Iatrogenic and Drug-Induced Hypertension

2004 ◽  
pp. 21-35 ◽  
Author(s):  
Ehud Grossman ◽  
Franz H. Messerli
Keyword(s):  
Drug Induced ◽  
Induced Hypertension

Abstract 16216: Increases in Renal Nkcc2 and Ncc Preceded the Elevation of Blood Pressure in Mice Treated With Clozapine

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Zhiyun Ren ◽  
Laureano D Asico ◽  
Xiaoyan Wang
Keyword(s):  
Protein Expression ◽  
Sodium Transport ◽  
Transport Proteins ◽  
No Synthase ◽  
Ros Generation ◽  
Serum Concentrations ◽  
Drug Induced ◽  
Induced Hypertension ◽  
Different Doses ◽  
Mini Pump

One of major side effects of clozapine, a common antipsychotic drug, is hypertension. In order to explore the pathogenesis of the drug-induced hypertension, we examined the renal sodium transport proteins and BP in the C57Bl6/J male mice treated with clozapine at different doses for 1 week. Clozapine at 20mg/kg/day via osmotic mini-pump increased SBP ( 110±0.6,mmHg, femoral artery, under anesthesia) and DBP (76.7±1) relative to vehicle (97.6±1.2/71.2±2.7) while the renal protein expression of NKCC2 (180±21, % of vehicle) and NCC (171±22), and ENaC-α (140±7), β(166±21) and γ(130±7) was increased without changes in NHE3 and α1-NKA (n=5/group). Clozapine at lower doses (5&10mg/kg/day,IP) did not change the conscious SBP and DBP monitored daily by tail-cuff, even on day 7 in 5 mg/kg group (115.61±1.6/90.1±1.3) and in 10mg/kg group (116.8±2/89.0±1.6) relative to vehicle (111.9±1.5/86.9±1.4) (n=4/group). Urinary excretion of Na + & K + and serum concentrations of Na + , K + , Cl - , creatinine were similar in all groups. However, renal protein expression of NKCC2 was increased in 5mg/kg (360±80, % of vehicle) and 10mg/kg (247±50) groups; NCC was increased at 5 mg/kg (175±9); α1-NKA was increased in 5mg/kg (216±5) and 10mg/kg (163±2) groups. No increases were found in the protein expression of NHE3 and ENaCs. Those increases in renal NKCC2 &NCC at 5 & 10 mg/kg were consistent with those at 20 mg/kg. AT1R was increased at 5 (221±20) &10mg/kg (255±21) while renin (186±15) and ACE1 (186±5), not ACE2, were increased at 5 mg/kg suggesting an activation of RAAS in kidney. NOX4, not NOX2, was increased at 5 mg/kg (453±69) while NOS3, not NOS1&2, was decreased at 5 (60±21) and 10mg/kg (64±5) groups. TNFα, not IL-6 was increased at 5 (222±18) &10 mg/kg (321±26). In cultured mouse distal convoluted tubule cells, clozapine also increased NCC and α1-NKA at 1nM (169±4;156±7) and 10nm(175±23;183±15) respectively ( 24h,n=4/group). Those changes in kidney, including increases in sodium transport proteins, RAAS components, ROS generation enzymes, inflammation factors and decrease in NO synthase, preceded the elevation of BP suggesting that direct or indirect regulations of clozapine on those proteins may play an important role in the pathogenesis of the drug-induced hypertension.

Drug-Induced Hypertension

Drugs ◽  
1976 ◽  
Vol 12 (3) ◽  
pp. 222-230 ◽  
Author(s):  
G. S. Stokes
Keyword(s):  
Drug Induced ◽  
Induced Hypertension

Drug-induced hypertension

1991 ◽  
Vol &NA; (354) ◽  
pp. 12
Author(s):  
&NA;
Keyword(s):  
Drug Induced ◽  
Induced Hypertension

Drug-Induced Hypertension

2007 ◽  
pp. 883-893
Author(s):  
Ehud Grossman ◽  
Franz H. Messerli
Keyword(s):  
Drug Induced ◽  
Induced Hypertension

Cardiovascular disorders

2011 ◽  
Author(s):  
Carl Waldmann ◽  
Neil Soni ◽  
Andrew Rhodes
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Bacterial Endocarditis ◽  
Endocrine Disorders ◽  
Heart Failure Management ◽  
Drug Induced ◽  
Failure Assessment ◽  
Induced Hypertension ◽  
The Uk ◽  
Secondary Causes

Hypertension 284Tachyarrhythmias 288Bradyarrhythmias 290Myocardial infarction: diagnosis 292NSTEMI 294STEMI 296Acute heart failure: assessment 300Acute heart failure: management 304Bacterial endocarditis 308Hypertension is defined as sustained SBP ≥140mm Hg and/or DBP ≥90mm Hg (Table 18.1.1). In the UK, the prevalence of hypertension is ~32%. Of these, only 22% have controlled BP (<140/90mm Hg). Essential (primary) hypertension accounts for 80–90% of cases. Secondary causes of hypertension include renal and endocrine disorders and drug-induced hypertension (...

