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Advanced Therapeutic Options in Acute Heart Failure
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Tiffany Dong, Aditi Nayak, Alanna Morris
With increasing diuretic use, many patients will develop diuretic resistance, which occurs when congestion persists despite diuretic therapy. The pathophysiology of diuretic resistance includes cell hypertrophy in the connecting tubule and collecting ducts of the kidney that may be driven by the renin-angiotensin and sympathetic systems.4 In these cases, adding a thiazide diuretic, such as chlorothiazide, or a thiazide-like diuretic, like metolazone, may be beneficial. The combination of a loop with a thiazide for diuresis is termed “dual nephron blockade,” as the thiazide blocks the sodium-chloride transporter in the ascending limb and distal tubule while the loop diuretic blocks the sodium, chloride, and potassium cotransporter of the loop of Henle. The combined effect leads to improved natriuresis.5
Cardiovascular Risk Factors
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
In contrast to sodium, minimally processed foods largely contain the nutrient, potassium. Potassium regulation within the body thus is not as important for physiologic responses as the body’s physiology system would have relied on steady intake through the diet. Interestingly, potassium supplementation or high dietary intake can promote natriuresis, loss of sodium within urine.
Hypertension
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Fenoldopam is a peripheral dopamine-1 agonist. It causes natriuresis, and systemic and renal vasodilation. The drug has a quick onset and a short half-life, so it is a good alternative to nitroprusside. Fenoldopam also does not cross the blood-brain barrier. Via IV infusion, the drug is titrated upward every 15 minutes to reach its maximum dose. Nitroglycerin affects the veins mostly, but also the arterioles. It can manage hypertension during and following acute MI, coronary artery bypass graft surgery, acute pulmonary edema, and unstable angina pectoris. If given IV, nitroglycerin is preferred over nitroprusside for severe CAD since nitroglycerin increases coronary flow. Doses are titrated upward every 5 minutes to achieve a maximal antihypertensive effect. Nitroglycerine must be used with other drugs to achieve long-term BP control. In about 2% of patients, a headache is the most common adverse effects. Other effects include nausea, vomiting, tachycardia, apprehension, muscular twitching, palpitations, and restlessness.
Inhibition of endoplasmic reticulum stress restores the balance of renal RAS components and lowers blood pressure in the spontaneously hypertensive rats
Published in Clinical and Experimental Hypertension, 2023
Jun Zhu, Anjing Shao, Chunyan Wang, Chensi Zeng, Hongyong Wang
Recent studies have shown that the activation of ER stress signaling pathways is closely related to the occurrence and development of hypertension (20). Inhibition of ER stress can stabilize protein conformation and promote the transfer of unfolded or misfolded proteins out of the endoplasmic reticulum (21), suggesting that inhibiting ER stress signaling may be an important target for hypertension treatment (22). The mechanisms by which ER stress contributes to hypertension are still being investigated. In the present study, we found that ER stress contributes to impaired natriuresis and diuresis in hypertension. The main findings of this study are as follows: (1) ER stress inhibitor, 4-PBA, decreased blood pressure in SHRs; (2) natriuretic function was impaired in SHRs and inhibition of ER stress improved renal sodium excretion function; (3) renal RAS components were imbalance in SHRs, which were restored by treatment of 4-PBA; and (4) 4-PBA decreased ER stress and oxidative stress, which was associated with the improvement of imbalance of renal RAS components in SHRs. These results suggest that increased ER stress is responsible for the imbalance of renal RAS components and impaired natriuresis and diuresis in SHRs, which were restored by 4-PBA treatment.
The anti-hypertensive effects of sodium-glucose cotransporter-2 inhibitors
Published in Expert Review of Cardiovascular Therapy, 2023
Luxcia Kugathasan, Lisa Dubrofsky, Andrew Advani, David Z.I. Cherney
It has been postulated that natriuresis, in part, may contribute to the SGLT2 mediated anti-hypertensive effect. Specifically, an acute and transient increase in natriuresis is observed in the early stages of SGLT2 inhibition [71]. Maximal natriuresis is reported within the first 3 days of treatment and eventually returns to baseline over time. Partially by the process of osmoregulation, acute sodium excretion is accompanied by a sustained 7.3% plasma volume contraction, as observed in patients following 8 weeks of dapagliflozin treatment [72,73]. Although the exact mechanisms outlining the transient nature of natriuresis are still unclear, it may be explained by way of a compensatory increase in distal tubule sodium reabsorption to offset the initial increase in sodium excretion at the proximal tubule and may suggest minimal contribution of natriuresis to BP reduction. Despite this, an acute increase in urinary sodium excretion by 10–20% was demonstrated in patients with T2D in response to SGLT2 inhibitor therapy, emphasizing a potential role for natriuresis [74].
Short-term effect of angiotensin-converting enzyme inhibitor on retinal vessel diameter in patients with systemic hypertension
Published in Cutaneous and Ocular Toxicology, 2022
Nazife Aşıkgarip, Emine Temel, Kemal Örnek, Ahmet Kıvrak
To date, the exact mechanism of ACE inhibitors has not been fully understood yet. These drugs interfere with the renin-angiotensin-aldosterone system (RAS), but their effect is not directly related to the renin levels in the blood. As the name indicates, ACE inhibitors prevent the conversion of angiotensin I to angiotensin II. Decreased production of angiotensin II enhances natriuresis, lowers blood pressure, and prevents remodelling of smooth muscle and cardiac myocytes. Also, the hypothesis is that ACE inhibitors interfere with the degradation of bradykinin, a peptide that causes vasodilation4. Previous studies have shown that the components of RAS are also found in the retina. Therefore, it can be proposed that the use of ACE inhibitors may cause changes in the retinal vessel diameters.