Pharmacodynamics and pharmacokinetics
The active substance directly affects the imidazoline receptors of the central nervous system located in the medulla oblongata . This leads to a decrease in sympathetic activity. With. , and blood pressure decreases.
Due to the fact that imidazole has low affinity for alpha-adrenergic receptors , such common side effects as dry mucous membranes and pronounced sedation practically do not occur.
Depending on food intake, within an hour after administration, the maximum concentration of the active substance in the blood is observed. About 7% is bound to plasma proteins . In the body it is metabolized into guanine and 4,5-dihydromoxonidine (they are eliminated within 5 hours). Moxonidine itself is excreted within 24 hours, mainly by the kidneys.
Pharmacokinetic parameters change in liver and kidney diseases and slightly in elderly people.
Physiotens
Centrally acting antihypertensive drug.
Moxonidine is an antihypertensive agent with a central mechanism of action. In the brain stem structures (rostral layer of the lateral ventricles), moxonidine selectively stimulates imidazoline-sensitive receptors that take part in the tonic and reflex regulation of the sympathetic nervous system. Stimulation of imidazoline receptors reduces peripheral sympathetic activity and blood pressure.
Moxonidine differs from other sympatholytic antihypertensive drugs in its lower affinity for α2-adrenergic receptors, which explains the lower likelihood of developing sedation and dry mouth.
The use of moxonidine leads to a decrease in systemic vascular resistance and blood pressure. The hypotensive effect of moxonidine has been confirmed in double-blind, placebo-controlled, randomized studies.
The results of a clinical study involving 42 patients with arterial hypertension and left ventricular hypertrophy demonstrated that, with a similar reduction in blood pressure, the use of a combination of angiotensin II receptor antagonists with moxonidine can reduce left ventricular hypertrophy to a greater extent compared with a free combination of a thiazide diuretic and a slow calcium channel blocker ( 15% versus 11%; p<0.05).
Moxonidine improves insulin sensitivity index by 21% (compared to placebo) in obese patients with insulin resistance and moderate hypertension.
Pharmacokinetics
Suction
After oral administration, moxonidine is rapidly and almost completely absorbed from the upper gastrointestinal tract. Absolute bioavailability is approximately 88%, indicating no significant first pass effect through the liver.
The time to reach Cmax is about 1 hour. Food intake does not affect the pharmacokinetics of the drug.
Distribution
Plasma protein binding is 7.2%.
Metabolism
The main metabolite of moxonidine is dehydrogenated moxonidine. The pharmacodynamic activity of dehydrogenated moxonidine is about 10% compared to moxonidine.
Removal
T1/2 of moxonidine and metabolite is 2.5 and 5 hours, respectively. Within 24 hours, more than 90% of moxonidine is excreted by the kidneys (about 78% unchanged and 13% as dehydriromoxonidine, other metabolites in the urine do not exceed 8% of the dose taken). Less than 1% of the dose is excreted through the intestines.
Pharmacokinetics in special clinical situations
Compared with healthy volunteers, patients with arterial hypertension show no changes in the pharmacokinetics of moxonidine.
Clinically insignificant changes in the pharmacokinetic parameters of moxonidine were noted in elderly patients, probably due to a decrease in the intensity of its metabolism and/or slightly higher bioavailability.
Moxonidine is not recommended for use in patients under the age of 18 years, and therefore pharmacokinetic studies have not been conducted in this group.
Moxonidine excretion is significantly correlated with CC. In patients with moderate renal failure (creatinine clearance 30-60 ml/min), steady-state plasma concentrations and final T1/2 are approximately 2 and 1.5 times higher than in individuals with normal renal function (creatinine clearance more than 90 ml/min). In patients with severe renal failure (creatinine clearance less than 30 ml/min), steady-state plasma concentrations and final T1/2 are 3 times higher than in patients with normal renal function. The administration of multiple doses of moxonidine leads to predictable accumulation in the body of patients with moderate to severe renal failure. In patients with end-stage renal failure (creatinine clearance less than 10 ml/min) on hemodialysis, steady-state plasma concentrations and final T1/2 are 6 and 4 times higher, respectively, than in patients with normal renal function. In patients with moderate renal failure, the Cmax of moxonidine in the blood plasma is 1.5-2 times higher. In patients with impaired renal function, the dose should be adjusted individually.
Moxonidine is excreted to a small extent during hemodialysis.
