Cyclosporin-induced hypertension Dotaz Zobrazit nápovědu
- MeSH
- antibakteriální látky škodlivé účinky MeSH
- cyklosporin škodlivé účinky MeSH
- hypertenze chemicky indukované komplikace epidemiologie terapie MeSH
- imunosupresiva škodlivé účinky MeSH
- incidence MeSH
- lidé MeSH
- takrolimus škodlivé účinky MeSH
- transplantace orgánů škodlivé účinky MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- antibakteriální látky MeSH
- cyklosporin MeSH
- imunosupresiva MeSH
- takrolimus MeSH
Transplantations of the heart are in recent years the therapeutic method in severe cardiac failure. One of the complications in the long-term follow-up of patients is the development of hypertension. The incidence of hypertension in patients treated with cyclosporin and prednisone is 70-90%. In the development of hypertension participates in addition to classical mechanisms (renin angiotensin system, fluid volume and peripheral resistance) also the negative effect of cardiac denervation, cyclosporin immunosuppression, corticoids and nephropathy. The nocturnal drop of pressure and pulse rate is lacking. Mechanisms of cyclosporin induced hypertension:enhancement of the vasoconstricting effect of endothelin 1, reduced NO production, activation of neurohumoral vasoconstrictors, increased calcium level in cytosols, increased thromboxane A production, reduced production of vasodilatating prostaglandins and activation of the sympathicus. The prerequisite of treatment are efforts to maintain the lowest possible effective cyclosporin level and if possible discontinue corticoids during the first year. The drug of first choice are calcium antagonists among others for their preventive effect on the vasculopathy of the graft. Other recommended groups of drugs are ACE inhibitors and diuretics.
- MeSH
- hypertenze farmakoterapie etiologie patofyziologie MeSH
- lidé MeSH
- transplantace srdce škodlivé účinky MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- anglický abstrakt MeSH
- časopisecké články MeSH
- přehledy MeSH
Endothelins are peptide tissue hormones with a powerful vasoconstrictor effect. The most important one among them, endothelin-1, is the most powerful vasoconstrictor substance in the human organism which causes constriction of the blood vessels, in particular renal, coronary, pulmonary and cerebral arteries, bronchioles, and inhibits the secretion of atrial natriuretic factor and vasopressin. Because of these effects importance in the pathogenesis of some diseases is ascribed to it, e.g. myocardial infarction, cardiac failure, asthma bronchiale, Raynaud a syndrome, renovascular disease, cyclosporin-induced nephrotoxicity and cerebrovascular attacks. Although there is little direct evidence on the role of endothelins in arterial hypertension, some authors prove its importance at least in some of its forms, e.g. salt sensitivity, or in complications of hypertension. The results of experimental and human studies with antagonists of endothelin receptors and endothelin-converting enzyme blockers also support the role of endothelin in the pathogenesis of hypertension. The use of these antagonists in the treatment of hypertension calls however for further long-term studies.
- MeSH
- endoteliny antagonisté a inhibitory chemie fyziologie MeSH
- hypertenze farmakoterapie patofyziologie MeSH
- lidé MeSH
- vazokonstrikce fyziologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- anglický abstrakt MeSH
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- endoteliny MeSH
Solid organ transplantation is an established treatment modality in patients with end-stage organ damage in cases where other therapeutic options fail. The long-term outcomes of solid organ transplant recipients have improved considerably since the introduction of the first calcineurin inhibitor (CNI) - cyclosporine. In 1984, the potent immunosuppressive properties of another CNI, tacrolimus, were discovered. The immunosuppressive effects of CNIs result from the inhibition of interleukin-2 synthesis and reduced proliferation of T cells due to calcineurin blockade. The considerable side effects that are associated with CNIs therapy include arterial hypertension and nephrotoxicity. The focus of this article was to review the available literature on the pathophysiological mechanisms of CNIs that induce chronic nephrotoxicity and arterial hypertension. CNIs lead to activation of the major vasoconstriction systems, such as the renin-angiotensin and endothelin systems, and increase sympathetic nerve activity. On the other hand, CNIs are known to inhibit NO synthesis and NO-mediated vasodilation and to increase free radical formation. Altogether, these processes cause endothelial dysfunction and contribute to the impairment of organ function. A better insight into the mechanisms underlying CNI nephrotoxicity could assist in developing more targeted therapies of arterial hypertension or preventing CNI nephrotoxicity in organ transplant recipients, including heart transplantation.
- MeSH
- hypertenze chemicky indukované patologie patofyziologie MeSH
- imunosupresiva škodlivé účinky MeSH
- inhibitory kalcineurinu aplikace a dávkování škodlivé účinky MeSH
- lidé MeSH
- nemoci ledvin chemicky indukované patologie patofyziologie MeSH
- reaktivní formy kyslíku metabolismus MeSH
- rejekce štěpu etiologie prevence a kontrola MeSH
- renin-angiotensin systém účinky léků MeSH
- transplantace srdce škodlivé účinky MeSH
- vazokonstrikce účinky léků MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- imunosupresiva MeSH
- inhibitory kalcineurinu MeSH
- reaktivní formy kyslíku MeSH
L-Lactate dehydrogenase pattern in tissues was determined by polyacrylamide gel electrophoresis adjusted to be more sensitive to LD1 and LD2. Three groups of rats (Wistar) were treated for 18 days with single oral daily doses of 45 mg consuprene/kg body weight to induce cyclosporine nephropathy. Two treated groups were further medicated either with carvedilol or BL-443 in single daily doses of 10 mg/kg b.w., unmedicated rats were given single i.p. daily doses of 1 ml saline. No significant difference in the LD(1-4) isoenzyme pattern in the liver between intact rats, rats with cyclosporine nephropathy, and rats with cyclosporine nephropathy medicated with carvedilol or BL-443 was found by F-test and t-test (p < 0.05). However, a significant difference in the LD(1-4) isoenzyme pattern in the myocardium between rats with cyclosporine nephropathy and intact rats was found. The present study reports the preliminary results of the effects of consupren on the LD(1-4) pattern in the muscle, spleen, and lung, as well as the effects of carvedilol and BL-443 in the tissues under the conditions of experimental cyclosporine nephropathy. The tissues with an increased risk of affection can be identified by evaluation of LD patterns that may become an additional tool to microscopic examination of the sample.
- MeSH
- adrenergní antagonisté terapeutické užití MeSH
- antihypertenziva terapeutické užití MeSH
- cyklosporin toxicita MeSH
- imunosupresiva toxicita MeSH
- izoenzymy analýza MeSH
- játra enzymologie MeSH
- karbamáty terapeutické užití MeSH
- karbazoly terapeutické užití MeSH
- karvedilol MeSH
- kosterní svaly enzymologie MeSH
- krysa rodu Rattus MeSH
- L-laktátdehydrogenasa analýza MeSH
- myokard enzymologie MeSH
- nemoci ledvin chemicky indukované farmakoterapie enzymologie MeSH
- plíce enzymologie MeSH
- potkani Wistar MeSH
- propanolaminy terapeutické užití MeSH
- slezina enzymologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- adrenergní antagonisté MeSH
- antihypertenziva MeSH
- BL443 MeSH Prohlížeč
- cyklosporin MeSH
- imunosupresiva MeSH
- izoenzymy MeSH
- karbamáty MeSH
- karbazoly MeSH
- karvedilol MeSH
- L-laktátdehydrogenasa MeSH
- propanolaminy MeSH