Il sistema catecolaminergico, farmaci e recettori adrenergici

Il sistema adrenergico

Il sistema nervoso autonomo simpatico (SNAS), grazie alle sue attività, è il sistema deputato alla regolazione fisiologia dell’organismo nei casi di lotta e fuga. Esso, in determinate situazioni, agisce sull’organismo attuando un sistema di difesa che determina:

  • una dilatazione della pupilla
  • una inibizione della salivazione
  • tachicardia
  • dilatazione bronchiale
  • inibizione della peristalsi (riduzione attività intestinali) e delle secrezioni
  • a livello epatico la conversione del glicogeno in glucosio
  • liberazione dell’adrenalina
  • contrazione della vescica

Il sistema nervoso autonomo parasimpatico bilancia queste attività avviate dal sistema simpatico determinando:

  • una stimolazione della salivazione
  • bradicardia
  • broncocostrizione
  • stimolazione peristalsi e secrezioni
  • stimolazione rilascio di bile
  • contrazione vescica

Il sistema ortosimpatico è parte di un sistema neuroendocrino dedicato alle risposte allo stress. In caso di stress, il rene recupera acqua e sodio dalle urine, reimmette queste sostanze nel sangue permettendo un aumento del volume ematico. Oltre a questo effetto, il sistema ortosimpatico, in caso di stress, permette la produzione di cortisolo il quale ha molteplici funzioni (aumento gittata cardiaca, aumento della glicemia, riduzione difese immunitarie ecc..).

Questo sistema è costituito da neuroni che liberano catecolamine: le principali catecolamine che fungono da neurotrasmettitore sono Adrenalina (epinephrine), Nor-Adrenalina (nor-epinephrine), Dopamina. Le risposte indotte dai neuroni dell’ortosimpatico sono dovute all’attivazione di recettori per le catecolamine presenti sulle cellule effettrici. I recettori per l’adrenalina, ad esempio, sono GPCR che producono secondi messaggeri i quali rappresentano un sistema di amplificazione del messaggio del neurotrasmettitore.

Recettori adrenergici

I farmaci attivi sui recettori adrenergici sono importanti modulatori delle funzioni cardio-circolatorie e respiratorie.  In base alle risposte dei farmaci, alla distribuzione nei tessuti e alle caratteristiche di struttura, i recettori per le catecolamine si distinguono in recettori Alfa e recettori Beta.

I recettori Alfa sono responsabili della vasocostrizione indotta dalle catecolamine in diversi tessuti. I recettori Alfa1 attivano PLC e fanno aumentare la concentrazione intracellulare di Ca, dunque stimolano la contrazione. I recettori Alfa2, invece, inibiscono la produzione di cAMP.

I recettori Beta stimolano la produzione di cAMP e dunque provocano il rilassamento delle cellule muscolari lisce. La loro distribuzione è la seguente:

  • I recettori Beta del cuore sono solo Beta1
  • I recettori Beta dei bronchi sono solo Beta2
  • I recettori Beta degli adipociti sono solo Beta3

In sintesi, i recettori Alfa fanno aumentare la concentrazione intracellulare di Ca++ provocando una contrazione, i recettori Beta fanno aumentare la concentrazione intracellulare di cAMP provocando un rilassamento.

Sui muscoli striati (scheletrico e cardiaco) l’aumento di cAMP provoca maggiore influsso di Ca++ attraverso canali al ca-volt-dipendenti e quindi potenzia la contrazione. L’attivazione dei recettori Beta del cuore provoca effetti inotropo e cronotropo positivi.

Sottotipi di recettori adrenergici e affinità recettoriale con i principali neurotrasmettitori. Fonte: Medicinapertutti.it

I farmaci attivi sui recettori adrenergici

I farmaci attivi sui recettori adrenergici sono di diverse tipologie:

  • Simpatico-mimetici diretti
  • Simpatico-mimetici indiretti
  • Agonisti non selettivi
  • Agonisti Beta 2
  • Antagonisti Alfa
  • Antagonisti Beta 1 (beta-bloccanti)

 

Solo i farmaci attivi sui recettori Beta sono di interesse per lo sport. I farmaci agonisti Beta sono interessanti per gli effetti di broncodilatazione e per la positività ino/cronotropa. I farmaci antagonisti sono interessanti perché riducono i tremori.

