Differential Effect of Prostaglandin A1 in Hypertensive Patients with Low, Normal and High Renin

1974 ◽  
Vol 48 (s2) ◽  
pp. 311s-313s
Author(s):  
L. R. Krakoff ◽  
N. Vlachakis ◽  
M. Mendlowitz ◽  
J. Stricker

1. Eighteen hypertensive in-patients were studied during a period of controlled electrolyte intake and, on the basis of determinations of mid-day plasma renin activity (PRA), were classified into low, normal and high renin sub-groups. 2. The responses of systemic arterial pressure, urine sodium excretion rate and PRA to infusion of prostaglandin A1 (PGA1) at a rate of 0.4 μg min−1 kg−1 for 60 min differed among the renin sub-groups. 3. The low renin sub-group displayed the greatest fall in arterial pressure and the greatest increase in sodium excretion rate during infusion of PGA1; PRA was unaffected. The normal renin group demonstrated a lesser reduction of arterial pressure and lesser rise in sodium excretion rate during infusion of PGA1 compared with the low renin group; PRA rose significantly during infusion of PGA1. No significant change in arterial pressure occurred in the high renin group during infusion of PGA1; sodium excretion rate rose less than that observed in the other two groups. Infusion of PGA1 caused striking increases in PRA in the high renin group. 4. The changes in PRA during infusion of PGA1 may explain the differences in arterial pressure and sodium excretion rate observed in the three renin sub-groups. The results also suggest that the role of the vasodilating prostaglandins may differ in the pathogenesis of low, normal and high renin hypertension.

Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Mary Cogswell ◽  
Chia-Yih Wang ◽  
Te-Ching Chen ◽  
Christine Pfeiffer ◽  
Paul Elliott ◽  
...  

Introduction: Reducing mean population sodium intake by ~1200 mg is projected to reduce thousands of deaths from heart disease and stroke and save billions of health care dollars annually. Twenty-four hour urine collection is recommended for assessing changes in mean population sodium intake, but can be difficult to implement. Predicting 24-hour urine sodium excretion using spot urines is not recommended due to diurnal variations in excretion. Further, sodium excretion patterns differ between black and white persons. We assessed the validity of previously published prediction equations for 24-hour sodium excretion in black and other young adults by timing of spot urine collection. Design: Of 481 adult volunteers aged 18-39 years (50% Blacks) asked to participate in a 2011 study in the Metropolitan DC area, 407 collected each urine void in a separate container for 24 hours. Four timed voids from the 24-h urine collection were selected (morning, afternoon, evening, and overnight) to use with previously published predictive equations. Predictive equations were based on one of two approaches; 1) an indirect approach using spot urine sodium-to-creatinine concentrations and predicted 24-hour creatinine excretion ( Tanaka, Kawasaki, Mage ), and 2) a direct approach using spot urine sodium, potassium, and creatinine concentrations, and age, and body mass index with separate equations by sex ( Brown ). We assessed mean differences between predicted and measured 24-hour sodium excretion (bias) and individual differences across levels of sodium excretion using Bland-Altman plots. Results: Among participants, mean measured 24-hour sodium excretion was ~3300 mg (SD ~1400 mg). Of the equations evaluated, mean bias in predicted 24-hour sodium excretion was least from Brown equations when using morning (-165 mg, 95% confidence interval [CI], -295, -36 mg), afternoon (-90 mg, 95% CI, -208, 28 mg) or evening ( -120 mg, 95% CI -230, -11 mg) spot urines. When using overnight spot urines, mean bias from Brown equations was greatest and statistically significant (-247 mg, 95% CI, -348, -151 mg). When using overnight spot urines, mean bias from Tanaka (-23 mg) or Mage (-145 mg) equations was not significant, however, when stratified by sex, mean biases were significant and in opposite directions. Among Blacks, mean biases from Brown were not significant (-167 to 122 mg) except using overnight specimens among Black females (-267 mg, 95% CI, -525, -47 mg). Across equations and time periods, Bland-Altman plots indicated significant bias at the individual level. Conclusions: Of the evaluated equations, predicted 24-hour urine sodium excretion using the Brown equations with morning, afternoon, or evening specimens may provide the least biased estimates of group mean sodium intake among young US adults. None of the equations adequately predicted individual 24-hour sodium excretion measured on the same day.


2019 ◽  
Vol 44 (2) ◽  
pp. 246-255 ◽  
Author(s):  
Anne Kathrine Nissen Pedersen ◽  
Charlotte Rud ◽  
Trine Levring Wilkens ◽  
Mette Borre ◽  
Jens Rikardt Andersen ◽  
...  

