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Hypertension
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
In contrast to the aorta and large central elastic arteries, many vasodilating drugs have a powerful effect on the peripheral muscular arteries, such that they dilate even though arterial pressure falls as a consequence of the peripheral effect of the drug on arterioles. This is a direct effect of the drug and not necessarily due to increased flow within the artery. Powerful arterial vasodilatation has been identified for nitrates, calcium antagonists and ACE inhibitors but not for pure arteriolar dilating drugs, such as hydralazine, dihydralazine and prazosin (Simon et al., 1982, 1983b, 1984; Safar et al., 1983; Levenson et al., 1984a, 1984b; Arcaro et al., 1991a, 1991b; Asmar et al., 1993; Chaignon et al., 1993; Bank et al., 1995; Merillon et al., 2014; Olsen et al., 2016). Vasodilatation has been shown too for pindolol, nebivolol and carvedilol but not propranolol or atenolol (Maarek et al., 1986; McEniery et al., 2004; Polónia et al., 2010). Conventional diuretics have no direct effect on these arteries (Smulyan et al., 1984; Levenson et al., 1992).
The Effects of Experimental Diabetes on the Cytochrome P450 System and Other Metabolic Pathways
Published in John H. McNeill, Experimental Models of Diabetes, 2018
Costas Ioannides, Peter R. Flatt, Christopher R. Barnett
The reactive intermediates of chemicals may also interact covalently with proteins, disturbing physiological homeostasis, leading to cell death. In the last decade, it has also become apparent that reactive intermediates can also function as haptens, conferring on proteins antigenic potential and eliciting immunotoxicity.4 Drugs such as tienilic acid, dihydralazine, and halothane are metabolically converted by the cytochrome P450–dependent mixed-function oxidases (see below) to metabolites that bind covalently to proteins to generate neoantigens resulting in the production of autoantibodies. Subsequent exposure to these drugs provokes an autoimmune response leading to hepatitis.
Physical activity and kidney function in health and disease
Published in Roy J. Shephard, Physical Activity and the Abdominal Viscera, 2017
In humans, indirect measurements of renal plasma flow using diodrast and para-amino hippurate clearance techniques suggest that exhausting endurance exercise quickly initiates a general visceral vasoconstriction. Renal vascular resistance can increase as much as fivefold[21] Renal blood flow is reduced by 70% or more[32–34] (Table 4.1), depending on the intensity of exercise,[22, 35] with the extent of vasoconstriction exacerbated by heat exposure or dehydration.[25] Changes seem related to the release of epinephrine and dopamine,[36] and they can persist for a substantial time following a sustained bout of exercise.[20, 22] One comparison of young and elderly men found little difference in flow reduction with age, but in this study the two groups had surprisingly similar levels of maximal oxygen intake,[37] suggesting that the older individuals were unusually fit. The flow reduction is abolished by the vasodilator dihydralazine.[38]
Predicting lupus flares: epidemiological and disease related risk factors
Published in Expert Review of Clinical Immunology, 2021
Samuel de Oliveira Andrade, Paulo Rogerio Julio, Diego Nunes de Paula Ferreira, Simone Appenzeller
More than 100 drugs commonly used in clinical practice are associated with rash, photosensitivity, arthralgia, arthritis, and white blood cell abnormalities [52,53]. These symptoms can be mistaken as lupus flare [52]. Drug-induced lupus (DIL) is an idiosyncratic side effect of treatments in which symptoms overlap with those of SLE and have been described in up to 10% of patients presenting with SLE symptoms [53]. Patients with DIL present usually with arthralgia or arthritis, myalgia, serositis, fever and rash, positive anti-nuclear antibodies and positive antihistone antibodies in over 75% of patients [53]. Positive ds-DNA can be observed in anti-Tumor necrosis factor (TNF) induced DIL [53]. After discontinuation of the drug, resolution of symptoms is commonly observed within weeks or months [53]. Risk factors for DIL are genetic predisposition [e.g human leukocyte antigen (HLA)‒DR4] and low rate of acetylation [53]. A definitive relationship with DIL was considered for procainamide, hydralazine, minocycline, quinidine, isoniazid, terbinafine, methyldopa, dihydralazine, and chlorpromazine [53]. Several other drugs have a probable or possible association [53].
N-acetyltransferase: the practical consequences of polymorphic activity in man
Published in Xenobiotica, 2020
The related antihypertensives, dihydralazine and endralazine, owing to their structural similarity to hydralazine, have been shown to undergo polymorphic N-acetylation but there was only a slight dissimilarity between the phenotypes with no significant differences in half-life (Reece et al., 1982; Waller et al., 1979). Endrazaline metabolism has been stated as being largely independent of the patient’s acetylator status (Quyyumi et al., 1983) but toxicity may be mediated via Phase I metabolites (Bourdi et al., 1994). Aminoglutethimide was introduced into medical usage as an anticonvulsant in the 1960s but was withdrawn a few years later owing to toxicity. A major metabolite is an N-acetylated derivative (Coombes et al., 1982; Goss et al., 1985) but acetylation does not appear to be associated with adverse events.