LOSARTAN (tablets)
Bisoprolol is also used for increased heart rate.
When I came to prescribe free medications in May of this year, Lorista was not available in pharmacies. I bought it in cash for two months. In July there was no Lorista or Amlodipine again. That's why they prescribed me this drug. Pranafarm Losartan tablets are an antihypertensive drug. Now I take it twice a day, one tablet in the morning and in the evening. And as an ambulance, just in case, I always have drugs such as Capoten or Captopril. Losartan tablets are sold in red and white cardboard packaging, which contains the minimum necessary information, such as a description of the tablets. Of course, it should be used only as prescribed by a doctor. There is a warning about the lactose content in the drug, because some people are intolerant. And of course there are storage conditions.
The active component of this medication is potassium salt. The manufacturer's details are also indicated on the packaging.
The release date, expiration date and series are embossed on the side.
The package contains three foil blisters of 10 tablets each. I have already started taking the second package.
On the reverse side is the name and description of the drug.
The tablets themselves are white, round in shape with a scoring line.
The instructions for use included in the package are quite extensive, so I’ll highlight only the most important things.
I also draw your attention to contraindications.
And a whole bunch of side effects are described (the photo may be deleted by the moderators). If you make a list of contraindications, you get 78 points.
The medicine can be taken both before and AFTER meals, that is, regardless of the time of meal. If necessary, you can gradually increase the dose. BUT!!! it should not exceed 100 milligrams per day. It turns out that I was immediately prescribed the maximum. For people with chronic heart failure, the standard maintenance dose of this drug is 50 milligrams, taken once a day. I accept the second package. The pressure remains even slightly lower. You probably need to reduce the dose. I don't really feel any side effects. Yes, there is drowsiness, but I have the opportunity to lie down with my grandson during the day)) Of course, I notice tachycardia and increased heart rate. I had pain in my lower extremities and back before. In general, of course, we all know that no medicine is 100% useful. As they say, “We treat one thing, we cripple another.” Nevertheless, you need to take it. I recommend, but with caution and only as prescribed by your doctor. The cost of the drug in our pharmacies is around 300 rubles. I will give the drug four stars, as there are a lot of side effects indicated. Health to everyone and once again health!!! Thanks for reading. With respect to you, the author of this review, Tatyana. See you again on the site!!!
Losartan
Mechanism of action
Angiotensin II is a powerful vasoconstrictor, the main active hormone of the renin-angiotensin-aldosterone system (RAAS), as well as a decisive pathophysiological link in the development of arterial hypertension (AH). Angiotensin II binds to AT1 receptors found in many tissues (vascular smooth muscle, adrenal glands, kidneys and heart) and performs several important biological functions, including vasoconstriction and aldosterone release. In addition, angiotensin II stimulates the proliferation of smooth muscle cells. AT2 receptors are the second type of receptor to which angiotensin II binds, but its role in regulating cardiovascular function is unknown.
Losartan is a selective antagonist of angiotensin II AT1 receptors, highly effective when taken orally. Losartan and its pharmacologically active carboxylated metabolite (E-3174), both in vitro and in vivo, block all physiological effects of angiotensin II, regardless of its source or route of synthesis. Unlike some peptide angiotensin II antagonists, losartan does not have agonist properties.
Losartan selectively binds to AT1 receptors and does not bind to or block receptors of other hormones and ion channels that play an important role in regulating the function of the cardiovascular system. In addition, losartan does not inhibit angiotensin-converting enzyme (ACE, kininase II), which is responsible for the destruction of bradykinin. Therefore, effects not directly related to AT1 receptor blockade, such as increased bradykinin-mediated effects or the development of edema (losartan 1.7%, placebo 1.9%), are not related to the action of losartan.
Losartan suppresses the increase in systolic and diastolic blood pressure (BP) during angiotensin II infusion. At the moment of reaching the maximum concentration of losartan in the blood plasma (Cmax) after taking losartan at a dose of 100 mg, the above effect of angiotensin II is suppressed by approximately 85%, and 24 hours after single and multiple doses - by 26-39%.
During the period of taking losartan, elimination of the negative feedback, which consists in the suppression of renin secretion by angiotensin II, leads to an increase in plasma renin activity (PRA). An increase in ARP leads to an increase in the concentration of angiotensin II in the blood plasma. With long-term (6-week) treatment of patients with hypertension with losartan at a dose of 100 mg/day, a 2-3-fold increase in the concentration of angiotensin II in the blood plasma was observed at the time the losartan Cmax was reached. Some patients experienced an even greater increase in angiotensin II concentrations. especially with a short duration of treatment (2 weeks). Despite this, during treatment, an antihypertensive effect and a decrease in plasma aldosterone concentrations appeared after 2 and 6 weeks of therapy, indicating effective blockade of angiotensin II receptors. After discontinuation of losartan, ARP and angiotensin II concentrations decreased within 3 days to the values observed before the start of losartan administration. Since losartan is a specific antagonist of angiotensin II AT1 receptors, it does not inhibit ACE (kininase II), an enzyme that inactivates bradykinin. A study comparing the effects of losartan at doses of 20 mg and 100 mg with the effects of an ACE inhibitor on angiotensin I, angiotensin II and bradykinin showed that losartan blocked the effects of angiotensin I and angiotensin II without affecting the effects of bradykinin. This is due to the specific mechanism of action of losartan. The ACE inhibitor blocked responses to angiotensin I and increased the severity of the effects due to the action of bradykinin, without affecting the severity of the response to angiotensin II. which demonstrates the pharmacodynamic difference between losartan and ACE inhibitors. Plasma concentrations of losartan and its active metabolite, as well as the antihypertensive effect of losartan, increase with increasing dose of the drug. Since losartan and its active metabolite are angiotensin II receptor antagonists (ARA II), they both contribute to the antihypertensive effect.
