The present study investigated in a rat model of hypertension whether the high conductance at acupoints is a result of the release of the neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP) during neurogenic inflammation in the referred pain area.
The present study investigates whether increased blood pressure in protein-restricted offspring would be associated with changes in the DRG cells and in renal pelvic wall expression of NK1R, SP and CGRP when compared to NP offspring.
In addition, there is an up-regulation of cerebellar CGRP1 (CRLR + RAMP1) and AM2 (CRLR + RAMP3) receptors and a down-regulation of AM1 (CRLR + RAMP2) receptor during hypertension associated with a decreased AM expression.
No significant differences were noted in the genotype distributions for AGTR1, PRRC2A, and CALCA polymorphisms in patients with hypertension (N = 500) and healthy controls (N = 506).
By comparing results from a range of human and animal studies, findings broadly suggest an association between CGRP and the pathophysiology of hypertension in terms of protective mechanisms, with possibly the RAMP1 component of the CGRP receptor playing a key role in the brain stem, in addition to peripheral receptors.
We also discuss the effects of direct administration of CGRP in the treatment of hypertension and of anti-hypertensive drugs that enhance the release or response of endogenous calcitonin gene-related peptide: angiotensin converting enzyme inhibitors, selective antagonists for the angiotensin II receptor, beta-blockers, magnesium sulphate for preeclampsia and rutaecarpine, as well as the possibilities using CGRP in gene therapy for prevention of vasospasm after subarachnoid haemorrage.
We recently reported that calcitonin gene-related peptide (CGRP) reversed the hypertension induced by nitric oxide inhibition in pregnant rats and that this effect appeared to be progesterone dependent.