Cardiovascular pharmacology of thyrotropin releasing hormone

Abstract

Thyrotropin releasing hormone (TRH) and its receptors are present in the cardiovascular nuclei of the brain as well as in the intermediolateral cell column of spinal cord. Anatomical, neurophysiological, functional and pharmacological studies suggest that TRH is a neurotransmitter/neuromodulator in the central nervous system. Administration of TRH to experimental animals or human subjects induces pressor and tachycardic responses and increases plasma levels of catecholamines. These effects are likely to be mediated by a central nervous system activation of the sympathoadrenomedullary system with no involvement of vasopressin or renin-angiotensin system. In the conscious rat, the TRH-induced pressor response is accompanied by an increment in cardiac output and a distinct change in organ blood flow, a hindquarter skeletal muscle vasodilation accompanied by renal and mesenteric vasoconstriction. The role of TRH in hypertension has not been studied. However, the extremely potent pressor and vasoconstrictor properties of TRH makes this tripeptide a candidate for neurotransmitters/modulators involved in the development and/or maintenance of hypertension. The role of TRH in the therapy of shock is at present controversial. Though preliminary experimental work raised hopes and expectations for therapeutic usage of TRH in shock and trauma, the more recent studies have shown no effect or a detrimental effect for TRH in some experimental shock states.