In a study with a single dose of 100 mg of losartan, which included healthy volunteers (men), oral administration of the drug under high- and low-salt diets did not affect the glomerular filtration rate (GFR), effective renal plasma flow and filtration fraction. Losartan had a natriuretic effect that was more pronounced with a low-salt diet and did not appear to be associated with suppression of early sodium reabsorption in the proximal renal tubules. Losartan also caused a transient increase in renal excretion of uric acid.
In patients with hypertension, proteinuria (at least 2 g/24 hours), without diabetes mellitus and taking losartan for 8 weeks at a dose of 50 mg with a gradual increase to 100 mg, a significant decrease in proteinuria (by 42%) and fractional excretion of albumin was observed and immunoglobulins (lgG). In these patients, losartan stabilized GFR and reduced the filtration fraction.
In postmenopausal women with hypertension who took losartan at a dose of 50 mg for 4 weeks, there was no effect of therapy on the renal and systemic levels of prostaglandins.
Losartan does not affect autonomic reflexes and does not have a long-term effect on the concentration of norepinephrine in the blood plasma.
In patients with hypertension, losartan in doses up to 150 mg/day did not cause clinically significant changes in the concentration of fasting triglycerides, total cholesterol and high-density lipoprotein cholesterol. At the same doses, losartan had no effect on fasting blood glucose concentrations.
The HEAAL clinical trial to evaluate the effect of high and low doses of ARB II (losartan) on the outcome of treatment in patients with chronic heart failure (CHF) included patients (n=3834) with CHF (II-IV functional class according to the NYHA classification) and intolerance to inhibitors APF. Patients were followed for more than 4 years (median follow-up 4.7 years) to compare the effects of losartan 50 mg/day and 150 mg/day on reducing all-cause mortality or hospitalization for heart failure. This study showed that losartan 150 mg/day significantly reduced the risk of all-cause mortality or hospitalization for heart failure compared with losartan 50 mg/day (hazard ratio [HR] 0.899, P = 0.027).
In general, losartan caused a decrease in serum uric acid concentrations (usually less than 0.4 mg/dL) that persisted during long-term treatment. In controlled clinical studies involving patients with hypertension, no cases of drug withdrawal due to an increase in creatinine concentration or serum potassium levels were recorded.
A 12-week parallel study, which included patients with left ventricular failure (NYHA functional class II-IV), most of whom were taking diuretics and/or cardiac glycosides, compared the effects of losartan at doses of 2.5, 10, 25 and 50 mg/day with placebo. At doses of 25 and 50 mg/day, the drug exhibited positive hemodynamic and neurohormonal effects, which persisted throughout the study. Hemodynamic effects included an increase in cardiac index and a decrease in pulmonary capillary wedge pressure, as well as a decrease in total peripheral vascular resistance, mean systemic blood pressure, and heart rate. The incidence of arterial hypotension in these patients depended on the dose of the drug. Neurohormonal effects included decreased concentrations of aldosterone and norepinephrine in the blood.
Use during pregnancy and children
The drug Giposart is contraindicated for use during pregnancy, because it has a direct effect on the RAAS and can cause developmental disorders of the fetus (especially in the second and third trimesters of pregnancy) or have a negative effect on the newborn, including death, if the drug was used during pregnancy.
It is known that therapy with angiotensin II receptor antagonists (ARA II) can cause fetal developmental disorders (impaired renal function, oligohydramnios, delayed ossification of the skull bones) and the development of complications in the newborn (renal failure, arterial hypotension, hyperkalemia). If the fact of pregnancy is established, the drug Giposart must be discontinued as quickly as possible.
When planning pregnancy, it is necessary to transfer the patient to adequate alternative therapy.
It is not known whether candesartan is excreted in breast milk, but it is known to be excreted in the milk of lactating rats.
During treatment with Hyposart, breastfeeding should be stopped. Newborns whose mothers took Hyposart during pregnancy should be under close medical supervision due to the likelihood of developing arterial hypotension.
Use in children
The use of the drug is contraindicated in children and adolescents under 18 years of age (efficacy and safety have not been established).
Contraindications for use
- Hypersensitivity to candesartan or other components of the drug;
- lactose intolerance, lactase deficiency, glucose-galactose malabsorption syndrome;
- pregnancy;
- breastfeeding period;
- children and adolescents under 18 years of age (efficacy and safety have not been established);
- severe liver dysfunction and/or cholestasis;
- simultaneous use with aliskiren and aliskiren-containing drugs in patients with diabetes mellitus or impaired renal function (GFR less than 60 ml/min).
With caution: severe renal dysfunction (creatinine clearance less than 30 ml/min), hemodialysis, bilateral renal artery stenosis or stenosis of the artery of a single kidney, hemodynamically significant stenosis of the aortic and/or mitral valve, hypertrophic obstructive cardiomyopathy (HOCM), condition after kidney transplantation, cerebrovascular disorders of ischemic origin and ischemic heart disease, hyperkalemia in patients with reduced blood volume, general anesthesia and surgical interventions (risk of developing arterial hypotension due to blockade of the RAAS), primary hyperaldosteronism.
