scholarly journals Renin gene polymorphism: its relationship to hypertension, renin levels and vascular responses

2011 ◽  
Vol 12 (4) ◽  
pp. 564-571 ◽  
Author(s):  
Bei Sun ◽  
Jonathan S Williams ◽  
Luminita Pojoga ◽  
Bindu Chamarthi ◽  
Jessica Lasky-Su ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin ◽  
Underlying Mechanism ◽  
Renin Activity ◽  
P Value ◽  
Nucleotide Polymorphisms ◽  
Gene Variation ◽  
Hypertension Risk ◽  
Increased Risk ◽  
Renin Gene

The renin gene has been previously reported to be associated with essential hypertension in a variety of ethnic groups. However, no studies have systematically evaluated the relationship between single nucleotide polymorphisms (SNPs) representing coverage of the entire renin gene and hypertension risk. To evaluate the association between renin gene variation and hypertension we investigated data on HyperPATH cohort with 570 hypertensive and 222 normotensive Caucasian subjects. Six tagging SNPs and resultant haplotypes were tested for associations with hypertension risk, followed by mean arterial pressure (MAP), plasma renin activity (PRA) and the change in MAP in response to angiotensin II (AngII) infusion (AngII ΔMAP). The A allele of SNP rs6693954 and the haplotype containing rs6696954A were significantly associated with higher risk for hypertension (OR = 1.98, p = 0.0001; OR = 1.63 p = 0.0005, respectively). The same haplotype block was also associated with altered PRA levels and blunted AngII ΔMAP (global p-value = 0.02, 0.047, respectively). Our results confirm that polymorphisms in the renin gene are associated with increased risk for hypertension in an independent cohort, and that the underlying mechanism may reside in the interaction of renin activity and vascular responsiveness to angiotensin II.

125 Increased plasma renin activity during wake in a repetitive sleep restriction protocol

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A51-A51
Author(s):  
Huan Yang ◽  
Michael Vazquez ◽  
Monika Haack ◽  
Janet Mullington
Keyword(s):  
Renal Function ◽  
Plasma Renin Activity ◽  
Impaired Renal Function ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sleep Restriction ◽  
Science Center ◽  
Percent Change ◽  
Recovery Sleep ◽  
Increased Risk

Abstract Introduction Insufficient sleep is associated with an increased risk of hypertension. It is well established that long-term BP regulation is modulated by the renin-angiotensin-aldosterone system (RAAS) and chronic kidney disease is a strong independent risk factor for development of cardiovascular disease. This study investigated the biomarkers of RAAS and renal function during repetitive exposures to controlled, experimental sleep restriction (SR). We hypothesized an upregulation of RAAS and increased markers of impaired renal function. Methods Twenty-one healthy participants (11 women, average age 31±2 years) completed the 22-day in-hospital SR protocol: permitted 4h of sleep/night from 0300-0700 for 3 nights followed by a recovery sleep, repeated 4 times. Blood samples were collected and plasma renin activity (PRA) was assessed in the morning (7:05am) and in the evening before bedtime (22:45pm) at baseline, experimental days (3rd day of each of the 4 blocks), and recovery. Urinary albumin to creatinine ratio (ACR) was measured from 24-h urinary collection at baseline, first and fourth SR blocks. Estimated glomerulus filtration rate (eGFR) was calculated based on the serum cystatin C levels at baseline and last block of SR. Results Percent change of evening PRA significantly increased during 4 blocks of SR and recovery (SR effect p=0.039), but not morning PRA (SR effect p=0.34). Specifically, evening PRA increased up to 98.4% in the first (p<0.01), 61.3% in the second (p=0.04) SR blocks, and 57.5% (p=0.05) in recovery. Urinary ACR showed no significant changes during first or fourth SR blocks (SR effect p=0.28). In addition, eGFR did not change in the fourth SR block compared to BL (paired t-test, p=0.27). Conclusion We did not see increased markers of impaired renal function (ACR or eGFR). Rather, short-term repetitive exposures to SR significantly increased percent change of PRA measured before bedtime, and evening PRA did not return to BL level during recovery. Our results suggested that sleep deficiency may contribute to hypertension through upregulation of RAAS during wake time. Support (if any) SRSF (CDA to Huan Yang), NIH (R01HL106782 to Dr. Janet Mullington), Harvard Catalyst, Harvard Clinical and Translational Science Center (UL1TR001102).

