Question: What is the role of TRH in hypertension?

Context:
We recently showed that diencephalic TRH may mediate the central leptin-induced pressor effect
that central TRH participates in the hypertension induced by body weight gain probably through its well-known action on sympathetic activity.
Five polymorphisms in five genes, CAST(calpastatin), LIPC (hepatic lipase), SLC4A1 (band 3 anion transporter), TRH (thyrotropin-releasing hormone), and VWF (von Willebrand factor), were significantly associated with both blood pressure variation and hypertension.
We previously reported that thyrotropin-releasing hormone (TRH) precursor gene overexpression induces hypertension in the normal rat and that spontaneously hypertensive rats have central TRH hyperactivity with increased TRH synthesis and release and an elevated TRH receptor number.
We propose that because leptin produces central TRH synthesis and release, obesity may induce hypertension through TRH system activation and that the TRH-leptin interaction may thus contribute to the strong association between hypertension and obesity.
We have described that TRH overexpression induces hypertension in a normal rat, which was reversed by TRH antisense treatment. 
his treatment also reduces the central TRH hyperactivity in spontaneously hypertensive rats and normalizes blood pressure.
Our findings support the hypothesis that the TRHR gene participates in the etiopathogenesis of essential hypertension.
Recently, we described that the TRH precursor gene overexpression induces hypertension in the normal rat. In addition, we published that spontaneously hypertensive rats (SHR) have central extrahypothalamic TRH hyperactivity with increased TRH synthesis and release and an elevated TRH receptor number.
the encephalic renin-angiotensin system seems to be crucial in the development and/or maintenance of hypertension in SHR, we investigated the effect of antisense inhibition of TRH on that system and found that TRH antisense treatment significantly diminished the elevated diencephalic angiotensin II (Ang II) content in the SHR without any effect in control animals, suggesting that the Ang II system is involved in the TRH cardiovascular effects.
he central TRH system seems to be involved in the etiopathogenesis of hypertension in this model of essential hypertension
ong-term treatment with enalapril (5 mg/kg twice daily), which was effective in inhibiting serum angiotensin-converting enzyme activity by more than 50%, decreased arterial blood pressure and preoptic area TRH content of SHR, whereas another vasodilator, diltiazem (10 mg/kg every 8 hours), failed to produce a similar change
the pressor effect of intravenous TRH is mediated primarily by a stimulation of alpha-adrenergic receptors. Adrenal medullectomy appears to enhance the blood pressure response to intravenous TRH. Activation of cardiac beta-adrenoceptors seems to contribute to the blood pressure increasing effect of intravenous TRH in medullectomized animals.
Centrally administered thyrotropin-releasing hormone exerts a well documented hypertensive effect.
These results provide evidence for a role of endogenous brain thyrotropin-releasing hormone in the maintenance of hypertension in spontaneously hypertensive rats.
in spontaneously hypertensive (SHR) rats the development of hypertension paralleled increases in brain receptors for thyrotropin-releasing hormone (TRH)
The results suggest that in addition to the brain, TRH receptors in the spinal cord of SHR rats are also up-regulated and may also play an important role in the regulation of blood pressure.
The results provide, for the first time, evidence for a parallel increase in the density of brain TRH receptors with elevation of blood pressure, and suggest that brain TRH receptors may play an important role in the pathophysiology of hypertension.

Answer: TRH gene overexpression induces hypertension in normal rats and spontaneously hypertensive rats have central TRH hyperactivity with increased TRH synthesis and release and an elevated TRH receptor number. TRH antisense treatment reduces hypertension.
central TRH participates in the hypertension induced by body weight gain probably through its well-known action on sympathetic activity.
the pressor effect of intravenous TRH is mediated primarily by a stimulation of alpha-adrenergic receptors.  Activation of cardiac beta-adrenoceptors seems to contribute to the blood pressure increasing effect of intravenous TRH. Ang II system is involved in the TRH cardiovascular effects. 
Polymorphisms in  TRH (thyrotropin-releasing hormone) are significantly associated with both blood pressure variation and hypertension.
TRH may mediate the central leptin-induced hypertension effect
A parallel increase in the density of brain TRH receptors with elevation of blood pressure has been shown and suggests that brain TRH receptors may play an important role in the pathophysiology of hypertension. TRH Receptor gene participates in the etiopathogenesis of essential hypertension.