Drug-Induced Hypertension

2019 ◽  
Vol 48 (4) ◽  
pp. 859-873 ◽  
Author(s):  
Matthew C. Foy ◽  
Joban Vaishnav ◽  
Christopher John Sperati
Keyword(s):  
Drug Induced ◽  
Induced Hypertension

Drug-Induced Hypertension

2020 ◽  
pp. 159-166
Author(s):  
Aurélien Lorthioir ◽  
Ines Belmihoub ◽  
Laurence Amar ◽  
Michel Azizi
Keyword(s):  
Drug Induced ◽  
Induced Hypertension

scholarly journals Drug-induced arterial hypertension

2019 ◽  
Vol 16 (2) ◽  
pp. 32-41
Author(s):  
Olga D Ostroumova ◽  
Mariia I Kulikova
Keyword(s):  
Blood Pressure ◽  
Antihypertensive Therapy ◽  
Antihypertensive Drugs ◽  
Smooth Muscles ◽  
Home Monitoring ◽  
New Drugs ◽  
Uncontrolled Hypertension ◽  
Drug Induced ◽  
Subsequent Increase ◽  
Induced Hypertension

This review is devoted to the problem of drug-induced hypertension (H). It summarizes the literature data on drugs and substances that can increase blood pressure, discusses the mechanisms of their hypertensive action. Many classes of drugs such as steroids, nonsteroidal anti-inflammatory drugs, sympathomimetics, immunosuppressants, oral contraceptives, antidepressants, erythropoietin, etc. can cause episodic or persistent increase in blood pressure, cause uncontrolled hypertension, reduce the effectiveness of antihypertensive drugs. The development of drug-induced hypertension is realized through a number of pathophysiological mechanisms: sodium retention with subsequent increase in the volume of circulating blood, activation of the sympathetic nervous system, direct effect on the smooth muscles of arterioles, there are other, not fully studied mechanisms. Drug-induced H may also be the result of pharmacokinetic or pharmacodynamic drug interactions. To suspect the presence of drug-induced hypertension, in the first place, should be in persons with newly diagnosed hypertension, as well as in patients who previously had a well-controlled hypertension (stable target blood pressure - BP levels) when they have episodes of unexplained increase in BP without a clear relationship with physical or psycho-emotional stress. It is very important to have a properly collected history with a focus on a thorough assessment of the medicines taken by the patient, especially newly prescribed, as well as those purchased at the pharmacy independently, including over-the-counter, this will avoid unnecessary and/or expensive studies and unnecessary prescriptions of additional antihypertensive drugs. The article presents these measures for the prevention and correction of drug-induced H. The appointment of new drugs by a doctor to patients receiving antihypertensive therapy should necessarily take into account their impact on the risk of drug-induced hypertension. Prescribing drugs that cause an increase in BP levels should either be avoided or, if alternative treatment regimens are not possible, strict control of the patient's BP level (including the method of home monitoring of BP) and, if necessary, the correction of antihypertensive therapy. When canceling a drug that causes drug-induced hypertension, BP returns to its original level, which is proof of the iatrogenic cause of hypertension.

scholarly journals Predictors of anti-VEGF drug-induced hypertension using different hypertension criteria: a secondary analysis of the COMPARZ study

2018 ◽  
Vol 10 ◽  
pp. 175883401875509 ◽  
Author(s):  
Arduino A. Mangoni ◽  
Ganessan Kichenadasse ◽  
Andrew Rowland ◽  
Michael J. Sorich
Keyword(s):  
Antihypertensive Drugs ◽  
Karnofsky Performance Status ◽  
Phase Iii ◽  
Drug Induced ◽  
Specific Patient ◽  
Post Hoc Analysis ◽  
Anti Vegf ◽  
Induced Hypertension ◽  
Grade 3 ◽  
Post Hoc

Background: There is inconsistency in the criteria used to define anti-vascular endothelial growth factor (VEGF) drug-induced hypertension (AVEGF-HT) in published studies. It is unknown whether specific patient characteristics similarly predict AVEGF-HT using different criteria. Methods: We assessed the associations between clinical and demographic factors ( n = 22) and AVEGF-HT, using six criteria based on predefined on-treatment blood pressure (BP) thresholds or absolute BP elevations versus baseline, in a post hoc analysis of a phase III trial of 1102 patients with renal cell carcinoma (RCC) randomized to pazopanib or sunitinib (COMPARZ study). Results: The cumulative incidence of AVEGF-HT at any time while on treatment ranged between 14.8% [criterion: grade ⩾3 toxicity, National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) v3.0] and 58.8% (criterion: absolute systolic BP increase ⩾20 mmHg versus baseline). After adjusting for anti-VEGF treatment and baseline BP, the number of significant ( p < 0.05) predictors ranged between one (criterion: absolute systolic BP increase ⩾20 mmHg, on-treatment systolic BP ⩾140 mmHg and diastolic BP ⩾90 mmHg) and nine (criterion: grade ⩾3 toxicity, NCI CTCAE v3.0). Age, use of antidiabetic drugs and use of antihypertensive drugs each significantly predicted four AVEGF-HT criteria. By contrast, sex, smoking, heart rate, proteinuria, Karnofsky performance status, and use of thiazide diuretics did not predict any criterion. Conclusions: There was a significant variability in the incidence, number and type of predictors of AVEGF-HT, using six different criteria, in a post hoc analysis of the COMPARZ study. The use of specific criteria might affect the assessment of the interaction between anti-VEGF drugs, AVEGF-HT and cancer outcomes.

Sign in / Sign up

Export Citation Format

Share Document