The hypertension associated with vitamin D deficiency is driven
by an increase in the levels of angiotensin II and ET-1, which are
responsible for activating cardiac hypertrophy and congestive heart
failure (CHF) [277]. In the presence of these two hormones, which
operate through the InsP3/Ca2þ signalling system, there are subtle
changes in the spatial and temporal properties of the individual
Ca2þ transients that drive contraction. The idea is that perinuclear
InsP3Rs function as coincident detectors that respond to both InsP3
and the brief Ca2þ transients that induce contraction to create a
nuclear Ca2þ microdomain responsible for driving the transcriptional
processes that initiate hypertrophy [278,279] (Fig. 8). There is
now considerable experimental evidence to show that InsP3Rs can
indeed function to enhance nuclear Ca2þ transients to control hypertrophy