scholarly journals The Influence of Long Term Hydrochlorothiazide Administration on the Relationship between Renin-Angiotensin-Aldosterone System Activity and Plasma Glucose in Patients with Hypertension

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Xu Xiao ◽  
Hong-jun Du ◽  
Wei-jian Hu ◽  
Peter X. Shaw
Keyword(s):  
Plasma Glucose ◽  
Density Lipoprotein ◽  
Plasma Renin ◽  
Ang Ii ◽  
Elevated Plasma ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Glucose Levels ◽  
One Year ◽  
The Relationship

Objective. To observe the relationship between changes in renin-angiotensin-aldosterone system (RAAS) activity and blood plasma glucose after administration of hydrochlorothiazide (HCTZ) for one year in patients with hypertension.Methods. 108 hypertensive patients were given 12.5 mg HCTZ per day for one year. RAAS activity, plasma glucose levels, and other biochemical parameters, as well as plasma oxidized low density lipoprotein (oxLDL) levels, were measured and analyzed at baseline, six weeks, and one year after treatment.Results. After one year of treatment, the reduction in plasma glucose observed between the elevated plasma renin activity (PRA) group (-0.26±0.26 mmol/L) and the nonelevated PRA group (-1.36±0.23 mmol/L) was statistically significant (P<0.05). The decrease of plasma glucose in the elevated Ang II group (-0.17±0.18 mmol/L) compared to the nonelevated Ang II group (-1.07±0.21 mmol/L) was statistically significant (P<0.05). The proportion of patients with elevated plasma glucose in the elevated Ang II group (40.5%) was significantly higher than those in the nonelevated Ang II group (16.3%) (P<0.05). The relative oxLDL level was not affected by the treatment.Conclusions. Changes in RAAS activity were correlated with changes in plasma glucose levels after one year of HCTZ therapy.

scholarly journals Effects of SGLT2 Inhibitors and GLP-1 Receptor Agonists on Renin-Angiotensin-Aldosterone System

2021 ◽  
Vol 12 ◽  
Author(s):  
Soraya Puglisi ◽  
Alessandro Rossini ◽  
Roberta Poli ◽  
Francesca Dughera ◽  
Anna Pia ◽  
...  
Keyword(s):  
Plasma Renin ◽  
Target Tissue ◽  
Protective Effects ◽  
Ang Ii ◽  
Osmotic Diuresis ◽  
Renin Angiotensin Aldosterone System ◽  
Glucose Lowering ◽  
Renin Angiotensin ◽  
Receptor Agonists

Sodium-glucose cotransporters inhibitors (SGLT2-i) and GLP-1 receptor agonists (GLP1-RA) are glucose-lowering drugs that are proved to reduce the cardiovascular (CV) risk in type 2 diabetes mellitus (T2DM). In this process, the renin-angiotensin-aldosterone system (RAAS) is assumed to play a role. The inhibition of SGLT2 improves hyperglycemia hampering urinary reabsorption of glucose and inducing glycosuria. This “hybrid” diuretic effect, which couples natriuresis with osmotic diuresis, potentially leads to systemic RAAS activation. However, the association between SGLT2-i and systemic RAAS activation is not straightforward. Available data indicate that SGLT2-i cause plasma renin activity (PRA) increase in the early phase of treatment, while PRA and aldosterone levels remain unchanged in chronic treated patients. Furthermore, emerging studies provide evidence that SGLT2-i might have an interfering effect on aldosterone/renin ratio (ARR) in patients with T2DM, due to their diuretic and sympathoinhibition effects. The cardio- and reno-protective effects of GLP-1-RA are at least in part related to the interaction with RAAS. In particular, GLP1-RA counteract the action of angiotensin II (ANG II) inhibiting its synthesis, increasing the inactivation of its circulating form and contrasting its action on target tissue like glomerular endothelial cells and cardiomyocytes. Furthermore, GLP1-RA stimulate natriuresis inhibiting Na+/H+ exchanger NHE-3, which is conversely activated by ANG II. Moreover, GLP1 infusion acutely reduces circulating aldosterone, but this effect does not seem to be chronically maintained in patients treated with GLP1-RA. In conclusion, both SGLT2-i and GLP1-RA seem to have several effects on RAAS, though additional studies are needed to clarify this relationship.

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.

scholarly journals Inhibition of Intestinal Bile Acid Transporter Slc10a2 Improves Triglyceride Metabolism and Normalizes Elevated Plasma Glucose Levels in Mice

PLoS ONE ◽  
2012 ◽  
Vol 7 (5) ◽  
pp. e37787 ◽  
Author(s):  
Thomas Lundåsen ◽  
Eva-Marie Andersson ◽  
Michael Snaith ◽  
Helena Lindmark ◽  
Johanna Lundberg ◽  
...  
Keyword(s):  
Bile Acid ◽  
Plasma Glucose ◽  
Elevated Plasma ◽  
Triglyceride Metabolism ◽  
Glucose Levels ◽  
Bile Acid Transporter ◽  
Acid Transporter

Angiotensin II inhibition with captopril on plasma ADH, PG synthesis, and renal function in humans

1986 ◽  
Vol 250 (6) ◽  
pp. F986-F990 ◽  
Author(s):  
M. Usberti ◽  
G. Di Minno ◽  
B. Ungaro ◽  
B. Cianciaruso ◽  
S. Federico ◽  
...  
Keyword(s):  
Urine Output ◽  
Filtration Rate ◽  
Enzyme Inhibitor ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Ang Ii ◽  
Urinary Osmolality ◽  
Endogenous Prostaglandins ◽  
The Relationship ◽  
Control Study

