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Drugs and Therapeutics
Published in James Sherifi, General Practice Under the NHS, 2023
Angiotensin receptor blockers (ARBs) work further down the angiotensin-rennin pathway and have the advantage of not causing cough, although, unlike ACE inhibitors, they have not been shown to reduce cardiac mortality. Nifedipine—1967, AmlodipineAngina, Hypertension, Chilblains Nifedipine was developed by Bayer and introduced to the UK market in the mid-1970s for the treatment of angina and hypertension. The drug had a cumbersome thrice-daily dosing regimen, leaving it wide open for replacement. This took a surprisingly long time to happen, until 1989, when once-daily amlodipine (Pfizer) came to market, with others including lacidipine, lercanidipine, and felodipine. Amlodipine came off patent in 2007, after which it pretty much had the market to itself.
Regulation of Arterial Blood Pressure
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The renin–angiotensin system is the most important renal–body fluid mechanism and, therefore, long-term blood pressure control. A decrease in arterial blood pressure causes a decrease in renal perfusion which is sensed by mechanoreceptors in the afferent arterioles of the kidneys. This results in renin secretion by the juxtaglomerular cells. Renin catalyses the conversion of angiotensinogen to angiotensin I in plasma. In the lungs and kidneys, angiotensin I is converted to angiotensin II. Angiotensin II activates G-protein-coupled angiotensin receptors (AT1) in adrenal cortex, vascular smooth muscle, kidneys and brain. Angiotensin II acts on the zona glomerulosa of the adrenal cortex to synthesize and secrete aldosterone. Aldosterone acts on the principal cells of the collecting duct to increase absorption and thereby increase blood and extracellular fluid (ECF) volume. Angiotensin II also stimulates the Na+/H+ exchanger in the proximal tubule of the kidneys and increases the reabsorption of Na+ and HCO3−. Angiotensin II also acts on the hypothalamus to increase thirst and water intake and stimulates ADH release, which increases water reabsorption in the collecting ducts. Angiotensin II binds to G-protein-coupled receptors on arterioles and activate the IP3/Ca++ second messenger system to cause vasoconstriction. The resulting increase in total peripheral resistance leads to an increase in arterial blood pressure.
The development of hypertension in transgenic rats, TGR (mREN2)27
Published in H. Saito, Y. Yamori, M. Minami, S.H. Parvez, New Advances in SHR Research –, 2020
Jörg Peters, Detlev Ganten, John J. Mullins
Angiotensin-converting enzyme inhibitors (Captopril, Lisinopril), and ATI-specific angiotensin antagonists (Losartan), were very effective at reducing the blood pressure of TGR (mREN2) 27 rats (Mullins et al., 1990; Bader et al., 1992; Barrett and Mullins, 1992). Oral administration of Captopril or Losartan, at doses as low as 10mg/kg BW reduced systolic blood pressure by at least 50 mmHg within 1 week. A single dose of captopril ( 1 mg/kg Bw ), when given intraperitoneally, reduced the diastolic blood pressure from 160 mmHg to Sprague Dawley control levels (105 mmHg) within 60 minutes. This demonstrates, that the generation of ANG II and its interaction with angiotensin receptors (ATI) are a prerequisite for the hypertensive phenotype.
Local renin-angiotensin system molecular mechanisms in intrauterine adhesions formation following gynecological operations, new strategy for novel treatment
Published in Journal of Obstetrics and Gynaecology, 2022
Sheida Shabanian, Majid Khazaie, Gordon A. Ferns, Mohammad-Hassan Arjmand
Renin-Angiotensin System (RAS) as an endocrine system plays a critical role in regular electrolytes, vascular resistance, and blood volume. RAS contains several peptides. Renin, an aspartic protease produced by the kidney, cleavage angiotensinogen to generate angiotensin I (Ang I), a 10 amino acids molecules, and then angiotensin convert enzyme (ACE) convert Ang I to angiotensin II (AngII), the main active peptide in the RAS, that exerts its actions by binding to angiotensin receptors (Kurdi et al. 2005). Angiotensin receptor types 1 and 2 (ATR1 and 2) mediate the actions of AngII and belong to trans-membrane G-protein (Aplin et al. 2009). Interactions between AngII and AT1R lead to increase cell proliferation, vasodilation, and activation signalling to stimulates organ fibrosis (Filippatos et al. 2001). Also, besides AngII and angiotensin receptors type 1 and 2, other components including Ang1-7, ACE2, and Mas receptors have been identified in the RAS system (Kibel et al. 2015).
Evaluation of pathophysiological relationships between renin-angiotensin and ACE-ACE2 systems in cardiovascular disorders: from theory to routine clinical practice in patients with heart failure
Published in Critical Reviews in Clinical Laboratory Sciences, 2021
Alberto Aimo, Giuseppe Vergaro, Claudio Passino, Aldo Clerico
An integrated approach that includes the biochemical pathways and physiological activities related to the RAS, NP, ACE/ACE2, and NEP systems is summarized in Figure 2. The pathophysiological effects of the RAS are mainly mediated by three different receptors (i.e. AT-1, AT-2, and Mas), which share different affinity and specificity for binding the active peptides, Angio-II and Angio-(1-7) [24,25,86,126,127]. Angiotensin receptor type I (AT-1) and II (AT-2) are seven-transmembrane G protein-coupled receptors that have a similar affinity for Angio-II, even though these two receptor proteins have a sequence homology of only 34% [128–132]. However, activation of both receptors is likely to stimulate different signaling mechanisms/pathways and produce distinct and often antagonistic biological responses (Figure 2).
Long-term amlodipine-based combination therapy attenuates seasonal variation of blood pressure in hypertensive patients
Published in Clinical and Experimental Hypertension, 2021
Hua-song Xia, Yue Liu, Ju-xiang Li, Hai Su, Yan-qing Wu
Previously, a few studies showed that some antihypertensive drugs, such as metoprolol and carvedilol could alleviate the BP responses to cold exposure (13,14), but little is known about the effect of various antihypertensive drugs on seasonal BP variation. At present, a lot of hypertensive patients need combination regimens for BP control (15). Calcium channel blockers (CCBs) and diuretics are widely used in China. The combination therapy with CCB+diuretics was effective in high-risk patients (16). Angiotensin receptor blockers (ARBs) are also in common use, especially for patients intolerant to ACEI. When they are used in combination with CCB, the peripheral edema caused by the latter can be offset. Both combination regimens have better efficacy and tolerance, however, no research was found to compare the effect of these two combination regimens on seasonal BP variation in hypertensive patients.