Dietary chloride modifies renin release in normal humans

1981 ◽  
Vol 241 (4) ◽  
pp. F361-F363 ◽  
Author(s):  
R. J. Koletsky ◽  
R. G. Dluhy ◽  
R. G. Cheron ◽  
G. H. Williams
Keyword(s):  
Sodium Intake ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Release ◽  
Upright Posture ◽  
Ang Ii ◽  
Low Salt ◽  
Normal Humans ◽  
The Mean ◽  
Induced Changes

The effect of high and low chloride diets on the responses of plasma renin activity (PRA), angiotensin II (ANG II), and aldosterone (Aldo) to upright posture was studied in the same normal subjects in balance on constant sodium intake. Diet 1 consisted of 10 meq Na/day (low Na) and either 50 or 150 meq Cl/day. Diet 2 consisted of 200 meq Na/day (high Na) and either 20 or 200 meq Cl/day. The mean recumbent PRA level on the high Na-high Cl diet tended to be lower than on the high Na-low Cl diet but was not significantly different. However, the absolute peak upright PRA levels, 8.8 +/- 1.0 vs. 4.4 +/- 0.8 ng . ml-1 . h-1, and the incremental difference (delta PRA) between recumbent and peak upright PRA levels, 5.5 +/- 0.8 vs. 2.2 +/- 0.5 ng . ml-1 . h-1, were significantly less on the high Na-high Cl diet compared with the high Na-low Cl diet. Similar significant changes were seen in ANG II and Aldo levels. However, there were no significant changes in PRA, ANG II, and Aldo responses to upright posture on the low Na diet when the dietary Cl was varied. It is concluded that dietary Cl is another factor modifying renin release. However, Cl is probably less important than Na because Cl-induced changes in PRA were not seen in the low salt state.

Comparison of the Renin Response to Dopamine and Noradrenaline in Normal Subjects and Patients with Autonomic Insufficiency

1974 ◽  
Vol 46 (4) ◽  
pp. 481-488 ◽  
Author(s):  
C. S. Wilcox ◽  
M. J. Aminoff ◽  
A. B. Kurtz ◽  
J. D. H. Slater
Keyword(s):  
Autonomic Failure ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Control Groups ◽  
Autonomic Reflexes ◽  
Fractional Increase ◽  
The Mean ◽  
Autonomic Insufficiency ◽  
Stimulation Of

1. The effect on plasma renin activity (PRA) of dopamine and noradrenaline infusions was studied in three patients with Shy—Drager syndrome, three patients with Parkinson's disease and normal autonomic reflexes, and three healthy volunteers. The patients with the Shy—Drager syndrome had functional evidence of a peripheral lesion of the sympathetic nervous system and subnormal PRA on a controlled sodium intake. 2. In all subjects catecholamines were infused step-wise for 4 min until a 30% rise in systolic blood pressure occurred. 3. In each subject, PRA fell after noradrenaline but rose after dopamine. The mean fractional increase in PRA after dopamine was no less in the Shy—Drager patients than in the control groups. 4. The results suggest, first, that stimulation of dopamine receptors can release renin, and secondly, that inadequate renin stores cannot explain the low PRA found in our patients with autonomic failure.

AT1 and TxA2/PGH2 receptors maintain hypertension throughout 2K,1C Goldblatt hypertension in the rat

1996 ◽  
Vol 271 (4) ◽  
pp. R891-R896 ◽  
Author(s):  
C. S. Wilcox ◽  
J. Cardozo ◽  
W. J. Welch
Keyword(s):  
Blood Pressure ◽  
Receptor Antagonist ◽  
Sodium Intake ◽  
Late Phase ◽  
Plasma Renin ◽  
Type I ◽  
Ang Ii ◽  
Control Groups ◽  
The Mean ◽  
Antihypertensive Response