Using captopril (C), an angiotensin (ANG) I converting-enzyme inhibitor, to increase endogenous prostaglandins (PGs) and to decrease endogenous ANG II synthesis, we studied the relationship between endogenous ANG II, PG, and antidiuretic hormone (ADH) release in seven normal volunteers before (control study) and after inhibition of PG synthesis by a single dose of aspirin (ASA study). In the control study, following the administration of 100 mg of C, there was a significant increase of plasma PGE2, plasma-renin activity (PRA), and urinary PGE2 and 6-keto-PGF1 alpha and a decrease of plasma ADH. Glomerular filtration rate (GFR) and renal plasma flow (RPF) were unaffected by C; urine output, fractional sodium excretion (FENa), and osmolal clearance (Cosmol) increased; and urinary osmolality (Uosmol) decreased significantly after C. In the ASA study PG were undetectable in plasma and significantly reduced in urine 1 h after aspirin and did not increase when C was added. Plasma ADH decreased and PRA increased, as in the control study, after C, whereas GFR, RPF, urine output, FENa, Cosmol, and Uosmol were unchanged. These results suggest that the effect of C on ADH release may be mediated, to a large extent, by a fall in endogenous circulating ANG II, since ADH decreased in the presence of both high or undetectable levels of PGE2. The results also suggest that the increase in PGE2 induced by C may precipitate the diuretic and natriuretic effects of acute C administration.

Characterization of the renin-angiotensin system in the turtle Pseudemys scripta

1984 ◽  
Vol 247 (1) ◽  
pp. R15-R23 ◽  
Author(s):  
M. D. Cipolle ◽  
J. E. Zehr
Keyword(s):  
Pressor Response ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Ang Ii ◽  
Freshwater Turtles ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Fourfold Increase ◽  
Inactive Form ◽  
Pseudemys Scripta

Studies were conducted in freshwater turtles Pseudemys scripta to define some characteristics of the renin-angiotensin system in this reptile. Dialyzed acid-treated kidney extract (1 g tissue per ml water) produced a prolonged pressor response in unanesthetized turtles, which was eliminated by boiling the extract or by pretreating the turtle with [Sar1, Ile8]angiotensin II. A rat pressor assay was employed because turtle angiotensin (ANG) was bound poorly by the anti-[Asp1, Ile5, His9]ANG I used in our radioimmunoassay. Kidney extract incubated with homologous plasma (pH 5.5 and 25 degrees C) produced a time-dependent pressor response in rats. The pressor activity of the product was eliminated by dialysis or by pretreating the rats with [Sar1, Ile8]ANG II. The pressor response in anesthetized turtles to ANG I was significantly reduced by captopril, whereas the ANG II response remained unchanged, thus demonstrating the presence of ANG-converting enzyme activity in these animals. We determined the velocity of turtle ANG formation at various dilutions of enzyme (kidney extract) or substrate (plasma). Turtle kidney extract incubated with homologous plasma displayed typical Michaelis-Menten kinetics. Finally we conducted experiments to determine whether a portion of turtle plasma renin exists in an inactive form. Trypsinization caused a slight increase in plasma renin activity (PRA), whereas acidification to pH 3.3 yielded a fourfold increase in PRA.

scholarly journals Effect of renal denervation on catecholamines and the renin–angiotensin–aldosterone system

2020 ◽  
Vol 21 (3) ◽  
pp. 147032032094309
Author(s):  
Lida Feyz ◽  
Sjoerd van den Berg ◽  
Robert Zietse ◽  
Isabella Kardys ◽  
Jorie Versmissen ◽  
...  
Keyword(s):  
Plasma Renin ◽  
Drug Regimen ◽  
Plasma Aldosterone ◽  
Renal Sympathetic Denervation ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Post Procedure ◽  
Endogenous Catecholamines ◽  
Significant Change ◽  
Renal Sympathetic

Introduction: The effect of renal sympathetic denervation (RDN) on neurohormonal responses is largely unknown. We aimed to assess the effect of RDN on the renin–angiotensin–aldosterone system (RAAS) and endogenous catecholamines. Methods: A total of 60 patients with hypertension underwent RDN and remained on a stable antihypertensive drug regimen. Samples for plasma aldosterone, plasma renin and urine (nor)metanephrine were collected at baseline and at 6 months post procedure. Ambulatory blood pressure (BP) recordings were obtained at baseline and at 6 months post procedure. Results: Mean age was 64±9 years, and 30/60 patients were male. At 6 months, average daytime systolic and diastolic ambulatory BP decreased by 10 and 6 mmHg, respectively ( p<0.001). No significant change was observed in plasma aldosterone (median=248.0 pmol/L (interquartile range (IQR) 113.3–369.5 pmol/L) vs. median=233.0 pmol/L (IQR 110.3–360.8 pmol/L); p=0.66); renin (median=19.5 µIU/mL (IQR 6.8–119.5 µIU/mL) vs. median=14.3 µIU/mL (IQR 7.2–58.0 µIU/mL); p=0.32), urine metanephrine (median=0.46 µmol/L (IQR 0.24–0.77 µmol/L) vs. median=0.46 µmol/L (IQR 0.22–0.88 µmol/L); p=0.75) and normetanephrine (median=1.41 µmol/L (IQR 0.93–2.00 µmol/L vs. median =1.56 (IQR 0.74–2.50 µmol/L); p=0.58) between baseline and 6 months, respectively. No correlation was found between the decrease in mean systolic daytime BP and changes in RAAS hormones or endogenous catecholamines. Conclusion: Despite significant reductions in ambulatory BP, RDN did not result in a significant change in endogenous catecholamines or in RAAS hormones at 6 months.

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