scholarly journals Relationship between Plasma Renin Activity and Blood Pressure Response to Antihypertensive Agents. A Proposal for Management of Essential and Renal Hypertension : Prognosis and Treatment of Renal Hypertension

1975 ◽  
Vol 39 (7) ◽  
pp. 805-810
Author(s):  
KENJIRO TANAKA ◽  
KOSHIRO FUKIYAMA ◽  
KENSHI KUMAMOTO ◽  
YOSHITAKA YAMAMOTO ◽  
HIDEO ONIKI ◽  
...  
1982 ◽  
Vol 63 (s8) ◽  
pp. 243s-246s
Author(s):  
M. S. Golub ◽  
M. E. Berger ◽  
N. D. Vlachakis ◽  
P. Eggena ◽  
M. P. Sambhi

1. Changes in plasma renin activity, plasma noradrenaline and adrenaline, and blood pressure were evaluated after mild haemorrhage (6 ml/kg) and subsequent intravenous captopril in conscious, restrained rabbits. Two protocols were followed. In the first, control animals (n = 8) were compared with rabbits receiving indomethacin (n = 8) in their drinking water for 5 days and intravenously during the haemorrhage and captopril study. In the second protocol, animals receiving propranolol in the drinking water and intravenously (n = 7) were compared with a group (n = 7) receiving propranolol plus indomethacin. 2. Urinary prostaglandin E excretion was decreased significantly with the oral administration of indomethacin in both protocols. Plasma renin activity levels were not significantly different at baseline, but the animals receiving indomethacin had significantly (P < 005) lower values after haemorrhage in both studies. The large increases in plasma renin activity after captopril were not influenced by indomethacin in either study. 3. The blood pressure response to captopril was significantly blunted in the indomethacin group in the first experiment. 4. Plasma noradrenaline and adrenaline levels were not affected by indomethacin treatment in either protocol. 5. It is concluded that the plasma renin activity response to haemorrhage in conscious rabbits is mediated in part by a cyclo-oxygenase-dependent component separable from the β-adrenoceptor. The renin response to converting enzyme inhibition is not influenced by cyclo-oxygenase inhibition. A component of the blood pressure response to captopril may involve a cyclo-oxygenase product.


1981 ◽  
Vol 60 (6) ◽  
pp. 625-631
Author(s):  
M. L. Watson ◽  
J. McCormick ◽  
A. Thom ◽  
P. Whelpdale ◽  
A. Ungar

1. Hypertension was induced in dogs by partial occulsion of one renal artery, the opposite kidney remaining intact, and the changes in blood pressure, plasma renin activity, aldosterone and prostaglandin E (PGE) were monitored. 2. Two days after induction of hypertension, the retained sodium and water were removed by haemodialysis and the animals were then maintained on a low dietary intake of sodium for the following 7 days. 3. Removal of the accumulated sodium and water had no immediate effect on blood pressure, but during the ensuing 7 days there was a small decrease in blood pressure, which again increased after re-institution of a normal sodium intake. 4. Plasma renin activity and aldosterone increased during development of hypertension and remained elevated during the period of sodium restriction. 5. Sodium and water retained during the development of hypertension was not responsible for the elevated blood pressure. 6. The concentration of PGE in arterial plasma and renal venous plasma from the undamped kidney were unchanged during the study, although we have previously shown that in the absence of sodium depletion, PGE rises. 7. PGE released from the kidney may be important in mediating the excretion of sodium and water that is retained during the development of renal hypertension.


Metabolites ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 645
Author(s):  
Mai Mehanna ◽  
Caitrin W. McDonough ◽  
Steven M. Smith ◽  
Yan Gong ◽  
John G. Gums ◽  
...  

Plasma renin activity (PRA) is a predictive biomarker of blood pressure (BP) response to antihypertensives in European–American hypertensive patients. We aimed to identify the metabolic signatures of baseline PRA and the linkages with BP response to β-blockers and thiazides. Using data from the Pharmacogenomic Evaluation of Antihypertensive Responses-2 (PEAR-2) trial, multivariable linear regression adjusting for age, sex and baseline systolic-BP (SBP) was performed on European–American individuals treated with metoprolol (n = 198) and chlorthalidone (n = 181), to test associations between 856 metabolites and baseline PRA. Metabolites with a false discovery rate (FDR) < 0.05 or p < 0.01 were tested for replication in 463 European–American individuals treated with atenolol or hydrochlorothiazide. Replicated metabolites were then tested for validation based on the directionality of association with BP response. Sixty-three metabolites were associated with baseline PRA, of which nine, including six lipids, were replicated. Of those replicated, two metabolites associated with higher baseline PRA were validated: caprate was associated with greater metoprolol SBP response (β = −1.7 ± 0.6, p = 0.006) and sphingosine-1-phosphate was associated with reduced hydrochlorothiazide SBP response (β = 7.6 ± 2.8, p = 0.007). These metabolites are clustered with metabolites involved in sphingolipid, phospholipid, and purine metabolic pathways. The identified metabolic signatures provide insights into the mechanisms underlying BP response.


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