Angiotension II (ANG II) increases the generation of vasoconstrictor prostaglandin endoperoxides (PGH2) and thromboxane A2 (TxA2). Two-kidney, one-clip (2K,1C) Goldblatt hypertensive rats have an increased plasma renin activity (PRA) and ANG II level during the early, but not the late, phases of hypertension. Therefore, the aim of these studies was to compare the antihypertensive efficacy of an ANG II type I (AT1) and a TxA2/PGH2 receptor antagonist during different phases of 2K,1C hypertension. Rats were maintained on a fixed sodium intake for 3 days before and throughout the period of drug administration. These studies assessed the antihypertensive response to administration of the AT1 receptor antagonist losartan (20 mg.kg-1.day-1), the TxA2/PGH2 receptor antagonist ifetroban (20 mg.kg-1.day-1) or vehicle given for 3 days to rats with early (2-4 wk postclip), intermediate (10-12 wk postclip), and late (36-42 wk post-clip) 2K,1C hypertension and to two control groups of rats corresponding in age to the early or intermediate and the late 2K,1C groups. The mean arterial pressure (MAP) was measured directly with indwelling arterial cannulas. The MAP of sham-operated rats was 109 +/- 5 mmHg. In the early phase of 2K,1C hypertension, the MAP was increased to 143 +/- 6 mmHg, and it was increased further to 162 +/- 5 mmHg during the intermediate and to 179 +/- 4 mmHg during the late phase. The PRA, compared with age-matched controls, was increased during early and intermediate, but not late phase 2K,1C hypertension. Neither drug lowered blood pressure in control rats. However, both drugs significantly reduced the blood pressure in the early, intermediate, and late phases of 2K, 1C hypertension. At the end of 3 days of administration, blood pressure in early 2K, 1C rats given losartan was reduced to levels of control rats, but remained slightly elevated in other groups and in those receiving ifetroban. In conclusion, AT1 and TxA2/PGH2 receptors maintain hypertension throughout the evolution of 2K, 1C hypertension in the rat, despite changes in PRA.

Age-Dependent Changes of Plasma Renin Concentration in Humans

1973 ◽  
Vol 45 (s1) ◽  
pp. 273s-278s ◽  
Author(s):  
K. Hayduk ◽  
D. K. Krause ◽  
W. Kaufmann ◽  
R. Huenges ◽  
U. Schillmöller ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Post Partum ◽  
Age Groups ◽  
Plasma Renin ◽  
Relative Increase ◽  
Upright Posture ◽  
Healthy Children ◽  
Absolute Increase ◽  
Plasma Renin Concentration ◽  
The Mean

1. Plasma renin concentration (PRC) in newborns greatly exceeded PRC in children and adults. PRC in cord plasma of newborns was higher than peripheral venous PRC in their mothers. PRC in the newborns increased further in the first 48 h post partum and then gradually decreased. 2. The mean PRC of healthy children and adults on free sodium intake decreased with age by an exponential function. 3. The absolute increase of PRC in response to upright posture (PRCupright — PRCrecumbent) decreased with age. The relative increase of PRC in response to upright posture (PRCuprjght:PRCrecumbent) remained unchanged with age, the PRC in upright posture being about twice the basal PRC in all age groups.

Hormonal responses to gradual changes in dietary sodium intake in humans

1989 ◽  
Vol 256 (6) ◽  
pp. R1171-R1175 ◽  
Author(s):  
G. A. Sagnella ◽  
N. D. Markandu ◽  
M. G. Buckley ◽  
M. A. Miller ◽  
D. R. Singer ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Progressive Increase ◽  
Plasma Aldosterone ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Initial Increase ◽  
Hormonal Responses

The effects of gradual (50 mmol/day) increases in dietary sodium intake from 10 to 350 mmol/day on plasma atrial natriuretic peptide (ANP), aldosterone, and plasma renin activity (PRA) were studied in six normal subjects. With the increases in sodium intake there was a progressive increase in urinary sodium from 12.2 +/- 4.4 to 314.8 +/- 31.4 mmol/24 h; plasma ANP increased gradually from 9.9 +/- 1.1 to 23.3 +/- 2.2 pg/ml, with the increases being closely associated with the changes in cumulative sodium balance. Plasma aldosterone decreased significantly from 2,519.7 +/- 147.4 pmol/l on the 10 mmol/day to 1,393.3 +/- 125.4 pmol/l when the sodium intake was increased to 50 mmol/day and decreased further to 251.6 +/- 78.7 pmol/l by the end of the study. The changes in PRA paralleled those in plasma aldosterone with the exception of no significant change in plasma PRA within 24 h of the initial increase in sodium intake. This marked sensitivity in the responses of both the ANP and the renin-aldosterone system to small increases in sodium intake clearly points to their importance in the renal adaptations to alterations in dietary sodium intake.

