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The Journal publishes articles on basic or clinical research relating to nephrology, arterial hypertension, dialysis and kidney transplants. It is governed by the peer review system and all original papers are subject to internal assessment and external reviews. The journal accepts submissions of articles in English and in Spanish languages. The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two receding years.

CiteScore measures average citations received per document published. Read more. SRJ is a prestige metric based on the idea that not all citations are the same. SJR uses a similar algorithm as the Google page rank; it provides a quantitative and qualitative measure of the journal's impact.

SNIP measures contextual citation impact by wighting citations based on the total number of citations in a subject field. These, are characterized by a smaller oral availability, a fast vasodilator action and a short duration of action. Manidipine arises as a dihydropyridine calcium antagonist of third generation with real additional advantages regarding to previous generations. They show high lipophilia, a more prolonged action and as well as a prolonged average life at the level of his receptor and, in addition, some theoretical advantages among others calcium antagonists, improvements on the renal function by reducing the intraglomerular pressure and microalbuminuria.

Nevertheless, the clinical evaluation of these last properties still depends on the results derived from clinical trials. Besides to go deep in its role in their antihypertensive effect, we presented a brief review on new cardiometabolic aspects of these dihydropyridines calcium antagonists focusing in manidipine..

Hypertension and insulin resistance are the most important risk factors for cardiovascular damage. Some studies 4,5 show that anti-hypertensive treatments that include calcium antagonists improve insulin sensitivity.

In a study of hypertensive patients with type-2 diabetes, the combination of manidipine and delapril showed results similar to those of olmesartan and hydrochlorothiazide as far as reducing arterial pressure, but with fewer changes in orthostatic arterial pressure, as well as fewer adverse metabolic effects.

These data are more interesting for this group of patients, which is especially prone to orthostatic hypotension associated with an increase in morbidity and mortality. Preliminary studies of diabetic patients with uncontrolled hypertension and microalbuminuria suggest that, despite adequate treatment with ACE inhibitors or ARBs, manidipine may be given in combination with the renin-angiotensin inhibitors to normalise blood pressure and urinary excretion of albumin in diabetic patients.

Calcium antagonists constitute a highly heterogeneous class of molecules that may be grouped into phenylalkylamine derivatives, such as verapamil, benzothiazepine derivatives whose prototype is diltiazem, and 1,4-dihydropyridine compounds that include manidipine. The first generation of dihydropyridine calcium channel blockers, such as nifedipine, are characterised by their instant release, their short half-life and their rapid absorption. Despite having a favourable metabolic profile, they present some adverse effects, such as sudden drops in arterial pressure, tachycardia and sympathetic activation.

In the second generation, that includes amongst others, felodipine and isradipine is characterised by a slower molecular release. The latest generation of calcium antagonists, with a long half-life and extended duration of action has shown a clear decrease in arterial pressure and a significant reduction in side effects.

On this subject, a trial with 30 obese hypertensive patients treated with amlodipine, manidipine and cilnidipine revealed that these long-acting calcium antagonists reduce arterial pressure, and in addition, reduce insulin resistance, suggesting important cardio-metabolic properties. Unlike the first calcium antagonists that only blocked L-type channels, third-generation blockers, such as manidipine, lercadipine, amlodipine, nivaldipine or efonidipine, are capable of blocking both L-type and T-type channels, the latter are only active during cellular proliferation.

L-type channels are activated by intense depolarisations, resulting in a prolonged calcium influx in a large variety of cell types. In this way, they play a central role in the contraction of cardiac and smooth muscle cells Cav1.

In the kidney, Cav1. Furthermore, we find other L-type channels in skeletal muscle Cav1. T-channels are expressed in the nervous system Cav3. T-type channels are activated by short depolarisations, which provoke a transitory flow of calcium. In post-glomerular or efferent arterioles, only T-type channels and no L-type channels are expressed and this implies that their tone must be controlled by T channels and AT1 angiotensin II receptors.

Manidipine and lercanidipine block T-type channels in efferent arterioles, thus diminishing the intraglomerular pressure and also the excretion of albumin; at the same time, they block L-type channels, favouring afferent arteriole dilation. In this way, T-type channel antagonists influence renal haemodynamics through their anti-hypertensive action.

Non-haemodynamic action of T-type channel antagonists may have multiple beneficial effects by inhibiting inflammatory processes inhibition of Rho kinase, NF-kB, leukocyte adhesion and blocking the renin-angiotensin system and the sympathetic nervous system. The lipotoxicity hypothesis suggests that in type-2 diabetes the adipose tissue looses the ability to accommodate an excess of calories. The loss of adipocyte differentiation causes the excess of calories to accumulate, mainly in the liver, pancreas and muscle tissue, which contributes to the development of insulin resistance.