1988 ◽  
Vol 75 (3) ◽  
pp. 331-336 ◽  
Author(s):  
Ingrid Mazanti ◽  
Kirstine Lintrup Hermann ◽  
Arne Høj Nielsen ◽  
Knud Poulsen

1. In order to study the role of the kidney in the elimination of endogenous plasma renin, renin was measured in the plasma and urine of female mice. 2. The renin concentration was two orders of magnitude lower in urine than in plasma, but it increased after intraperitoneal injection of submandibular mouse renin. No correlation between the plasma renin concentration and the urinary renin concentration and renin excretion rate could be demonstrated. 3. Blockade of the tubular reabsorption of proteins by intraperitoneal injection of the basic amino acid lysine increased the urinary renin concentration, renin excretion rate and renin clearance two to three orders of magnitude, without affecting the plasma renin concentration. 4. This finding demonstrates that ultrafiltered renin is reabsorbed almost completely in the renal tubules and that the mechanism most likely is the same as for other filtered proteins. 5. The large renal renin clearance obtained after intraperitoneal lysine is in accordance with a major role of the kidneys in the elimination of renin from the circulation, by a glomerular ultrafiltration and tubular reabsorption and metabolization of renin.


1983 ◽  
Vol 244 (1) ◽  
pp. R74-R77 ◽  
Author(s):  
J. Schwartz ◽  
I. A. Reid

The role of vasopressin in the regulation of blood pressure during water deprivation was assessed in conscious dogs with two antagonists of the vasoconstrictor activity of vasopressin. In water-replete dogs, vasopressin blockade caused no significant changes in mean arterial pressure, heart rate, plasma renin activity (PRA), or plasma corticosteroid concentration. In the same dogs following 48-h water deprivation, vasopressin blockade increased heart rate from 85 +/- 6 to 134 +/- 15 beats/min (P less than 0.0001), increased cardiac output from 2.0 +/- 0.1 to 3.1 +/- 0.1 1/min (P less than 0.005), and decreased total peripheral resistance from 46.6 +/- 3.1 to 26.9 +/- 3.1 U (P less than 0.001). Plasma renin activity increased from 12.4 +/- 2.2 to 25.9 +/- 3.4 ng ANG I X ml-1 X 3 h-1 (P less than 0.0001) and plasma corticosteroid concentration increased from 3.2 +/- 0.7 to 4.9 +/- 1.2 micrograms/dl (P less than 0.05). Mean arterial pressure did not change significantly. When the same dogs were again deprived of water and pretreated with the beta-adrenoceptor antagonist propranolol, the heart rate and PRA responses to the antagonists were attenuated and mean arterial pressure decreased from 103 +/- 2 to 91 +/- 3 mmHg (P less than 0.001). These data demonstrate that vasopressin plays an important role in blood pressure regulation during water deprivation in conscious dogs.


2018 ◽  
Vol 314 (1) ◽  
pp. F70-F80 ◽  
Author(s):  
Weijian Shao ◽  
Carla B. Rosales ◽  
Camila Gonzalez ◽  
Minolfa C. Prieto ◽  
L. Gabriel Navar

Serelaxin is a novel recombinant human relaxin-2 that has been investigated for the treatment of acute heart failure. However, its effects on renal function, especially on the renal microcirculation, remain incompletely characterized. Our immunoexpression studies localized RXFP1 receptors on vascular smooth muscle cells and endothelial cells of afferent arterioles and on principal cells of collecting ducts. Clearance experiments were performed in male and female normotensive rats and Ang II-infused male rats. Serelaxin increased mean arterial pressure slightly and significantly increased renal blood flow, urine flow, and sodium excretion rate. Group analysis of all serelaxin infusion experiments showed significant increases in GFR. During infusion with subthreshold levels of Ang II, serelaxin did not alter mean arterial pressure, renal blood flow, GFR, urine flow, or sodium excretion rate. Heart rates were elevated during serelaxin infusion alone (37 ± 5%) and in Ang II-infused rats (14 ± 2%). In studies using the in vitro isolated juxtamedullary nephron preparation, superfusion with serelaxin alone (40 ng/ml) significantly dilated afferent arterioles (10.8 ± 1.2 vs. 13.5 ± 1.1 µm) and efferent arterioles (9.9 ± 0.9 vs. 11.9 ± 1.0 µm). During Ang II superfusion, serelaxin did not alter afferent or efferent arteriolar diameters. During NO synthase inhibition (l-NNA), afferent arterioles also did not show any vasodilation during serelaxin infusion. In conclusion, serelaxin increased overall renal blood flow, urine flow, GFR, and sodium excretion and dilated the afferent and efferent arterioles in control conditions, but these effects were attenuated or prevented in the presence of exogenous Ang II and NO synthase inhibitors.


2013 ◽  
Vol 23 (6) ◽  
pp. 450-455 ◽  
Author(s):  
Srinivas Subramanian ◽  
Boon Wee Teo ◽  
Qi Chun Toh ◽  
Yun Yin Koh ◽  
Jialiang Li ◽  
...  

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