, or plasma potassium. It is concluded that natriuresis is a homeostatic response to dehydration as a means of ameliorating the rise in body fluid osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Plasma and Electrolyte Changes in Exercising Humans After Ingestion of Multiple Boluses of Pickle Juice

2015 ◽  
Vol 50 (2) ◽  
pp. 141-146 ◽  
Author(s):  
Michael A. McKenney ◽  
Kevin C. Miller ◽  
James E. Deal ◽  
Julie A. Garden-Robinson ◽  
Yeong S. Rhee
Keyword(s):  
Body Weight ◽  
Relative Humidity ◽  
Blood Sample ◽  
Plasma Volume ◽  
Potassium Concentration ◽  
Plasma Osmolality ◽  
Plasma Potassium ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Plasma Sodium Concentration

Context: Twenty-five percent of athletic trainers administer pickle juice (PJ) to treat cramping. Anecdotally, some clinicians provide multiple boluses of PJ during exercise but warn that repeated ingestion of PJ may cause hyperkalemia. To our knowledge, no researchers have examined the effect of ingesting multiple boluses of PJ on the same day or the effect of ingestion during exercise. Objective: To determine the short-term effects of ingesting a single bolus or multiple boluses of PJ on plasma variables and to characterize changes in plasma variables when individuals ingest PJ and resume exercise. Design: Crossover study. Setting: Laboratory. Patients or Other Participants: Nine euhydrated men (age = 23 ± 4 years, height = 180.9 ± 5.8 cm, mass = 80.7 ± 13.8 kg, urine specific gravity = 1.009 ± 0.005). Intervention(s): On 3 days, participants rested for 30 minutes, and then a blood sample was collected. Participants ingested 0 or 1 bolus (1 mL·kg−1 body weight) of PJ, donned sweat suits, biked vigorously for 30 minutes (approximate temperature = 37°C, relative humidity = 18%), and had a blood sample collected. They either rested for 60 seconds (0- and 1-bolus conditions) or ingested a second 1 mL·kg−1 body weight bolus of PJ (2-bolus condition). They resumed exercise for another 35 minutes. A third blood sample was collected, and they exited the environmental chamber and rested for 60 minutes (approximate temperature = 21°C, relative humidity = 18%). Blood samples were collected at 30 and 60 minutes postexercise. Main Outcome Measure(s): Plasma sodium concentration, plasma potassium concentration, plasma osmolality, and changes in plasma volume. Results: The number of PJ boluses ingested did not affect plasma sodium concentration, plasma potassium concentration, plasma osmolality, or changes in plasma volume over time. The plasma sodium concentration, plasma potassium concentration, and plasma osmolality did not exceed 144.6 mEq·L−1 (144.6 mmol·L−1), 4.98 mEq·L−1 (4.98 mmol·L−1), and 289.5 mOsm·kg−1H2O, respectively, in any condition at any time. Conclusions: Ingesting up to 2 boluses of PJ and resuming exercise caused negligible changes in blood variables. Ingesting up to 2 boluses of PJ did not increase plasma sodium concentration or cause hyperkalemia.

Enhancement of the Antihypertensive Effect of Hydrochlorothiazide in Dogs after Suppression of Renin Release by Beta-Adrenergic Blockade

1975 ◽  
Vol 48 (2) ◽  
pp. 147-151
Author(s):  
C. S. Sweet ◽  
M. Mandradjieff
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Antihypertensive Effect ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Antihypertensive Activity ◽  
Adrenergic Blockade ◽  
Arterial Blood

1. Renal hypertensive dogs were treated with hydrochlorothiazide (8−2 μmol/kg or 33 μmol/kg daily for 7 days), or timolol (4.6 μmol/kg daily for 4 days), a potent β-adrenergic blocking agent, or combinations of these drugs). Changes in mean arterial blood pressure and plasma renin activity were measured over the treatment period. 2. Neither drug significantly lowered arterial blood pressure when administered alone. Plasma renin activity, which did not change during treatment with timolol, was substantially elevated during treatment with hydrochlorothiazide. 3. When timolol was administered concomitantly with hydrochlorothiazide, plasma renin activity was suppressed and blood pressure was significantly lowered. 4. These observations suggest that compensatory activation of the renin-angiotensin system limits the antihypertensive activity of hydrochlorothiazide in renal hypertensive dogs and suppression of diuretic-induced renin release by timolol unmasks the antihypertensive effect of the diuretic.