Therefore, favouring adipogenesis will contribute to lowering insulin resistance in type-2 diabetics. The improvement of insulin sensitivity gained with dihydropyridine calcium antagonists is almost imperceptible. Nifedipine, only blocks L-type channels, worsens insulin resistance and inhibits the release of glucose. The latter is an indicator of adipogenesis and possibly expressed after induction of the former figure 1.

These results suggest that manidipine increases insulin sensitivity in hypertensive diabetic patients by stimulating the formation of new adipocytes unpublished observations. In addition it has been observed that the increase in intracellular calcium inhibits pre-adipocyte differentiation.

Calcium homeostasis was studied with particular attention to the calreticulin, the principal protein that binds to calcium in the lumen of the endoplasmic reticulum, and which is largely responsible for rapid calcium exchange. A study of stem cells and 3T3-L1 pre-adipocytes shows that calreticulin could modulate adipogenesis by means of a negative feedback mechanism.

The action of manidipine as a calcium channel blocker may prevent calcium from entering the cell thus, decreasing the concentration of calcium in the endoplasmic reticulum and therefore, the concentration of calreticulin, favouring adipocyte differentiation. Oxidative stress plays a fundamental role in the development of atherosclerosis. Several studies demonstrate the beneficial effect of dihydropiridine calcium antagonists on atherosclerotic lesions.

Furthermore, manidipine shows another beneficial effect on atherogenesis, since it inhibits the expression of LOX-1, a low-density lipoprotein receptor induced by angiotensin II.

Treatment with nifedipine or dinitrophenol inhibits the action of the calcitriol, which reveals a mechanism that is dependent on calcium and mitochondrial uncoupling. Therefore, it would seem that blocking calcium channels with manidipine would produce an antioxidant, antiinflammatory effect by lowering the intracellular calcium level.

L-type channels are activated by intense depolarisations that are responsible for the tone of smooth arterial muscle. Ttype channels are activated by short depolarisations, which provoke a transitory flow of calcium. Home Articles in press Archive. ISSN: Previous article Next article.

June Pages DOI: Cardio-metabolic properties of manidipine: beyond lowering arterial pressure?. Download PDF. This item has received. Article information. Palabras clave:. Resistencia a la insulina. Besides to go deep in its role in their antihypertensive effect, we presented a brief review on new cardiometabolic aspects of these dihydropyridines calcium antagonists focusing in manidipine.

Insulin resistance. Calcium antagonists. Obesity: effects on cardiovascular disease and its diagnosis. Board Fam. Association between the number of cardiovascular risk factors and each risk factor level in elementary school children.

Hypertension ; Effects of the long-acting calcium channel blockers, amlodipine, manidipine and cilnidipine on steroid hormones and insulin resistance in hypertensive obese patients. Renal protection in hypertensive patients: selection of antihypertensive therapy. Drugs ; 65 Suppl 2: [Pubmed]. Calcium-antagonist drugs. Concomitant calcium entry blockade and inhibition of the renin-angiotensin system: a rational and effective means for treating hypertension.

Atherosclerosis-related molecular alteration of the human CaV1. A ; [Pubmed]. Physiol Cell Physiol ; CC Trials with manidipine]. Effect of calcium antagonists on glomerular arterioles in spontaneously hypertensive rats. Hypertension ; [Pubmed]. Angiotensin blockade prevents type 2 diabetes by formation of fat cells. Manidipne but not amlodipine , increases insulin sensitivity and rises plasma adiponectin cocentrations in hypertensive non-diabetic patients with metabolic syndrome and impaired fasting glucose.

Diabetologia ; 48 Suppl 1: A Manidipine prevents hepatic C-reactive protein production and reactive oxygen species generation by down-regulation of the age receptor expression, dependent on PPAR-gamma activation. Journal of Hypertension ; SS Manidipine has a marked non-haemodynamic nephroprotective action; Partly dependent on PPAR-gamma activation, and synergistic with angiotensin receptor blockade.

Journal of Hypertension ; S8. Cell Biol. Calreticulin inhibits commitment to adipocyte differentiation. Effects of calcium channel blockers on atherosclerosis: new insights. Acta Cardiol. Ion channels and regulation of intracellular calcium in vascular endothelial cells. Different antioxidative potencies of dihydropyridine calcium channel modulators in various models.

Calcium channel blockades exhibit anti-inflammatory and antioxidative effects by augmentation of endothelial nitric oxide synthase and the inhibition of angiotensin converting enzyme in the N G -nitro-L-arginine methyl ester-induced hypertensive rat aorta: vasoprotective effects beyond the blood pressure-lowering effects of amlodipine and manidipine. Calcium [corrected] channel blockers reduce angiotensin II-induced superoxide generation and inhibit lectin-like oxidized low-density lipoprotein receptor-1 expression in endothelial cells.

Calcitriol and calcium regulate cytokine production and adipocyte-macrophage cross-talk.


Intoxicación por antagonistas del calcio

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