Effect of chloride on renal blood flow in angiotensin II induced hypertension

1991 ◽  
Vol 69 (4) ◽  
pp. 507-511 ◽  
Author(s):  
John C. Passmore ◽  
Agnes E. Jimenez
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Sodium Chloride ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Dietary Sodium ◽  
Maximum Increase ◽  
High Sodium ◽  
Low Sodium ◽  
Chloride Effect

The effect of selective dietary sodium and (or) chloride loading on blood pressure and renal blood flow (RBF) in the rat angiotensin II (AII) model of hypertension was determined. AII (200 ng/min) or saline was infused intraperitoneally. Diets were provided with either high or low concentrations of sodium, chloride or both ions for 22 days. The blood pressure of saline-treated animals was not increased by the high sodium chloride diet. Animals on a high sodium, high chloride diet had a significantly greater increase of blood pressure at 8, 15, 18, and 22 days of AII infusion compared with AII-treated animals on a low sodium, low chloride diet (p < 0.05). Selective dietary loading of either high sodium or chloride in AII-treated rats produced no greater elevation of blood pressure than AII with the low sodium, low chloride diet. Selective high dietary chloride was associated with a lower RBF in AII- and vehicle-treated rats compared with low dietary chloride. The chloride effect on RBF was greater in AII-treated animals. In conclusion, both sodium and chloride are necessary to produce the maximum increase of blood pressure in AII animals. AII enhances the decreased RBF induced by dietary chloride.Key words: angiotensin II, sodium chloride, blood pressure.

Excessive Zinc Intake Increases Systemic Blood Pressure and Reduces Renal Blood Flow via Kidney Angiotensin II in Rats

2012 ◽  
Vol 150 (1-3) ◽  
pp. 285-290 ◽  
Author(s):  
Miyoko Kasai ◽  
Takashi Miyazaki ◽  
Tsuneo Takenaka ◽  
Hiroyuki Yanagisawa ◽  
Hiromichi Suzuki
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Zinc Intake

Renal vasodilatation after inhibition of renin or converting enzyme in marmoset

1986 ◽  
Vol 251 (5) ◽  
pp. H897-H902
Author(s):  
D. Neisius ◽  
J. M. Wood ◽  
K. G. Hofbauer
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Enzyme Inhibitor ◽  
Renal Vascular Resistance ◽  
Converting Enzyme ◽  
Renin Inhibition ◽  
Renal Vascular

The relative importance of angiotensin II for the renal vasodilatory response after converting-enzyme inhibition was evaluated by a comparison of the effects of converting-enzyme and renin inhibition on renal vascular resistance. Renal, mesenteric, and hindquarter blood flows were measured with chronically implanted ultrasonic-pulsed Doppler flow probes in conscious, mildly volume-depleted marmosets after administration of a converting-enzyme inhibitor (enalaprilat, 2 mg/kg iv), a synthetic renin inhibitor (CGP 29,287, 1 mg/kg iv), or a renin-inhibitory monoclonal antibody (R-3-36-16, 0.1 mg/kg iv). Enalaprilat reduced blood pressure (-16 +/- 4 mmHg, n = 6) and induced a selective increase in renal blood flow (27 +/- 8%, n = 6). CGP 29,287 and R-3-36-16 induced comparable reductions in blood pressure (-16 +/- 4 mmHg, n = 6 and -20 +/- 4 mmHg, n = 5, respectively) and selective increases in renal blood flow (36 +/- 12%, n = 6 and 34 +/- 16%, n = 4, respectively). The decrease in renal vascular resistance was of similar magnitude for all of the inhibitors (enalaprilat -28 +/- 3%, CGP 29,287 -32 +/- 6%; and R-3-36-16 -33 +/- 7%). These results indicate that the renal vasodilatation induced after converting-enzyme or renin inhibition is mainly due to decreased formation of angiotensin II.

scholarly journals Pre-treatment with the angiotensin receptor 1 blocker losartan protects renal blood flow and oxygen delivery after propofol-induced hypotension in pigs

