Tachycardic responses to stimulation of β-adrenoceptors in the brain parenchyma in conscious rats

- This study examined cardiac actions of forebrain beta-adrenoceptors in rats.
- Isoproterenol was locally injected into many brain regions including the forebrain.
- Isoproterenol increased heart rate and noradrenaline, without changing blood pressure.
- Its cardiac action was inhibited by treatments with propranolol or hexamethonium.
- The tachycardia may be due, at least in part, to excitation of sympathetic nerves.

This study aimed to investigate how stimulation of β-adrenoceptors in the anteroventral third ventricular region (AV3V; a pivotal forebrain area for autonomic functions) and other brain regions affects heart rate (HR) in conscious rats. Topical injections of the β-adrenergic agonist isoproterenol (Isop) into the AV3V caused dose-related and reversible increases in HR. Only its highest dose utilized significantly affected blood pressure (BP), inducing a decrease. The tachycardia due to AV3V Isop lasted significantly longer than that elicited by hypotension, and was inhibited by AV3V administration of the β-adrenergic antagonist propranolol or systemic infusion of a ganglion blocker hexamethonium. Plasma noradrenaline indicative of sympathetic nerve activity increased in parallel with rises in HR after the AV3V application of Isop. When Isop was locally injected into various brain regions other than the AV3V, region-related effectiveness in provoking tachycardia was observed that tended to be large in limbic structures and the hypothalamic paraventricular nucleus. No region responded to Isop applications with decreases in HR. These results suggest that β-adrenoceptors in the AV3V and other brain regions may be able to produce tachycardia by enhancing, at least in part, the efferent sympathetic nerve activity controlling cardiac function.