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Perfusion flow rate in the isolated elasmobranch rectal gland, perfused at in vivo pressures, was measured in Scyliorhinus canicula L. and Squalus acanthias L. Flow through the secretory parenchyma of the gland was reduced in the presence of concentrations of catecholamines in the physiological range, an effect mediated via alpha-adrenergic receptors within the gland vasculature. Flow through the non-secretory vascular shunts of the rectal gland was unaffected. The vasoconstriction induced by noradrenaline was blocked by the addition of cyclic AMP + theophylline or adenosine at concentrations known to stimulate secretion by the gland. In Squalus, a similar effect was seen with the secretagogue vasoactive intestinal peptide, but this agent had no effect in the glands of Scyliorhinus. Experiments indicate that the blockage of the noradrenaline effect by the secretory agents does not involve any stimulation of vasodilatory beta-adrenergic receptors and, furthermore, that the vasomotor effects of these agents appear to be entirely independent of their actions on the secretory cells. Evidence is presented indicating that the vasomotor action of adenosine may be mediated via receptors specific for the ribose moiety of the nucleoside (Ra receptors) activating adenylate cyclase, and that this may, in turn, explain the observed effects of the addition of exogenous cyclic AMP. The significance of the observed vascular effects in the overall control of secretion rate by the gland in vivo is discussed.

Haemodynamic Effects of Secretory Agents On the Isolated Elasmobranch Rectal Gland