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Respiratory, endocrine, cardiac, and renal topics
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
Captopril has a short duration of action, with an elimination half-life of 2 hours, and therefore must be given in 3 doses per day. Initial dose is 500 mcg/kg/day, mean dose 2 mg/kg/day, and maximum 4 mg/kg/day. An initial test dose of one tenth the mean daily dose should be given, especially in infants, and blood pressure must be measured at regular intervals thereafter.
Cardiovascular Drugs
Published in Radhwan Nidal Al-Zidan, Drugs in Pregnancy, 2020
Risk Summary: Captopril is contraindicated during the 2nd and 3rd Trimesters because the pregnancy experience in humans showed a profound potentiality of teratogenicity and severe fetal toxicity associated with its use during this period.
Cardiac Preload Control: An Important Function of Cardiac Chemical Receptors*
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
David M. Nganele, Thomas H. Hintze
Myocardial ischemia and congestive heart failure are usually accompanied by increases in preload. This can be very detrimental to a heart that is already diseased. The reduction in preload represents a positive approach in alleviating the pathophysiological condition. The results of this study add a new dimension to the protective nature of a metabolite of arachidonic acid, PGI2, for the ischemic myocardium. The reduction in preload would reduce the oxygen demand/supply ratio that increases during ischemia. PGI2 is being tested clinically for the potential management of congestive heart failure (Yui et al., 1982) and myocardial ischemia (Blasko et al., 1983). Its preload reducing property could represent a major component of its therapeutics. The present study has also provided a mechanism for the preload reduction by captopril, which can be important in clinical use of captopril that is now utilized for the management of heart failure (Davis et al., 1979). In summary, stimulation of inhibitory cardiac receptors results in withdrawal of α-adrenergic tone from capacitance vessels causing a reduction in preload. These effects are more pronounced in the absence of the baroreflexes. This reduction in preload, by reducing wall stress, may provide a powerful physiological control mechanism for the regulation of myocardial oxygen consumption as well as be beneficial in pathophysiological states where oxygen supply is limited.
Angiotensin II receptor blockers in dermatology: a narrative review
Published in Journal of Dermatological Treatment, 2022
ACEIs is one of the most common triggers for drug-induced pemphigus (DIP), but ARBs can also induce pemphigus (34–36), including telmisartan, valsartan, losartan and candesartan. However, it is difficult to differentiate between DIP and idiopathic pemphigus, due to the similar clinical and histologic features; furthermore, indirect immunofluorescence also cannot be used to differentiate between these two entities (34). Although a previous study revealed that immunostaining of a monoclonal antibody (32-2B) can be useful for the diagnosis of DIP and is an indicator of a good prognosis (35), it is rarely used in clinical practice. Some articles reported a good prognosis with thiol-induced pemphigus (36), but one review article reported no difference within thiol and non-thiol groups for the outcome (34). The time for remission varies for the drugs, according to the previous review article (34), the median time to remission for the cases induced by penicillamine is 90 days, and 60 days for the cases induced by captopril. The possible mechanism of ARBs for DIP is that nonthiol and nonphenol drugs lead to autoantibody production and the loss of keratinocyte adhesion (34). Studies have reported the appearance of lesions 2–6 months after ARBs administration (37–39). Furthermore, some case reports have revealed that ARBs induce bullous pemphigoid (40). However, diuretics were the most common antihypertensive drug contributing to BP (41,42), especially loop diuretics (42). Due to the high prevalence of hypertension in elderly patients, ARBs should be considered when dealing with DIP.
Angiotensin converting enzyme and angiotensin converting enzyme inhibitors in dermatology: a narrative review
Published in Expert Review of Clinical Pharmacology, 2022
ACEI could possibly be considered a possible treatment choice for infantile hemangioma (IH), possibly related to the fact that the endothelium of proliferating IH express components of RAS [27]. Tan et al. reported the efficacy of captopril for IH in eight patients, under a dose of 0.1 mg kg(−1) test dose orally, followed by 0.15 mg kg(−1) every 8 hours over 24 hours [28]. But captopril did not demonstrate sustainable effects of corticosteroid-induced involution for 7 (58%) patients, according to the other case series [29]. One randomized controlled trial reported that both propranolol and captopril can reduce the levels of ATII and vascular endothelial growth factor, but propranolol showed a significantly better response [30]. Interestingly, the genotype ID of ACE was associated with a better treatment response to captopril [30]. Serum levels of renin, ACE and ATII have been measured for the treatment modalities for treating IH [31]. ATII had a significant decline under captopril but ACE did not, which may indicate that ACE does not play a major role for IH. Currently, β-blockers are the mainstream treatment for IH, and the evidence for ACE is still limited [32].
Captopril suppresses hepatic mammalian target of rapamycin cell signaling and biomarkers of inflammation and oxidative stress in thioacetamide-induced hepatotoxicity in rats
Published in Archives of Physiology and Biochemistry, 2021
Fahaid Al-Hashem, Suliman Al Humayed, Mohamed A. Haidara, Noha S. Abdel Latif, Bahjat Al-Ani
Captopril is widely used to treat hypertension via the inhibition of the angiotensin-converting enzyme (ACE) that leads to the inhibition of angiotensin II production and hence hypertension (Loloi et al.2018). It also ameliorates several types of liver diseases such as hepatic fibrosis (Karimian et al.2008, Aldahmash and El-Nagar 2016), nonalcoholic fatty liver disease (Ackerman et al.2005), acute pancreatitis (El-Ashmawy et al.2018), acute pancreatitis-associated lung injury (Yu et al.2016), and lipopolysaccharide (LPS)-induced inflammation and hepatic injury (Azizi-Malekabadi et al. 2008). However, the effects of captopril on TAA-induced liver injury enzymes, inflammation, oxidative stress, hypertension, and upregulation of the cell signaling molecules, mTOR and TIMP-1 that play essential roles in the development of liver fibrosis in animal models is unknown. Therefore, we speculated that activation of the mTOR and these parameters by TAA in rats could be inhibited by captopril.