The Renal Extraction and the Natriuretic Action of GLP-1 in Humans Depend on Interaction With the GLP-1 Receptor

2020 ◽  
Vol 106 (1) ◽  
pp. e11-e19
Author(s):  
Ali Asmar ◽  
Per K Cramon ◽  
Meena Asmar ◽  
Lene Simonsen ◽  
Charlotte M Sorensen ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Fold Increase ◽  
Receptor Activation ◽  
Ang Ii ◽  
Healthy Humans ◽  
Natriuretic Effect ◽  
Glucagon Like Peptide 1 ◽  
Arterial Plasma

Abstract Purpose The natriuretic effect of glucagon-like peptide-1 (GLP-1) in humans is independent of changes in renal plasma flow (RPF) and glomerular filtration rate (GFR) but may involve suppression of angiotensin II (ANG II) and a significant (~45%) renal extraction of GLP-1. The current study was designed to investigate the consequences for the renal extraction and the natriuretic effect of blocking GLP-1 receptors with the specific GLP-1 receptor antagonist, Exendin 9–39 (Ex 9–39). Methods Under fixed sodium intake for 4 days before each study day, 6 healthy male participants were recruited from our recent study where GLP-1 or vehicle was infused (1). In the present new experiments, participants were examined during a 3-hour infusion of GLP-1 (1.5 pmol/kg/min) together with a 3.5-hour infusion of Ex 9–39 (900 pmol/kg/min). Timed urine collections were conducted throughout the experiments. Renal extraction of GLP-1 as well as RPF and GFR were measured via Fick’s principle after catheterization of a renal vein. Arterial plasma renin, ANG II, and aldosterone concentrations were measured. Results Co-infusion of Ex 9–39 significantly reduced renal extraction of GLP-1 to ~25% compared with GLP-1 infusion alone (~45%). Urinary sodium excretions remained at baseline levels during co-infusion of Ex 9–39 as well as vehicle. By contrast, GLP-1 infusion alone resulted in a 2-fold increase in natriuresis. Ex 9–39 abolished the GLP-1-induced decrease in arterial ANG II concentrations. RPF and GFR remained unchanged during all experiments. Conclusions Renal extraction of GLP-1 and its effect on natriuresis are both dependent on GLP-1 receptor activation in healthy humans.

Effect of ouabain on pressor responsiveness in normal man

1994 ◽  
Vol 267 (5) ◽  
pp. E642-E647
Author(s):  
G. B. Pidgeon ◽  
A. M. Richards ◽  
M. G. Nicholls ◽  
R. R. Bailey ◽  
K. L. Lynn ◽  
...  
Keyword(s):  
Heart Rate ◽  
Healthy Volunteers ◽  
Plasma Levels ◽  
Plasma Renin ◽  
Ang Ii ◽  
Short Term ◽  
Vasoactive Hormones ◽  
Normal Man ◽  
The Mean ◽  
Mean Heart Rate

To assess the effects of ouabain on pressor and vasoactive hormone responsiveness, 10 healthy volunteers were pretreated with ouabain (0.5 mg i.v. 42 and 18 h before study) or placebo before pressor challenge with angiotensin II (ANG II; 2, 4, and 8 ng.kg-1.min-1 for 30 min/dose) and norepinephrine (NE; 5, 15, and 45 ng.kg-1.min-1 for 15 min/dose). There were no differences at baseline between the two study days regarding mean arterial pressure (MAP) or heart rate. Baseline pulse pressure, however, was significantly greater after ouabain (47 +/- 3 vs. 41 +/- 1 mmHg; P < 0.05). The mean maximum increments in MAP during ANG II and NE infusions were 17.5 +/- 1.1 and 10.5 +/- 1.3 (SE) mmHg, respectively, after ouabain and 19.2 +/- 1.3 and 10.4 +/- 1.5 mmHg after placebo (not significant). The mean heart rate was lower during both infusion periods on the ouabain study day compared with control (P < 0.05). Baseline plasma levels of ANG II, aldosterone, plasma renin activity, atrial and brain natriuretic peptide, guanosine 3',5'-cyclic monophosphate, NE, and epinephrine and achieved levels during the two infusions were similar on the two study days. We conclude that short-term ouabain administration does not alter pressor responsiveness or plasma levels of vasoactive hormones in healthy volunteers.

Cardiovascular and renin responses to desmopressin in humans: role of prostacyclin and beta-adrenergic systems

1991 ◽  
Vol 260 (4) ◽  
pp. H1031-H1036 ◽  
Author(s):  
K. Hasunuma ◽  
K. Yamada ◽  
Y. Tamura ◽  
S. Yoshida
Keyword(s):  
Blood Pressure ◽  
Pulse Rate ◽  
Plasma Renin ◽  
Cardiovascular Responses ◽  
Normal Subjects ◽  
Receptor Activation ◽  
Renin Release ◽  
Beta Adrenoceptor ◽  
V2 Receptor

