The effect of alprenolol on the beta-receptor and adenylate cyclase activity in rabbit heart membranes.
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Biomedical subjects
Publications and source records attributed to M Wollemann.
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The author summarizes the current literature on neurotransmitters (dopamine, noradrenaline, serotonin and histamine) acting through adenlyate cyclase and also those ating direcctly without the intermission of c-AMP. The criteria of receptor binding are also stressed. The characteristics of D1 and D2 dopaminergic, beta1 adrenergic, H1 and H2 histaminergic receptors, their localisation and specific antagonists resp. agonists are emphasized too. Finally a new model is presented where adenylate cyclase and ionophore share a common receptor.
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Triton X-100 and Lubrol PX at similar concentrations extracted more phospholipid than protein from rat liver and rabbit heart membranes, as compared with their original protein and phospholipid contents, respectively. All the types of membrane phospholipid were solubilized from rat liver membrane with the used non ionic detergents, but less sphingomyelin was extracted than phosphatidylcholine and phosphatidylethanolamine.
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Among opiatelike peptides, stimulatory as well as inhibitory effects are encountered on adenylate cyclase activity. These actions are dependent not only on the investigated brain region but also on the applied peptide. Met-enkephalin stimulates adenylate cyclase activity in the rat brain stem (D-Met2, Pro5)-enkephalinamide and beta-endorphin inhibited it, whereas all three peptides inhibited the activity of cortex. Naloxone antagonized the effects of the applied peptides in the presence of sodium chloride.
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The effect of capsaicin on the adenylate cyclase activity in different regions of the rat brain (preoptic area of the hypothalamus, cerebral cortex and cerebellum) was investigated. Capsaicin added in vitro (10(-7)-10(-5) M) increased the adenylate cyclase activity of different brain regions. Following systemic capsaicin desensitization adenylate cyclase activity was significantly increased in the preoptic area. The enhanced adenylate cyclase activity in the preoptic area was inhibited by the vitro addition of capsaicin or 5-HT, whereas desensitization did not affect the in vitro activating effect of capsaicin in other brain regions (cerebral cortex, cerebellum). It is assumed that the pharmacological effect of capsaicin in the preoptic area is mediated through the activation of adenylate cyclase. Since capsaicin induces irreversible impairment of the function of warmsensitive hypothalamic neurons it is assumed that adenylate cyclase is involved in maintaining normal thermoregulatory functions.
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