Abstract
Primary or essential hypertension is a major risk factor for many cardiovascular diseases. Since it has no identifiable cause, deducing its pathophysiology has been a major research focus in order to understand the underlying mechanisms contributing to high blood pressure. Dysfunction of the cardiac sympathetic nervous system causing sympathetic overdrive in the heart is one such mechanism linked to hypertension. This project was proposed to study the cellular level changes occurring in the superior cervical ganglion (SCG) and its influence on cardiac sympathetic neurotransmission of hypertensive animals. Here, I used the Spontaneously Hypertensive Rat (SHR), an animal model of primary hypertension to study these changes in vivo, at birth (P2), pre-hypertensive (3 weeks) and hypertensive (8 and 12 weeks) states. I found that SCGs of hypertensive rats have an elevated neuronal density at 3 weeks old which is restored to values comparable to those of normotensive WKY rats by 8 weeks of age. There were no significant differences in the glial cell density and glial neuronal ratio
between WKY and SHR SCGs. However, an increase in the glial neuronal ratio was observed with age in both strains which can be correlated with the decrease in their neuronal densities. On quantifying the glial envelope area estimated by S100β expression, a trend of higher S100β expression in SHRs than in WKY rats at each time point studied was observed with a significant difference in 8 weeks old males. The results on studying glial activation in the SCG showed that 8- and 12- weeks old SHR males exhibit significantly higher GFAP
expression compared to age-matched WKY males. This suggests that satellite glial cells are more activated at older ages in hypertensive males than in age-matched controls. These findings showing an increased expression of glial proteins, S100β and GFAP might indicate
increased neuron-glial communication within the SCGs of hypertensive animals. Further experiments might validate these findings and future work is needed to elucidate how these observed developmental neuronal and satellite glial cell changes in the SCG and other modulatory factors may contribute to the impaired cardiac sympathetic activity seen in hypertensive animals.