Increases in arterial blood pressure in the rat in response to a new vertebrate neuropeptide, LPLRFamide, and a related molluscan peptide, FMRFamide

Vasopressor responses in urethane-anaesthetized rats were evoked by a new peptide from chicken brain, LPLRFamide, and the immunochemically related molluscan neuropeptide, FMRFamide. In doses of 50 to 200 nmol X kg-1, i.v., both peptides produced a rapid increase in arterial pressure that returned to basal in 1-2 min. When given intracisternally in similar doses the two peptides again increased arterial pressure, but the time to peak response (1-2 min) and the duration of the responses (5-8 min) were prolonged. There was a marked, reversible, specific, tachyphylaxis following intracisternal but not intravenous injection of LPLRFamide, indicating separate sites of action after administration by these routes. Guanethidine and phentolamine blocked the responses to both intravenous and intracisternal administration, and hexamethonium significantly reduced the response to intracisternal administration. Both by intravenous and intracisternal routes it is therefore likely that responses are mediated by noradrenaline release from sympathetic endings. In addition, following adrenalectomy and propranolol the response to intravenous (but not intracisternal) LPLRFamide was increased, suggesting that adrenaline released from the adrenal medulla might act at beta-adrenoreceptors causing vasodilatation. The physiological significance of these observations remains to be established, but it is significant that peptides immunochemically related to FMRFamide and LPLRFamide occur in areas of rat brain concerned with autonomic control.