In this context it may be significant that alteration in excitability seen in our study was restricted to MVC like SPN and did not extend to changes in CVC like neuronal activity, implying a functional, cell-type selectivity in the deficit, rather than a global phenotype.
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Increased intrinsic excitability of muscle vasoconstrictor preganglionic neurons may contribute to the elevated sympathetic activity in hypertensive rats.
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