Regulation of parotid kallikrein secretion-role of the alpha 2- and beta-adrenergic system.
The effects of pharmacologically induced alterations of alpha 1, alpha 2 and beta-adrenergic system on kallikrein secretion - measured as amidolytic activity - in rat parotid gland were tested in vivo. Beta and alpha 1/2-adrenergic stimulation (Orciprenaline, alpha-methylnorepinephrine) caused a comparably significant increase of parotid kallikrein secretion. Alpha 2-receptor blockade (yohimbine) but not the alpha 1-antagonist prazosin, partly abolished the effect of alpha-methylnorepinephrine. The effects of the alpha 1-adreno-receptor agonist norfenephrine on kallikrein secretion were significantly lower compared to alpha 1/2-adreno-receptor-stimulation.
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000818:Animals; D007610:Kallikreins / Q000378:metabolism*; D008297:Male; D010306:Parotid Gland / Q000187:drug effects / Q000201:enzymology*; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D011943:Receptors, Adrenergic, beta / Q000502:physiology*
D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D007610:Kallikreins