The Effects of C-Type Natriuretic Peptide on Catecholamine Release in the Pacific Spiny Dogfish (Squalus acanthias)

Abstract

The interaction between homologous C-type natriuretic peptide (dfCNP) and catecholamine release in cardiovascular control was assessed in the marine dogfish (Squalus acanthias). This was accomplished by evaluation of the dynamics of the dfCNP-elicited secretion of catecholamines in situ and in vivo. With an in situ saline-perfused postcardinal sinus preparation, it was demonstrated that perfusion with saline containing dfCNP (10−9 mol L−1) did not affect the secretion of either noradrenaline or adrenaline. However, the presence of dfCNP in the perfusate significantly enhanced carbachol-evoked secretion of noradrenaline. In vivo, intravascular injection of dfCNP (10−9 mol kg−1) caused a biphasic pressor–depressor response consisting of a brief increase in caudal artery blood pressure (PCA) followed by a prolonged reduction in PCA. Furthermore, although systemic resistance initially increased, it was subsequently maintained at baseline values in the face of persistent decreases in both PCA and cardiac output. Bolus injection of dfCNP elicited significant increases in plasma noradrenaline levels that peaked within 10 min; plasma adrenaline levels were unaffected. The release of noradrenaline elicited by dfCNP was unaffected by prior blockade of the renin–angiotensin system (RAS) (with the angiotensin converting enzyme inhibitor lisinopril) or by pretreatment with the nicotinic receptor blocker hexamethonium. The delayed decrease in PCA was not observed in the hexamethonium-treated fish. Prior blockade of β-adrenoreceptors (with sotalol) or α-adrenoreceptors (with prazosin) either significantly reduced (sotalol) or abolished (prazosin) the increase in plasma noradrenaline levels after dfCNP injection. The results of this investigation demonstrate that the elevation of plasma noradrenaline levels observed in vivo following dfCNP injection is not caused by a direct effect of dfCNP on catecholamine secretion from axillary body chromaffin cells. Furthermore, the dfCNP-mediated increase of plasma noradrenaline appears to be unrelated to changes in PCA and is insensitive to blockade of the RAS or nicotinic receptors. However, stimulation of adrenergic receptors, in particular the α-adrenoreceptors, appears to be a key mechanism underlying the dfCNP-elicited secretion of noradrenaline.