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The Treatment of Hypertension with Nutrition, Nutritional Supplements, Lifestyle and Pharmacologic Therapies
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Nebivolol (vasodilating and increases nitric oxide) and carvedilol (an alpha-/beta-blocker with antioxidant activity) are the BB of choice. One should avoid other older BB for hypertension as they do not reduce CVD or CHD compared to the other antihypertensive agents. Renin inhibitors (DRI) are appropriate for add-on treatment but should not be given with an ACEI or an ARB. An ACEI should not be administered with an ARB. Spironolactone 12.5–25 mg QD is very effective in resistant hypertension or in patients with LRH or those with the genetic SNP CYP11 B2. Amiloride 5–20 mg/day is very effective in patients with hyperactive epithelial sodium channel with a genetic SNP CYP4A11 or LRH.
The Renin-Angiotensin System
Published in Austin E. Doyle, Frederick A. O. Mendelsohn, Trefor O. Morgan, Pharmacological and Therapeutic Aspects of Hypertension, 2020
When a constant amount of dog renin was added to the plasma of animals nephrec-tomized 24 and 48 hr previously, the rate of angiotensin-I generation increased independently of renin substrate580 (Figure 76). In addition, it was found that normal plasma would inhibit the reaction between dog renin and nephrectomized-dog plasma. These observations led to a search for a renin inhibitor in kidney.580,584 A phospholipid was isolated from dog kidney which inhibited dog renin in vitro and reduced its pressor effects in nephrectomized rats. The inhibitor resembled, but was not identical to, phosphatidyl serine in that it contained a β-hydroxy α-amino acid that was neither serine nor threonine, and it had an unusually high content of a fatty acid migrating on GLC as arachadonic acid. The compound was subsequently found to be a precursor of a more active lysophospholipid which could be produced by the action of phospholipase A on the “preinhibitor’’.580
Cardiovascular Medications in Pregnancy
Published in Afshan B. Hameed, Diana S. Wolfe, Cardio-Obstetrics, 2020
One of the causes of morbidity and mortality in pregnant women and their fetus is heart failure. However, due to its nonspecific symptoms, it is sometimes difficult to diagnose. Women experience swelling to their lower extremities, dyspnea on exertion, and fatigue, but all of these symptoms can be considered normal in pregnancy [4]. Patient complaints need to be assessed carefully based on the heart failure guidelines. Once it is diagnosed, the management is not significantly different from patients who are not pregnant, except teratogenic medications need to be avoided. The goal of managing heart failure is improving prognosis and symptoms. Heart failure should be treated according to guidelines on acute and chronic heart failure. During pregnancy, ACE inhibitors, ARBs, and renin inhibitors are contraindicated because of fetotoxicity.
An international multicenter observational non-interventional prospective study of the efficacy of azilsartan medoxomil in overweight or obese patients with arterial hypertension (CONSTANT)
Published in Current Medical Research and Opinion, 2021
Irina E. Chazova, Yulia V. Zhernakova
The primary goal of antihypertensive therapy is to maintain BP at target levels of < 140/90 mmHg (or, in accordance with the recommendations relevant at the time of the initiation of the study, < 140/85 mmHg for patients with DM). Despite the significant expansion of the number of antihypertensive drugs, the problem of effective BP control remains relevant14,15. In particular, according to the results of an ESSE-RF epidemiological study, only half of Russian patients achieve the target BP during antihypertensive treatment15. One of the mechanisms for BP control involves RAAS, which can be affected by ACE inhibitors, angiotensin II receptor blockers, aldosterone antagonists, and direct renin inhibitors16. In this study, which was the first major observational international study of real clinical practice in the Russian Federation and in the Republic of Kazakhstan, azilsartan medoxomil showed high efficacy in monotherapy or as a part of combination therapy with other antihypertensive drugs. This is consistent with the results of other studies.
Aliskiren and valsartan in combination is a promising therapy for hypertensive renal injury in rats
Published in Clinical and Experimental Hypertension, 2018
In the present study, aliskiren at the dose used was found to produce renoprotection. Concern has been raised that treatment with aliskiren might induce renal tissue damage by activating the (pro)renin receptor [(P)RR], which might be a limiting factor to the protective effects of renin inhibitors. The possible explanation and relationship between renoprotection of aliskiren and the function of the (P)RR and its implication in renal disease was studied by Feldman et al. (6). In situ hybridization indicates that aliskiren-induced suppression of gene expression of (P)RR in vivo. However, incubation of aliskiren with mesangial cells in vitro did not alter gene expression of (P)RR in these cells, arguing against a direct effect of aliskiren on the (P)RR expression in vivo. This lack of in vitro effect may reflect the absence of physiological mechanisms that may be required for aliskiren to indirectly reduce the (P)RR expression in vivo; possibly by (1) reducing renal/plasma Ang II levels (2), increasing renal/plasma (pro) renin levels (3), recruiting intracellular promyelocytic zinc finger, or simply (4) by lowering BP.
Evidence for angiotensin mediation of the late histopathological effects of pulmonary fat embolism: Protection by losartan in a rat model
Published in Experimental Lung Research, 2018
Alan Poisner, Devin Bass, Amanda Fletcher, Ashwin Jain, Janessa Pennington England, Mariah Gawlik Davis, Dauod Arif, Agostino Molteni
These results support our previous suggestion that the use of angiotensin blockade in clinical situations where FE is suspected would be beneficial3 and our studies with the renin inhibitor aliskiren4 suggest that renin blockade may also be of clinical benefit. The increase in renin staining that we found at 6 weeks after triolein also support this view17 In addition, based on our studies on the second hit effects of LPS, it is possible that in other cases of chronic or acute respiratory distress, an initial respiratory insult or trauma may have occurred in the recent or more distant past. As evidenced by the widespread undiagnosed incidence of fat embolism,1 trauma long forgotten may be a precursor of respiratory distress. Thus current respiratory clinical symptoms may be a result of a second hit and also benefit from pharmacological intervention in the renin-angiotensin system.