The Clinical Effects of Losartan (Cozaar) on Hypertensive Patients

Abstract

Background Losartan potassium, one of an orally active, selective type 1 angiotensin receptor blocker, has been introduced recently as an antihypertensive agent. Method Losartan, angiotensin receptor blocker, was administrated as an initial antihypertensive agent over 12 weeks in 30 patients 11 male, 19 female, 60.1 7.2 years with stage 1 to 3 hypertension in order to observe the clinical effects. Changes in quality of life, side effects, electrocardiogram and left ventricular function were also evaluated before and after losartan therapy. Results 1 After 12 weeks treatment with 50 to 100 mg of losartan, blood pressure was lowered markedly in 18 60% , moderately in 9 30% and mildly in 1 3% out of 30 patients studied. The average of blood pressures of the 30 subjects were systolic 159.0 13.2 mmHg and diastolic 100.7 9.4 mmHg before treatment, which were lowered to 130.7 15.6 and 85.9 9.1 mmHg respectively after 12 weeks p 0.005 . 2 Heart rates were not changed with losartan. 3 Quality of life including general well-being, physical symptom, sleep and sexual dysfunction improved markedly in 2 7% and slightly in 17 57% out of 30 subjects. 4 Laboratory findings revealed no significant changes. 5 In electrocardiographic and echocardiographic follow-up 1 patient with ST-T abnormality and 2 patients with mild LV systolic dysfunction improved to normal. 6 Undesirable side effects were observed in 2 cases with dizziness, 1 dry cough, 1 skin rash, 1 leg edema and 1 epigastric discomfort, among whom one with dizziness stopped losartan. 7 In the final clinical assessment according to the scores of hypotensive effect, quality of life, LV function and side effect, losartan was very useful in 3 10% , useful in 18 60% and slightly useful in 3 10% out of 30 hypertensive patients. Conclusion Losartan can be used as an effective initial agent for the treatment of hypertension of various severities with the improvement of quality of life and low side effects.

Identification of a neural development gene expression signature in colon cancer stem cells reveals a role for EGR2 in tumorigenesis

“…During embryogenesis EGR2 has a conserved role in regulating embryonic master transcriptional regulator HOX genes and the stem cell regulator SOX2 (Chavrier et al, 1990;Desmazie `res et al, 2009;Ghislain et al, 2003;Jang et al, 2010;Kim et al, 1998;Manzanares et al, 2002;Nonchev et al, 1996aNonchev et al, , 1996bSham et al, 1993;Topilko et al, 1994;Vesque et al, 1996). In addition, several HOX genes and SOX2 have recently been shown to regulate colon CSCs (Bhatlekar et al, 2014(Bhatlekar et al, , 2018bNovak et al, 2019;Schaefer and Lengerke, 2020;Takeda et al, 2018).…”

“…EGR2 is a conserved regulator and marker of NCSCs that acts upstream of several HOX genes and SOX2 to control cell fate in embryonic and nervous system stem cells (Chavrier et al, 1990;Desmazie `res et al, 2009;Ghislain et al, 2003;Grose et al, 2002;Jang et al, 2010;Kim et al, 1998;Manzanares et al, 2002;Nonchev et al, 1996aNonchev et al, , 1996bSham et al, 1993;Topilko et al, 1994;Vesque et al, 1996). In addition, EGR2 expression is rapidly activated after wounding in embryonic and adult mouse skin (Grose et al, 2002) and is a marker of hair follicle matrix progenitor cells that give rise to the hair shaft (Liao et al, 2017).…”

“…During embryonic development of the neural crest, which gives rise to the peripheral nervous system (PNS) and several nonneuronal cell types (Bronner and LeDouarin, 2012), HOX and SOX genes are regulated by retinoic acid (Duester, 2008;Nolte et al, 2014;Tremblay et al, 2012), a product of the normal tissue stem cell and CSC marker aldehyde dehydrogenase (ALDH1A1) (Douville et al, 2008;Huang et al, 2009;Vassalli, 2019), and by the neural crest stem cell (NCSC) zinc finger transcription factor and wound response gene EGR2 (KROX20) (Chavrier et al, 1990;Desmazie `res et al, 2009;Ghislain et al, 2003;Grose et al, 2002;Jang et al, 2010;Kim et al, 1998;Manzanares et al, 2002;Nonchev et al, 1996aNonchev et al, , 1996bSham et al, 1993;Topilko et al, 1994;Vesque et al, 1996).…”

Peculiarities detected in formation of speficic hapten sensitization to phenol in children

“…Negative effects produced by phenol on the immune system and associated with development of allergic reactions have been discussed over the last decades in many research papers [9][10][11]. Immune-modulating effects produced by phenol are assumed to be mediated by the chemical being tropic to estrogen receptors (ER), peroxisome proliferator-activated receptors (PPAR), aryl hydrocarbon receptors (AhR), and its ability to induce Th2-shift in the cytokine profile [8,[12][13][14][15].…”

“…It is also a significant participant in regulation of inflammation and fibrosis [16]. Several experimental and clinical studies established that phenol and its metabolites (hydroquinone) were able to induce hyperproduction of interleukin 4 and elevated levels of IgE [10,12,13]. Th2dependent deviation in the immune response was studied using experimental models of asthma and turned out to make for generation of reactive oxygen species in considerable quantities thus making the inflammatory process more severe [16].…”