The exercise pressor reflex (EPR), a neurocirculatory control mechanism, is exaggerated in hypertensive humans and rats. Disease-related abnormalities within the afferent arm of the reflex loop, including mechano- and metabosensitive receptors located at the terminal end of group III/IV muscle afferents, may contribute to the dysfunctional EPR in
hypertension. Using control (WKY) and spontaneous hypertensive (SHR) rats, we examined dorsal root ganglion (DRG) gene and
protein expression of molecular receptors recognized as significant determinants of the EPR. Twelve lumbar DRGs (6 left, 6 right) were harvested from each of 10 WKY [arterial blood pressure (MAP): 96 ± 9 mmHg] and 10 SHR (MAP: 144 ± 9 mmHg). DRGs from the left side were used for
protein expression (Western blotting; normalized to GAPDH), whereas right-side DRGs (i.e., parallel structure) were used to determine
mRNA levels (
RNA-sequencing, normalized to TPM). Analyses focused on metabosensitive (ASIC3,
Bradykinin receptor B2, EP4, P2X3, TRPv1) and mechanosensitive (Piezo1/2) receptors. Although Piezo1 was similar in both groups (P = 0.75),
protein expression for all other receptors was significantly higher in SHR compared with WKY. With the exception of a greater
Bradykinin-receptor B2 in SHR (P < 0.05),
mRNA expression of all other receptors was not different between groups (P > 0.18). The higher
protein content of these sensory receptors in SHR indirectly supports the previously proposed hypothesis that the exaggerated EPR in
hypertension is, in part, due to disease-related abnormalities within the afferent arm of the reflex loop. The upregulated receptor content, combined with normal
mRNA levels, insinuates that posttranscriptional regulation of sensory receptor
protein expression might be impaired in
hypertension.