Plasma Renin Activity and Adrenal Angiotensin II Receptors in Fetal, Newborn, Adult and Pregnant Rabbits

Neonatology ◽  
1979 ◽  
Vol 36 (3-4) ◽  
pp. 119-127 ◽  
Author(s):  
M.G. Pernollet ◽  
M.A. Devynck ◽  
G.J. Macdonald ◽  
P. Meyer
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin Ii Receptors

Effect of enalapril (MK-421), an orally active angiotensin I converting enzyme inhibitor, on blood pressure, active and inactive plasma renin, urinary prostaglandin E2, and kallikrein excretion in conscious rats

1984 ◽  
Vol 62 (1) ◽  
pp. 116-123 ◽  
Author(s):  
Ernesto L. Schiffrin ◽  
Jolanta Gutkowska ◽  
Gaétan Thibault ◽  
Jacques Genest
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Ace Inhibition ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin I Converting Enzyme

The angiotensin I converting enzyme (ACE) inhibitor enalapril (MK-421), at a dose of 1 mg/kg or more by gavage twice daily, effectively inhibited the pressor response to angiotensin I for more than 12 h and less than 24 h. Plasma renin activity (PRA) did not change after 2 or 4 days of treatment at 1 mg/kg twice daily despite effective ACE inhibition, whereas it rose significantly at 10 mg/kg twice daily. Blood pressure fell significantly and heart rate increased in rats treated with 10 mg/kg of enalapril twice daily, a response which was abolished by concomitant angiotensin II infusion. However, infusion of angiotensin II did not prevent the rise in plasma renin. Enalapril treatment did not change urinary immunorcactive prostaglandin E2 (PGE2) excretion and indomethacin did not modify plasma renin activity of enalapril-treated rats. Propranolol significantly reduced the rise in plasma renin in rats receiving enalapril. None of these findings could be explained by changes in the ratio of active and inactive renin. Water diuresis, without natriuresis and with a decrease in potassium urinary excretion, occurred with the higher dose of enalapril. Enalapril did not potentiate the elevation of PRA in two-kidney one-clip Goldblatt hypertensive rats. In conclusion, enalapril produced renin secretion, which was in part β-adrenergically mediated. The negative short feedback loop of angiotensin II and prostaglandins did not appear to be involved. A vasodilator effect, apparently independent of ACE inhibition, was found in intact conscious sodium-replete rats.

L-arginine analogues inhibit aldosterone secretion in rats

1995 ◽  
Vol 268 (5) ◽  
pp. R1137-R1142 ◽  
Author(s):  
J. C. Simmons ◽  
R. H. Freeman
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Methyl Ester ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Bilateral Nephrectomy ◽  
Aldosterone Secretion ◽  
Series Of Experiments

L-Arginine analogues, e.g., NG-nitro-L-arginine methyl ester (L-NAME), increase arterial pressure and suppress renin release in the rat. On the basis of these observations, it was hypothesized that L-arginine analogues also would attenuate aldosterone secretion. This hypothesis was tested in anesthetized rats treated with L-NAME or NG-nitro-L-arginine (L-NNA, 185 mumol/kg ip). The aldosterone secretion rate, plasma renin activity, and adrenal blood flow were attenuated in rats treated with L-NAME and L-NNA compared with control animals. Similar experiments were performed in anephric rats to examine the effects of L-NAME on aldosterone secretion independent of the circulating reninangiotensin system. The administration of L-NAME reduced adrenal blood flow but failed to reduce aldosterone secretion in these anephric rats. Bilateral nephrectomy reduced plasma renin activity essentially to undetectable levels in these animals. In a third series of experiments, two groups of anephric rats were infused with angiotensin II (3 micrograms/kg body wt iv) to provide a stimulus for aldosterone secretion. Aldosterone secretion and adrenal blood flow were markedly reduced in angiotensin II-infused rats pretreated with L-NAME compared with the control anephric animals infused with angiotensin II. Overall these results suggest that L-arginine analogues attenuate aldosterone secretion by inhibiting the adrenal steroidogenic effects of endogenous or exogenous angiotensin II and/or by reducing plasma levels of renin/angiotensin.