To investigate the involvement of prostacyclin and the sympathetic nervous system in cardiovascular responses to 1-desamino-8-D-arginine vasopressin (DDAVP), a selective V2-receptor agonist, in normal subjects, DDAVP (0.4 micrograms/kg) was infused with or without indomethacin, a cyclooxygenase inhibitor, or propranolol, a beta-adrenoceptor antagonist. A decrease in blood pressure and increases in pulse rate and plasma renin activity (PRA) were observed by DDAVP infusion. Indomethacin did not influence the DDAVP-induced changes in blood pressure and pulse rate but suppressed the increases in PRA and urinary 6-ketoprostaglandin F1 alpha excretion after DDAVP infusion. Even with propranolol administration, DDAVP produced a similar decrease in blood pressure with a reduction of the increased pulse rate. The DDAVP-induced increase in PRA was not affected either. Indomethacin or propranolol alone did not affect the basal levels of the parameters. DDAVP stimulated the in vitro renin release from rabbit renal cortical slices. The stimulation was inhibited by indomethacin or d(CH2)5[D-Ile2,Ile4]AVP, a selective V2-receptor antagonist. These findings suggest that DDAVP primarily elicits vasodilation, probably through the prostacyclin-independent endothelium-derived relaxation and DDAVP also causes an increase in renin release, which would be partly attributed to the increased synthesis of prostacyclin due to vasculoendothelial V2-like receptor activation but not mainly due to an increase in sympathetic nerve activity.

Obesity augments vasoconstrictor reactivity to angiotensin II in the renal circulation of the Zucker rat

2007 ◽  
Vol 293 (4) ◽  
pp. H2537-H2542 ◽  
Author(s):  
David W. Stepp ◽  
Erika I. Boesen ◽  
Jennifer C. Sullivan ◽  
James D. Mintz ◽  
Clark D. Hair ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Angiotensin Ii ◽  
Vascular Reactivity ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Zucker Rats ◽  
Ang Ii ◽  
Renal Vasoconstriction ◽  
Insulin Resistant

Obesity is an emerging risk factor for renal dysfunction, but the mechanisms are poorly understood. Obese patients show heightened renal vasodilation to blockade of the renin-angiotensin system, suggesting deficits in vascular responses to angiotensin II (ANG II). This study tested the hypothesis that obesity augments renal vasoconstriction to ANG II. Lean (LZR), prediabetic obese (OZR), and nonobese fructose-fed Zucker rats (FF-LZR) were studied to determine the effects of obesity and insulin resistance on reactivity of blood pressure and renal blood flow to vasoconstrictors. OZR showed enlargement of the kidneys, elevated urine output, increased sodium intake, and decreased plasma renin activity (PRA) vs. LZR, and renal vasoconstriction to ANG II was augmented in OZR. Renal reactivity to norepinephrine and mesenteric vascular reactivity to ANG II were similar between LZR and OZR. Insulin-resistant FF-LZR had normal reactivity to ANG II, indicating the insulin resistance was an unlikely explanation for the changes observed in OZR. Four weeks on a low-sodium diet (0.08%) to raise PRA reduced reactivity to ANG II in OZR back to normal levels without effect on LZR. From these data, we conclude that in the prediabetic stages of obesity, a decrease in PRA is observed in Zucker rats that may lead to increased renal vascular reactivity to ANG II. This increased reactivity to ANG II may explain the elevated renal vasodilator effects observed in obese humans and provide insight into early changes in renal function that predispose to nephropathy in later stages of the disease.

Plasma renin system during exercise in normal men

1987 ◽  
Vol 63 (1) ◽  
pp. 188-194 ◽  
Author(s):  
J. Staessen ◽  
R. Fagard ◽  
P. Hespel ◽  
P. Lijnen ◽  
L. Vanhees ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Peak Exercise ◽  
Ang Ii ◽  
Similar Extent ◽  
Bicycle Ergometry ◽  
Arterial Blood ◽  
Intensity Of Exercise ◽  
Normal Men

The exercise-related increase in plasma renin activity (PRA) and in the plasma concentration of angiotensin II (ANG II) and aldosterone (Aldo) was studied in 43 healthy volunteers whose 24-h urinary sodium excretion (UVNa) ranged from 10 to 250 mmol. Arterial blood samples were obtained at rest and during bicycle ergometry. Compared with rest, PRA, ANG II, and Aldo rose to a similar extent during light and moderate exercise. However, at peak exercise ANG II increased significantly more (P less than 0.001) than PRA and Aldo. Thus, with increasing intensity of exercise, the slope of the linear regression of ANG II on PRA became significantly (P less than 0.001) steeper, whereas at maximal exercise the Aldo response did not follow the acute rise in ANG II. At rest as well as during exercise, Aldo rose with increasing ANG II, but the stimulatory effect of ANG II on Aldo was attenuated with higher sodium intake, as estimated from UVNa. Finally, independent of the level of physical activity, UVNa was negatively correlated with PRA, ANG II, and Aldo.

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