Captopril Pharmacokinetics, Blood Pressure Response and Plasma Renin Activity in Normotensive Children with Renal Scarring

1991 ◽  
Vol 16 (4) ◽  
pp. 185-193 ◽  
Author(s):  
Maurice Levy ◽  
Gideon Koren ◽  
Julia Klein ◽  
Gordon McLorie ◽  
J. Williamson Balfe
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Blood Pressure Response ◽  
Renal Scarring ◽  
Plasma Renin ◽  
Pressure Response ◽  
Renin Activity

Effect of Cyclo-Oxygenase Inhibition on Renin, Catecholamine and Blood Pressure Responses to Haemorrhage and Captopril in Conscious Rabbits

1982 ◽  
Vol 63 (s8) ◽  
pp. 243s-246s
Author(s):  
M. S. Golub ◽  
M. E. Berger ◽  
N. D. Vlachakis ◽  
P. Eggena ◽  
M. P. Sambhi
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Plasma Renin Activity ◽  
Blood Pressure Response ◽  
Plasma Renin ◽  
Pressure Response ◽  
Renin Activity ◽  
Plasma Noradrenaline ◽  
Conscious Rabbits ◽  
Noradrenaline And Adrenaline

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.

scholarly journals Metabolomics Signature of Plasma Renin Activity and Linkage with Blood Pressure Response to Beta Blockers and Thiazide Diuretics in Hypertensive European American Patients

Metabolites ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 645
Author(s):  
Mai Mehanna ◽  
Caitrin W. McDonough ◽  
Steven M. Smith ◽  
Yan Gong ◽  
John G. Gums ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Blood Pressure Response ◽  
Beta Blockers ◽  
Plasma Renin ◽  
Predictive Biomarker ◽  
Renin Activity ◽  
European American ◽  
Using Data ◽  
Metabolic Signatures

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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