Analogues of Physiotenza
Level 4 ATC code matches: Tenzotran
Moxonitex
Albarel
Moxonidine
Clonidine
The most common analogue of Physiotens is a drug called moxogama . It contains the same active ingredient.
Other analogues: tenaxum, clonidine (various productions), estupik .
Physiotenza price (where to buy)
The price of Physiotenza with a dosage of 0.4 mg is about 420 rubles for 14 pieces. The cost of the same amount of 0.2 mg is 266 rubles.
- Online pharmacies in RussiaRussia
- Online pharmacies in KazakhstanKazakhstan
ZdravCity
- Physiotens tablets p.p.o.
0.4 mg 28 pcs. JSC Nobel Almaty Pharmaceutical Factory/JSC VEROPHARM 830 rub. order - Physiotens film-coated tablets 0.2 mg No. 28AO Veropharm
RUR 549 order
- Physiotens tab. p/o captivity. 0.4 mg 14 pcs. JSC Veropharm
440 rub. order
- Physiotens tab. p/o captivity. 0.4 mg 28 pcs. JSC Veropharm
RUR 876 order
- Physiotens film-coated tablets 0.2 mg No. 14AO Veropharm
RUB 283 order
Pharmacy Dialogue
- Physiotens tablets 0.2 mg No. 28Nobel Almatinksaya FF/Veropharm
RUR 574 order
- Physiotens tablets 0.4 mg No. 28Nobel Almatinksaya FF/Veropharm
RUB 885 order
- Physiotens tablets 0.2 mg No. 28Maylan
RUR 579 order
- Physiotens tablets 0.4 mg No. 14Nobel Almatinksaya FF/Veropharm
450 rub. order
- Physiotens tablets 0.2 mg No. 14Rottendorf/Maylan
RUB 281 order
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PHYSIOTENZ COATED TAB 0.4 MG N14
Suction
After oral administration, moxonidine is rapidly and almost completely absorbed from the upper gastrointestinal tract. Absolute bioavailability is approximately 88%, indicating no significant first-pass effect.
The time to reach maximum concentration is about 1 hour. Food intake does not affect the pharmacokinetics of the drug.
Distribution
The binding to plasma proteins is 7.2%.
Metabolism
The main metabolite is dehydrogenated moxonidine. The pharmacodynamic activity of dehydrogenated moxonidine is about 10% compared to moxonidine.
Removal
The half-life (T1/2) of moxonidine and metabolite is 2.5 and 5 hours, respectively. Within 24 hours, over 90% of moxonidine is excreted by the kidneys (about 78% unchanged and 13% as dehydriromoxonidine, other metabolites in the urine do not exceed 8% of the dose taken). Less than 1% of the dose is excreted through the intestines.
Pharmacokinetics in patients with arterial hypertension
Compared with healthy volunteers, patients with arterial hypertension show no changes in the pharmacokinetics of moxonidine.
Pharmacokinetics in old age
Clinically insignificant changes in the pharmacokinetic parameters of moxonidine were noted in elderly patients, probably due to a decrease in the intensity of its metabolism and/or slightly higher bioavailability.
Pharmacokinetics in children
Moxonidine is not recommended for use in persons under 18 years of age, and therefore no pharmacokinetic studies have been conducted in this group.
Pharmacokinetics in renal failure
Moxonidine excretion is significantly correlated with creatinine clearance (CC). In patients with moderate renal failure (creatinine clearance in the range of 30–60 ml/min), steady-state plasma concentrations and final T1/2 are approximately 2 and 1.5 times higher than in individuals with normal renal function (creatinine clearance more than 90 ml/min). min).
In patients with severe renal failure (creatinine clearance less than 30 ml/min), steady-state plasma concentrations and final T1/2 are 3 times higher than in patients with normal renal function.
The administration of multiple doses of moxonidine leads to predictable accumulation in the body of patients with moderate and severe renal failure.
In patients with end-stage renal failure (creatinine clearance less than 10 ml/min) on hemodialysis, steady-state plasma concentrations and final T1/2 are 6 and 4 times higher, respectively, than in patients with normal renal function. In patients with moderate renal failure, the maximum concentration of moxonidine in the blood plasma is 1.5–2 times higher. In patients with impaired renal function, the dosage should be adjusted individually. Moxonidine is excreted to a small extent during hemodialysis.