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Stephanie Franzén ◽  
Robert Frithiof
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Oxygen Delivery ◽  
Induced Hypotension ◽  
Renal Vasoconstriction ◽  
Arterial Blood ◽  
Pre Treatment ◽  
Renal Oxygen

Abstract Hypotensive events are strongly correlated to the occurrence of perioperative acute kidney injury, but the underlying mechanisms for this are not completely elucidated. We hypothesised that anaesthesia-induced hypotension causes renal vasoconstriction and decreased oxygen delivery via angiotensin II-mediated renal vasoconstriction. Pigs were anaesthetised, surgically prepared and randomised to vehicle/losartan treatment (0.15 mg*kg−1). A deliberate reduction in arterial blood pressure was caused by infusion of propofol (30 mg*kg−1) for 10 min. Renal function and haemodynamics were recorded 60 min before and after hypotension. Propofol induced hypotension in all animals (p < 0.001). Renal blood flow (RBF) and renal oxygen delivery (RDO2) decreased significantly regardless of treatment but more so in vehicle-treated compared to losartan-treated (p = 0.001, p = 0.02, respectively). During recovery RBF and RDO2 improved to a greater extent in the losartan-treated compared to vehicle-treated (+ 28 ml*min−1, 95%CI 8–50 ml*min−1, p = 0.01 and + 3.1 ml*min−1, 95%CI 0.3–5.8 ml*min−1, p = 0.03, respectively). Sixty minutes after hypotension RBF and RDO2 remained depressed in vehicle-treated, as renal vascular resistance was still increased (p < 0.001). In losartan-treated animals RBF and RDO2 had normalised. Pre-treatment with losartan improved recovery of renal blood flow and renal oxygen delivery after propofol-induced hypotension, suggesting pronounced angiotensin II-mediated renal vasoconstriction during blood pressure reductions caused by anaesthesia.

Abstract P050: Reproducibility of Blood Pressure Responses to Dietary Sodium and Potassium Interventions: the GenSalt Study

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Jiang He ◽  
Dongfeng Gu ◽  
Jichun Chen ◽  
Qi Zhao ◽  
Lydia A Bazzano ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Urinary Excretion ◽  
Dietary Intervention ◽  
Correlation Coefficients ◽  
Dietary Sodium ◽  
High Sodium ◽  
Low Sodium ◽  
Potassium Supplementation ◽  
Study Participants ◽  
Sodium And Potassium

Blood pressure (BP) responses to dietary sodium and potassium interventions vary among individuals (salt- and potassium-sensitivity). However, it is unknown whether salt- and/or potassium-sensitivity is a reproducible trait. We repeated the dietary sodium and potassium intervention among 488 Han Chinese who participated in the Genetic Epidemiology Network of Salt Sensitivity (GenSalt) four years after the original dietary intervention. The same dietary intervention protocol, which included a 7-day low sodium-feeding (51.3 mmol/day), a 7-day high sodium-feeding (307.8 mmol/day), and a 7-day high sodium-feeding with an oral potassium supplementation (60 mmol/day), was applied in both the original and repeated studies. Three BP measurements were obtained during each of the 3 days of baseline observation and on days 5, 6, and 7 of each intervention period. Three timed urinary samples were collected to measure sodium and potassium excretion at baseline and during each intervention phase. On average, study participants were 39.7 years old and 49.4% of them were male. Study participants had a mean body mass index of 23.7 kg/m 2 , systolic BP of 118.1 mmHg, diastolic BP of 74.4 mmHg, urinary excretion of sodium of 258.8 mmol/24-hrs, and urinary excretion of potassium of 38.8 mmol/24-hrs. The results from the 24-h urinary excretions of sodium and potassium showed excellent compliance with the study diet. BP responses to dietary intervention in the original and repeated studies were highly correlated. For example, the correlation coefficients for systolic BP between original and repeated studies were 0.7681 at baseline, 0.7902 during low-sodium, 0.8045 during high-sodium, and 0.8232 during high-sodium and potassium supplementation intervention (all p<0.0001). The correlation coefficients for systolic BP changes between original and repeated studies were 0.3659 from baseline to low-sodium, 0.3655 from low to high-sodium, and 0.2850 from high-sodium to potassium supplementation (all p<0.0001). These data indicate that BP responses to dietary sodium and potassium intervention are reproducible traits. Furthermore, our study suggests that identification of individuals who are more sensitive to dietary sodium and potassium intake may improve the efficiency of targeted dietary intervention for hypertension prevention among high-risk individuals.