Renin, aldosterone, electrolyte, and cortisol responses to hypoxic decompression

1977 ◽  
Vol 43 (3) ◽  
pp. 421-424 ◽  
Author(s):  
J. R. Sutton ◽  
G. W. Viol ◽  
G. W. Gray ◽  
M. McFadden ◽  
P. M. Keane
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Cortisol ◽  
Acute Mountain Sickness ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Plasma Aldosterone Concentration ◽  
Urinary Potassium ◽  
Mountain Sickness

Responses of plasma renin activity, plasma aldosterone, plasma cortisol, and plasma electrolyte concentration and urinary electrolyte and aldosterone excretion were studied in four men during hypoxic decompression to a stimulated altitude of 4,760 m in a pressure chamber. Three of the four subjects developed significant acute mountain sickness. Plasma sodium and potassium concentrations were unchanged. No significant change in plasma renin activity was observed, but values tended to fall. Plasma aldosterone concentration was depressed while plasma cortisol was elevated and diurnal variation lost. Urinary sodium excretion was unchanged, but urinary potassium and aldosterone excretion were decreased. The decrease in plasma and urinary aldosterone and urinary potassium in the absence of change in plasma renin activity or plasma potassium is of uncertain origin. It is unlikely to be due to a decrease in adrenocorticotropin secretion since plasma cortisol rose during the same time. None of the changes could be causally implicated in the development of acute mountain sickness although the increase in plasma cortisol was greatest in the most ill.

Renin, Angiotensin and Aldosterone in Human Pregnancy and the Menstrual Cycle

1971 ◽  
Vol 16 (3) ◽  
pp. 183-196 ◽  
Author(s):  
J. I. S. Robertson ◽  
R. J. Weir ◽  
G. O. Düsterdieck ◽  
R. Fraser ◽  
M. Tree
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin ◽  
Normal Pregnancy ◽  
Maternal Plasma ◽  
Plasma Aldosterone ◽  
Sodium Depletion ◽  
Aldosterone Secretion ◽  
Renin Substrate ◽  
Plasma Aldosterone Concentration ◽  
In Pregnancy

Aldosterone secretion is frequently, although not invariably, increased above the normal non-pregnant range in normal pregnancy. Substantial increases in plasma aldosterone concentration have also been demonstrated as early as the sixteenth week. In pregnancy, aldosterone secretion rate responds in the usual way to changes in sodium intake. Plasma renin concentration is frequently, but not invariably, raised above the normal non-pregnant range. Plasma renin-substrate is consistently raised in pregnancy. Plasma angiotensin II has also been shown usually to be raised in a series of pregnant women. A significant positive correlation has been shown between the maternal plasma aldosterone concentration and the product of the concurrent plasma renin and renin-substrate concentrations. This suggests that the increased plasma aldosterone in pregnancy is the consequence of an increase in circulating angiotensin II, which in turn is related to the level of both renin and its substrate in maternal blood. For these reasons, estimations of renin activity in pregnancy are of dubious value. The increased renin, angiotensin and aldosterone concentrations may represent a tendency to maternal sodium depletion, probably mainly a consequence of the increased glomerular filtration rate. It is possible that the nausea and other symptoms of early pregnancy may be a consequence of this tendency to sodium depletion, with its attendant hormonal changes. In ‘pre-eclampsia’, renin and aldosterone values are generally slightly lower than in normal pregnancy. Human chorion can apparently synthesize renin independently of the kidney. The physiological significance of this remains at present obscure, but it seems unlikely that this source contributes much, if at all, to the often elevated maternal plasma renin. Plasma renin, renin-activity and angiotensin II concentrations, and aldosterone secretion are increased in the luteal phase of the menstrual cycle.

Independence of salt intake induced by calcium deprivation from the renin-angiotensin-aldosterone system

1993 ◽  
Vol 264 (3) ◽  
pp. R492-R499 ◽  
Author(s):  
M. G. Tordoff ◽  
D. M. Pilchak ◽  
R. L. Hughes
Keyword(s):  
Salt Intake ◽  
Plasma Renin ◽  
Calcium Deficiency ◽  
Plasma Aldosterone ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Receptor Blockade ◽  
Renin Angiotensin Aldosterone System ◽  
Angiotensin System ◽  
Renin Angiotensin