Alcuni farmaci permettono un aumento della propria performance: tra questi, spiccano i Beta-2 agonisti (impiegati in clinica per il trattamento dell’asma).

Un classico esempio di Beta-2 agonista è il Clenbuterolo. Esso ha una lunga durata d’azione e, rispetto agli altri B2 agonisti, presenta una maggiore attività anabolizzante. Il suo effetto diminuisce dopo 8-10 giorni per la downregulation* dei recettori B2. Pertanto viene assunto con uno schema di tipo ciclico. Nei periodi di wash out** possono presentarsi sintomi di astinenza per la diminuzione degli effetti stimolanti il SNC. Le dosi come doping sono generalmente 4-5 volte superiori quelle terapeutiche (20-40 mcg/day). Le reazioni avverse sono quelle tipiche dei B2 agonisti (tachicardia, aritmie cardiache, cefalea, tremori, agitazione).

I motivi per cui i farmaci beta-agonisti sono considerati farmaci del doping sono molteplici e tutti legati all’effetto che ricorda la stimolazione del sistema nervoso vegetativo simpatico:

  • aumento delle prestazioni cardiache
  • aumento del calibro bronchiale
  • aumento della vascolarizzazione del tessuto muscolare
  • effetti metabolici che favoriscono la produzione di substrati energetici muscolari
  • aumento della forza di contrazione muscolare

Ecco uno schema di alcune localizzazioni dei recettori Beta adrenergici e i relativi effetti in seguito a stimolazione ed inibizione.

Tessuto Recettore Stimolazione Inibizione
Vasi sanguigni B1; B2 Dilatazione Contrazione
Cuore B1 Effetto inotropo e cronotropo positivo Effetto inotropo e cronotropo negativo
Muscolatura scheletrica B1; B2 Tremori, aumento massa muscolare e velocità di contrazione muscolare Diminuzione tremori
Bronchi B2 Dilatazione Contrazione

 

Beta bloccanti, antagonisti dei recettori Beta per le catecolamine

Sono farmaci utilizzati nello sport in determinate discipline.

Alcuni beta-bloccanti, soprattutto selettivi per i Beta1, sono l’atenololo, bisoprololo, metoprololo (utilizzato nella terapia di fondo di profilassi dell’emicrania) e il nebivololo.

Esistono altri beta-bloccanti che sono “non selettivi”. A questo gruppo appartengono il propanololo, nadololo, timololo, pindololo e il labetololo (quest’ultimo è un Alfa1 antagonista).

Hanno un’azione bradicardizzante, un effetto anti-tremore ed uno ansiolitico. Essi sono usati negli sport in cui è importante una buona coordinazione posturale: tiro con l’arco, tiro al piattello, bowling, bob, trampolino, tuffi, nuoto sincronizzato, pentathlon ecc. ed hanno effetti negativi sulla resistenza fisica.

Vengono utilizzati clinicamente per l’ipertensione, l’angina pectoris, infarto del miocardio, aritmie, scompenso cardiaco e profilassi dell’emicrania. Le loro principali reazioni avverse provocano broncospasmo (controindicati negli asmatici), ipoglicemia, crampi, aritmie, insufficienza cardiaca, insonnia, incubi, depressione, diminuzioni libido, diplopia ecc…

Gli effetti indesiderati che possono presentarsi con l’assunzione di questi farmaci sono:

  • la riduzione del flusso renale
  • asma
  • blocco AV

Sono controindicati in caso di:

  • asma
  • insufficienza cardiaca
  • anomalie AV o SA
  • diabete insulino-dipendente
  • tossicità: sindrome da astinenza

*La downregulation (sottoregolazione) è un processo attraverso il quale una cellula riduce la quantità di una componente cellulare, come un particolare RNA o proteina, in risposta a una variabile esterna.

**Periodo in cui i livelli di un farmaco nell’organismo devono essere gradualmente ridotti a zero.

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