Abstract P234: Genetic Variants of the Kallikrein-kinin System Associated with the Salt Sensitivity of Blood Pressure: The GenSalt Study

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Dongfeng Gu ◽  
Qi Zhao ◽  
Tanika N Kelly ◽  
James E Hixson ◽  
Dabeeru C Rao ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Genetic Variants ◽  
Dietary Intervention ◽  
Linkage Disequilibrium Block ◽  
Salt Sensitivity ◽  
Dietary Sodium ◽  
Kinin System ◽  
High Sodium ◽  
Low Sodium ◽  
Kallikrein Kinin System

The kallikrein-kinin system (KKS) has been implicated in the pathogenesis of salt-sensitive hypertension in animal models. We comprehensively examined the association between genetic variants of the KKS and blood pressure (BP) response to dietary sodium intervention among participants of the Genetic Epidemiology Network of Salt Sensitivity (GenSalt) study. A 7-day low-sodium dietary intervention followed by a 7-day high-sodium dietary intervention was carried out among 1,906 GenSalt participants from rural areas of north China. Nine BP measurements were obtained at baseline and on the last three days of each intervention period using a random-zero sphygmomanometer. The percentage changes in mean BP from baseline to low-sodium intervention and from low-sodium to high-sodium intervention were used to assess individual salt-sensitivity. A total of 205 tagSNPs and functional SNPs of eleven genes of the KKS ( BDKRB1 , BDKRB2 , CPN1 , CPN2 , CPM , ECE1 , KLK1 , KLKB1 , KNG1 , MME , SERPINA4 ) were selected and genotyped in this study. Single marker analyses were conducted using the Family Based Association Test program. Genetic variants in the bradykinin receptor B2 ( BDKRB2 ) and endothelin converting enzyme 1 ( ECE1 ) genes showed significant associations with salt sensitivity even after adjusting for multiple testing using the false discovery rate method. SNP rs11847625 of BDKRB2 was significantly associated with systolic BP (SBP) response to low-sodium intervention ( P = 0.0001). Compared to its major allele G, carriers of the minor allele C had greater SBP decrease during low-sodium intervention. Furthermore, a haplotype containing allele C was associated with greater SBP increase to high-sodium intervention ( P = 0.0009). Seven SNPs of ECE1 , one of the degrading enzymes of kinins, were significantly associated with diastolic BP (DBP) response to low-sodium intervention ( P values ranged from 0.0003 to 0.002). Two haplotypes in the linkage disequilibrium block including these seven SNPs were significantly associated with DBP response to low-sodium intervention (P=0.0004 and 0.003, respectively). Our study found that the genetic variants of the KKS were associated with salt sensitivity of BP. Replication and functional studies of the identified variants are warranted in the future.

scholarly journals Central Blood Pressure Responses to Dietary Sodium and Potassium Interventions

2018 ◽  
Vol 31 (5) ◽  
pp. 582-589 ◽  
Author(s):  
Xiaolong Xing ◽  
Fangchao Liu ◽  
Xueli Yang ◽  
Chen Huang ◽  
Dingding Zhang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Augmentation Index ◽  
Dietary Sodium ◽  
Central Hemodynamics ◽  
High Sodium ◽  
Metabolic Traits ◽  
Low Sodium ◽  
Potassium Supplementation ◽  
Sodium And Potassium ◽  
Linear Trends