We investigated whether the elevated NaCl intake shown by calcium-deprived rats is mediated by the renin-angiotensin-aldosterone system. First, we looked for manifestations of altered renin-angiotensin-aldosterone system activity during the progression of calcium deficiency. There were no differences between control and calcium-deprived rats in plasma aldosterone concentrations, plasma renin activity, plasma sodium concentrations, sodium balance, or blood pressure. Second, we used selective pharmacological antagonists to examine whether disruption of the renin-aldosterone-angiotensin system influenced salt intake. Blockade of aldosterone receptors with spironolactone (25 mg.kg-1 x day-1 sc for 7 days) had no effect on NaCl intake of control or calcium-deprived rats. Angiotensin AT1 receptor blockade with losartan potassium (0.5-10 mg/kg orally) had no effect on NaCl intake of control or calcium-deprived rats but doses > 0.5 mg/kg decreased NaCl intake of adrenalectomized rats. Taken together, these findings indicate that the renin-angiotensin-aldosterone system does not mediate the increased NaCl intake produced by calcium deficiency. The appetite for salt produced by calcium deficiency involves a different physiological substrate from most other models of NaCl intake.

Hypertension in dogs during antidiuretic hormone and hypotonic saline infusion

1979 ◽  
Vol 236 (2) ◽  
pp. H314-H322 ◽  
Author(s):  
R. D. Manning ◽  
A. C. Guyton ◽  
T. G. Coleman ◽  
R. E. McCaa
Keyword(s):  
Arterial Pressure ◽  
Antidiuretic Hormone ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Saline Infusion ◽  
Plasma Sodium ◽  
Experimental Hypertension ◽  
Plasma Aldosterone Concentration ◽  
Plasma Sodium Concentration ◽  
Hypotonic Saline

Experimental hypertension was produced in 7 dogs by continuously infusing suppressor amounts of antidiuretic hormone (ADH) and hypotonic saline after renal mass had been surgically reduced to 30% of normal. Data were collected during 9 days of control measurements, 14 days of ADH and saline infusion, and then 3 days of saline infusion to 1) determine the chronic effects of ADH on arterial pressure and 2) determine whether hypertension could be maintained during hyponatremia. During the period of ADH infusion, arterial pressure increased to hypertensive levels while plasma sodium concentration decreased almost 20 meq/1. Also, during the ADH infusion period, the dogs demonstrated decreases in heart rate, plasm potassium concentration, plasma renin activity, and plasma aldosterone concentration. Fluid volume expansion was evidenced by sustained increases in blood volume and sodium space. We conclude that when renal function is compromised, subpressor amounts of ADH can contribute to the development of hypertension, probably due to its fluid-retaining properties and in spite of the attendant hyponatremia.

The influence of streptozotocin-induced diabetes mellitus on fluid and electrolyte handling in rats

1986 ◽  
Vol 70 (1) ◽  
pp. 111-117 ◽  
Author(s):  
R. A. Hebden ◽  
S. M. Gardiner ◽  
T. Bennett ◽  
I. A. MacDonald
Keyword(s):  
Food Intake ◽  
Plasma Potassium ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Diabetic Group ◽  
Control Group ◽  
Plasma Sodium ◽  
Steady Increase ◽  
Urinary Potassium ◽  
Streptozotocin Induced Diabetes

1. Intakes and urine outputs of fluid and electrolytes were measured daily in rats before, and for 3 weeks after, induction of diabetes by intraperitoneal injection of streptozotocin (STZ; 60 mg/kg); control animals received saline. 2. Water intakes and urine outputs were increased on and after the first day after injection with STZ; after a transient period of negative water balance, fluid intakes and urine outputs increased in parallel. 3. Food intake was reduced for the first 3 days after injection of STZ but thereafter there was a steady increase. On the final experimental day, the food intake of the diabetic group was 60% greater than that of the control group. 4. Urinary electrolyte excretion was increased after injection of STZ; at the end of the experiment, the increase in urinary sodium excretion was similar to the increase in intake but the increase in urinary potassium excretion was less. 5. On day 21 after injection of STZ plasma sodium concentration and packed cell volume were significantly reduced in the diabetic group but plasma potassium concentration was not. 6. There was a difference between the measured osmolality and the calculated osmolarity of the plasma of the diabetic animals which was not seen in the controls. This difference was not due to pseudohyponatraemia, but was probably due to the presence of unidentified solutes, since there was a significant gap between the urinary osmolal and osmolar excretion in the diabetic animals that was not present in the control animals.

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