Participation of capsaicin-sensitive neurons in the cardiovascular effects of neurotensin in guinea pigs.
Intravenous (IV) infusions of neurotensin (NT) in anesthetized guinea pigs elicited dose-dependent pressor effects and tachycardia. Both effects were significantly reduced or abolished in guinea pigs given a chronic treatment with the neurotoxin capsaicin. In guinea pig isolated atria NT evoked a positive inotropic and chronotropic effect. Both effects were completely abolished in atria derived from capsaicin-treated guinea pigs. The positive inotropic and chronotropic effects of NT in guinea pig atria were mimicked by capsaicin and calcitonin gene-related peptide (CGRP). These results were interpreted as an indication that NT produces its cardiovascular effects in guinea pigs by activating capsaicin-sensitive sensory neurons.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects*; D015740:Calcitonin Gene-Related Peptide; D002211:Capsaicin / Q000494:pharmacology*; D005260:Female; D006168:Guinea Pigs; D006339:Heart Rate / Q000187:drug effects*; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects*; D009388:Neostigmine / Q000494:pharmacology; D009479:Neuropeptides / Q000494:pharmacology; D009496:Neurotensin / Q000494:pharmacology*; D013373:Substance P / Q000494:pharmacology
D009479:Neuropeptides; D013373:Substance P; D009496:Neurotensin; D009388:Neostigmine; D001285:Atropine; D015740:Calcitonin Gene-Related Peptide; D000109:Acetylcholine; D002211:Capsaicin