Abstract BACKGROUND To explore how central hemodynamics respond to dietary sodium and potassium interventions, and whether the responses are associated with metabolic traits. METHODS We conducted a dietary intervention study including a 7-day low-sodium (51.3 mmol sodium/day) intervention, a 7-day high-sodium (307.8 mmol sodium/day) intervention, and a 7-day high-sodium with potassium supplementation (60.0 mmol potassium/day) intervention among 99 northern Chinese subjects aged 18–60 years. Five metabolic traits included abdominal obesity, high triglycerides, low HDL cholesterol, raised blood pressure (BP), and high glucose. Central hemodynamics were measured at baseline and during each intervention. RESULTS Central systolic BP (SBP), diastolic BP (DBP), pulse pressure (PP), and augmentation index (AIx@75) significantly decreased during low-sodium intervention, increased during high-sodium intervention, and then decreased during potassium supplementation. We observed potential linear trends toward significance of central SBP and PP responses to low-sodium intervention, and significant linear trends of responses to high-sodium intervention as the number of metabolic traits grows. For example, among participants with 0 or 1, 2 or 3, and 4 or 5 metabolic traits, central SBP responses to high-sodium intervention were 8.8 [95% confidence interval (5.8, 11.8)], 9.3 (7.1, 11.6), and 14.0 (11.6, 16.3) mmHg, respectively (P for trend = 0.009). Significant linear trends of central SBP and DBP responses to potassium supplementation were also observed. CONCLUSIONS Central BP and AIx@75 were lowered by sodium reduction and potassium supplementation, and elevated by sodium-loading. The responses of central BP were pronounced among individuals with metabolic traits clustering. CLINICAL TRIALS REGISTRATION Trial Number NCT00721721 (The current study is registered on ClinicalTrials.gov; https://clinicaltrials.gov).

Angiotensin II and prostaglandins in control of vasa recta blood flow

1988 ◽  
Vol 254 (3) ◽  
pp. F417-F424 ◽  
Author(s):  
W. A. Cupples ◽  
T. Sakai ◽  
D. J. Marsh
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Renal Medulla ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Electromagnetic Flow Probe ◽  
Angiotensin Blockade

Angiotensin II has been implicated in the regulation of medullary blood flow and is known to interact with prostaglandins at sites within the kidney. Therefore the role of angiotensin in control of vasa recta blood flow was studied in antidiuretic, Munich-Wistar rats. We also tested the hypothesis that prostaglandins act to modulate the effect of angiotensin. Total renal blood flow was measured by an electromagnetic flow probe, vasa recta blood flow by a dual-slit method. Captopril was used to confirm that angiotensin blockade increased renal blood flow (by 15 +/- 4%). Captopril and saralasin were used to show that angiotensin blockade increased vasa recta blood flow (by 23 +/- 9 and 14 +/- 7%, respectively). The results demonstrate a tonic constrictor effect of angiotensin in the renal medulla. Exogenous angiotensin II, delivered intravenously, failed to mimic the effect of endogenous angiotensin. Indomethacin did not alter blood pressure or renal blood flow but did reduce vasa recta blood flow by 20 +/- 3%, suggesting that prostaglandins act preferentially on the medullary circulation. Nor did it alter the response of blood pressure, of renal blood flow, or of vasa recta blood flow to captopril. Moreover, prior angiotensin blockade with either captopril or saralasin enhanced the medullary vasoconstrictor effect of indomethacin (P less than 0.05). These results are not consistent with the hypothesis that prostaglandins act primarily as angiotensin modulators. They suggest that the medullary interaction between angiotensin and prostaglandins differs from that in the cortex.

Abstract 55: Sodium Sensitivity, Sodium Resistance, and Incidence of Hypertension

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Jiang He ◽  
Jian-Feng Huang ◽  
Jing Chen ◽  
Ji-Chun Chen ◽  
Xiangfeng Lu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Incident Hypertension ◽  
High Sodium ◽  
Sodium Sensitivity ◽  
Low Sodium ◽  
Blood Pressure Responses