Water deprivation-induced drinking in rats: role of angiotensin II

1983 ◽  
Vol 244 (2) ◽  
pp. R244-R248 ◽  
Author(s):  
C. C. Barney ◽  
R. M. Threatte ◽  
M. J. Fregly
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Water Intake ◽  
Water Deprivation ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Renin Activity ◽  
Deprivation Period ◽  
Dependent Component

The role of angiotensin II in the control of water intake following deprivation of water for varying lengths of time was studied. Male rats were deprived of water for 0, 12, 24, 36, or 48 h. Water intakes were measured with and without pretreatment with the angiotensin I-converting enzyme inhibitor, captopril (50 mg/kg, ip). Captopril had no significant effect on water intake following either 0 or 12 h of water deprivation. However, captopril significantly attenuated water intake following 24-48 h of water deprivation with the magnitude of the attenuation increasing as the length of the period of water deprivation increased. Plasma renin activity was significantly increased over control levels after 24-48 h of water deprivation but not after 12 h of water deprivation. Plasma renin activity tended to increase as the length of the water-deprivation period increased. Serum osmolality and sodium concentration were significantly increased over control levels following 12-48 h of water deprivation. Serum osmolality and sodium concentration failed to show any further increases with increasing length of water deprivation beyond the increases following 12 h of water deprivation. The data indicate that the water intake of water-deprived rats can be divided into an angiotensin II-dependent component and angiotensin II-independent component. The angiotensin II-independent component appears to be more important in the early stages of water deprivation whereas the angiotensin II-dependent component becomes more important as the length of the water-deprivation period increases.

scholarly journals Effects of Ramipril on the Aldosterone/Renin Ratio and the Aldosterone/Angiotensin II Ratio in Patients With Primary Aldosteronism

Hypertension ◽  
2020 ◽  
Vol 76 (2) ◽  
pp. 488-496 ◽  
Author(s):  
Zeng Guo ◽  
Marko Poglitsch ◽  
Diane Cowley ◽  
Oliver Domenig ◽  
Brett C. McWhinney ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Ace Inhibitors ◽  
Primary Aldosteronism ◽  
Characteristic Curve ◽  
False Negative ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Aldosterone Concentration

The aldosterone/renin ratio (ARR) is currently considered the most reliable approach for case detection of primary aldosteronism (PA). ACE (Angiotensin-converting enzyme) inhibitors are known to raise renin and lower aldosterone levels, thereby causing false-negative ARR results. Because ACE inhibitors lower angiotensin II levels, we hypothesized that the aldosterone/equilibrium angiotensin II (eqAngII) ratio (AA2R) would remain elevated in PA. Receiver operating characteristic curve analysis involving 60 patients with PA and 40 patients without PA revealed that the AA2R was not inferior to the ARR in screening for PA. When using liquid chromatography-tandem mass spectrometry to measure plasma aldosterone concentration, the predicted optimal AA2R cutoff for PA screening was 8.3 (pmol/L)/(pmol/L). We then compared the diagnostic performance of the AA2R with the ARR among 25 patients with PA administered ramipril (5 mg/day) for 2 weeks. Compared with basally, plasma levels of equilibrium angiotensin I (eqAngI) and direct renin concentration increased significantly ( P <0.01 or P <0.05) after ramipril treatment, whereas eqAngII and ACE activity (eqAngII/eqAngI) decreased significantly ( P <0.01). The changes of plasma renin activity and plasma aldosterone concentration in the current study were not significant. On day 14, 4 patients displayed false-negative results using ARR_direct renin concentration (plasma aldosterone concentration/direct renin concentration), 3 of whom also showed false-negative ARR_plasma renin activity (plasma aldosterone concentration/plasma renin activity). On day 15, 2 patients still demonstrated false-negative ARR_plasma renin activity, one of whom also showed a false-negative ARR_direct renin concentration. No false-negative AA2R results were observed on either day 14 or 15. In conclusion, compared with ARR which can be affected by ACE inhibitors causing false-negative screening results, the AA2R seems to be superior in detecting PA among subjects receiving ACE inhibitors.

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