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The vertebrate heart is regulated by excitatory adrenergic and inhibitory cholinergic innervations, as well as non-adrenergic non-cholinergic (NANC) factors that may be circulating in the blood or released from the autonomic nerves. As an example of NANC signaling, an increased histaminergic tone, acting through stimulation of H2 receptors, contributes markedly to the rise in heart rate during digestion in pythons. In addition to the direct effects of histamine, it is also known that histamine can reinforce the cholinergic and adrenergic signaling. Thus, to further our understanding of the histaminergic regulation of the cardiovascular response in pythons, we designed a series of in vivo experiments complemented by in vitro experiments on sinoatrial and vascular ring preparations. We demonstrate the tachycardic mechanism of histamine works partly through a direct binding of cardiac H2 receptors and in part through a myocardial histamine-induced catecholamine release, which strengthens the sympathetic adrenergic signaling pathway. [ABSTRACT FROM AUTHOR]

The cardiovascular system of vertebrates is regulated by a vast number of regulatory factors, including histamine. In pythons, histamine induces a strong tachycardia and dilates the systemic vasculature, which resembles the cardiovascular response to the elevated metabolic rate during digestion. In fact, there is an important role of increased histaminergic tone on the heart during the initial 24 h of digestion in pythons. Whilst the cardiovascular effects of histamine are well studied in pythons, little is known about the effects in other groups of reptiles. The histaminergic effects on the heart vary among species and histamine may exert either pressor and depressor effects by causing either constrictive or dilatory vascular responses. Here, we investigated the cardiovascular effects of histamine in three species of reptiles with very different cardiovascular and pulmonary morphologies. Experiments were performed on both anesthetized and recovered animals. We show a species-dependent effect of histamine on the systemic vasculature with dilation in rattlesnakes and constriction in turtles and caimans but no effect on the pulmonary circulation. The histamine-induced dilation in rattlesnakes was mediated through an activation of H-receptors, whereas the histamine-induced constriction in caimans was mediated through both adrenergic signaling and H-receptors activation. In all three species, histamine-induced tachycardia by direct stimulation of histaminergic receptors as well as an indirect activation of adrenoreceptors. This finding highlights a more complex mechanism underlying the action of histamine than previously recognized in reptiles. [ABSTRACT FROM AUTHOR]

The functional role of nitric oxide (NO) was investigated in the systemic and pulmonary circulations of the South American rattlesnake,Crotalus durissus terrificus. Bolus, intra-arterial injections of the NO donor, sodium nitroprusside (SNP) caused a significant systemic vasodilatation resulting in a reduction in systemic resistance (Rsys). This response was accompanied by a significant decrease in systemic pressure and a rise in systemic blood flow. Pulmonary resistance (Rpul) remained constant while pulmonary pressure (Ppul) and pulmonary blood flow (Qpul) decreased. Injection ofL-Arginine (L-Arg) produced a similar response to SNP in the systemic circulation, inducing an immediate systemic vasodilatation, while Rpul was unaffected. Blockade of NO synthesis via the nitric oxide synthase inhibitor, L-NAME, did not affect haemodynamic variables in the systemic circulation, indicating a small contribution of NO to the basal regulation of systemic vascular resistance. Similarly, Rpul and Qpul remained unchanged, although there was a significant rise in Ppul. Via injection of SNP, this study clearly demonstrates that NO causes a systemic vasodilatation in the rattlesnake, indicating that NO may contribute in the regulation of systemic vascular resistance. In contrast, the pulmonary vasculature seems far less responsive to NO. [ABSTRACT FROM AUTHOR]