Adrenergic and non‐adrenergic cardiovascular effects of thyrotropin‐releasing hormone (TRH) in the anaesthetized rabbit

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Abstract
The effects of thyrotropin‐releasing hormone (TRH) on regional blood flows were studied in urethane‐anaesthetized rabbits. Experiments were performed both with and without adrenergic antagonist pretreatment. The tracer microsphere method was used to measure blood flow. TRH (0.1 mg kg‐1) caused an increase in mean arterial blood pressure (MAP) from 9.8 ± 1 to 11.8 ± 0.8; a higher dose (1 mg kg‐1) increased the blood pressure to 15.2±1 kPa (P < 0.001). Total cerebral blood flow (CBFtot) increased to 137 ± 10% (P< 0.05) of control at the lower dose and to 214±16% (P< 0.001), at the higher dose. A reduction in blood flow at both doses of TRH in several peripheral organs indicates that the pressor effect was mainly due to an effect on the peripheral vascular resistance. In prazosin‐pretreated animals in which the MAP was normalized by ligation of the thoracic aorta, TRH elicited an increase in the CBFtotto 131 ± 12% (P< 0.05) of control. In the iris, TRH caused vasodilation in prazosin‐pretreated animals. In experiments with combined α‐ and β‐adrenergic blockade, a non‐adrenergic vasoconstricting effect of TRH was seen in some peripheral organs.The results indicate that TRH activates the sympathetic nervous system thus causing an increased vascular resistance and MAP; these effects are mediated mainly by an α1‐adrenergic mechanism. In the spleen, the gastric mucosa and the adrenal glands, the vasoconstriction caused by TRH was partly non‐adrenergic. The vasodilation seen in the small intestine and the anterior uvea after TRH treatment and adrenoceptor blockade may be explained by effects on the parasympathetic nervous system. The vasodilating effect of TRH in the brain does not seem to involve α‐ or β‐adrenergic mechanisms.