Background: Blood pressure responses to dietary sodium intake vary among individuals. However, it is unknown whether sodium sensitivity and sodium resistance predict incidence of hypertension. Methods: We conducted a feeding study, including a 7-day low-sodium diet (51.3 mmol/day) and a 7-day high-sodium diet (307.8 mmol/day), among 1,718 Chinese individuals with normal blood pressure in 2003-2005 and follow-up studies in 2008-2009 and 2011-2012. Three blood-pressure measurements and 24-hour urinary sodium excretion were obtained on each of 3 days during baseline, low- and high-sodium interventions, and follow-up visits. Latent class models were used to identify subgroups that share a similar underlying trajectory in blood-pressure responses to dietary sodium intake. Results: Three trajectories of systolic blood pressure responses to dietary sodium intake were identified (Figure). Mean (standard deviation) changes in systolic blood pressure were -13.7 (5.5), -4.9 (3.0), and 2.4 (3.0) mmHg during the low-sodium intervention, and 11.2 (5.3), 4.4 (4.1) and -0.2 (4.1) mmHg during the high-sodium intervention ( P< 0.001 for group differences) in high sodium-sensitive, moderate sodium-sensitive, and sodium-resistant groups, respectively. Compared to individuals with moderate sodium sensitivity, multiple-adjusted odds ratio (95% confidence intervals) for incident hypertension were 1.44 (1.03 to 1.99) for those with high sodium sensitivity and 1.42 (1.02 to 1.97) for those with sodium resistance ( P <0.001 for quadratic trend). Furthermore, a J-shaped association between systolic blood pressure responses to high sodium intake and incident hypertension was identified ( P <0.001). Similar results were observed for diastolic blood pressure. Conclusions: Individuals with either high sodium sensitivity or sodium resistance are at an increased risk for developing hypertension.

Soybean proteins counteract heart remodeling in wistar rats fed a high sodium chloride diet

2019 ◽  
Vol 23 (6) ◽  
pp. 92-99
Author(s):  
I. G. Kayukov ◽  
O. N. Beresneva ◽  
M. M. Parastaeva ◽  
G. T. Ivanova ◽  
A. N. Kulikov ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Chloride ◽  
Cardiac Remodeling ◽  
Wistar Rats ◽  
Salt Intake ◽  
Left Ventricular ◽  
High Salt ◽  
Soy Proteins ◽  
High Sodium ◽  
Heart Remodeling

BACKGROUND. Increased salt intake is associated with a number of cardiovascular events, including increased blood pressure (BP) and the development of left ventricular hypertrophy (LVH). However, there is much evidence that a high content of sodium chloride in the diet does not always lead to an increase in BP, but almost inevitably causes cardiac remodeling, in particular, LVH. Many aspects of myocardial remodeling induced by high sodium content in the food have not been studied enough. THE AIM of the study was to trace the echocardiographic changes in Wistar rats fed the high salt ration and the high salt ration supplemented with soy proteins.MATERIAL AND METHODS. Echocardiography and BP measurements were performed on male Wistar rats, divided into three groups. The first (control; n = 8) included rats that received standard laboratory feed (20.16 % animal protein and 0.34 % NaCl); the second (n = 10) – animals that received standard feed and 8 % NaCl (high salt ration). The third group (n = 10) consisted of rats who consumed a low-protein diet containing 10 % soy protein isolate (SUPRO 760) and 8 % NaCl. The follow-up period was 2 and 4 months.THE RESULTS of the study showed that: (1) the intake of a large amount of salt with a diet does not necessarily lead to the formation of arterial hypertension; (2) despite the absence of a distinct increase in BP, under these conditions signs of cardiac remodeling, in particular, LVH, appear rather quickly; (3) supplementing a high-salt diet with soy isolates counteracts the development of LVH.CONCLUSION. High salt intake with food can cause heart remodeling, regardless of blood pressure, while soy proteins can counteract this process.

Effect of Prolonged High Sodium Chloride Ingestion and Withdrawal upon Blood Pressure of Dogs.

1951 ◽  
Vol 77 (3) ◽  
pp. 379-382 ◽  
Author(s):  
C. M. Wilhelmj ◽  
E. B. Waldmann ◽  
T. F. McGuire
Keyword(s):  
Blood Pressure ◽  
Sodium Chloride ◽  
High Sodium
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