title: Differences between rat and guinea pig aorta in postreceptor mechanisms of alpha 1-adrenoceptors.
abstract: The relative importance of different postreceptor mechanisms associated with alpha 1-adrenoceptor activation in guinea pig aorta and rat aorta was compared. In both tissues, a concentration-dependent correlation was observed between contractile responses produced by high concentrations of norepinephrine (NE) and inositol-1-phosphate (IP1) accumulation. Blockade of Ca2+ entry through voltage-dependent membrane channels by nifedipine had no inhibitory action on NE-induced contractile responses in guinea pig aorta, but significantly inhibited NE-induced contractile responses in rat aorta. Nifedipine had no major effect on NE-induced IP1 accumulation in either tissue. A medium with no Ca2+ inhibited NE-induced contractile responses and IP1 accumulation in guinea pig aorta, but had a more marked effect on contractile responses and IP1 accumulation in rat aorta. The combination of a high concentration of nifedipine and a medium with no Ca2+ almost completely inhibited NE-induced contractile responses and IP1 accumulation in both tissues. Exposure to EGTA also virtually completely inhibited NE-induced contractile response and IP1 accumulation in both tissues. Significant 45Ca2+ entry was stimulated in rat aorta by NE, and this entry was completely blocked by nifedipine. No significant 45Ca2+ entry was stimulated by NE in guinea pig aorta. We conclude that the most important postreceptor event linked to alpha 1-adrenoceptor stimulation in guinea pig aorta is activation of the phosphatidylinositol pathway, whereas in rat aorta Ca2+ entry through voltage-dependent membrane channels is as important as activation of the phosphatidylinositol pathway. We also conclude that activation of the phosphatidylinositol pathway in both tissues is critically dependent on the presence of a small amount of Ca2+, which may enter from the external medium.
authors.affiliation: Department of Medicine, University of Melbourne, Royal Melbourne Hospital, Parkville, Victoria, Australia.
authors.forename: R A
authors.initials: RA
authors.lastname: Jenkin
authors.forename: M A
authors.initials: MA
authors.lastname: Baldi
authors.forename: V
authors.initials: V
authors.lastname: Iwanov
authors.forename: R F
authors.initials: RF
authors.lastname: Moulds
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism*; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism; D002132:Calcium Radioisotopes; D006224:Cricetinae; D004533:Egtazic Acid / Q000494:pharmacology; D006168:Guinea Pigs; D066298:In Vitro Techniques; D007291:Inosine Monophosphate / Q000378:metabolism; D008566:Membranes / Q000187:drug effects / Q000378:metabolism; D009119:Muscle Contraction / Q000187:drug effects; D009543:Nifedipine / Q000494:pharmacology; D009638:Norepinephrine / Q000037:antagonists & inhibitors / Q000494:pharmacology; D010716:Phosphatidylinositols / Q000378:metabolism; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects*; D013045:Species Specificity
chemical_list: D015220:Calcium Channels; D002132:Calcium Radioisotopes; D010716:Phosphatidylinositols; D011942:Receptors, Adrenergic, alpha; D007291:Inosine Monophosphate; D004533:Egtazic Acid; D011189:Potassium Chloride; D009543:Nifedipine; D009638:Norepinephrine