Functional Modifications in Blood Vessels of Hypertensive Rats
It has been reported that vascular smooth muscle from hypertensive animals shows hypersensitivity for vasoconstrictors (Holloway and Bohr 1973; Thompson et al. 1987; Boonen and De Mey 1990; Bodin et al. 1993). This hyperre-activity has been suggested to arise either from a change in receptor affinity (Nyborg and Bevan 1988), in receptor number, or in the transduction mechanisms of the receptor (Asano et al. 1988; Johnson et al. 1991). In addition to these observations, several reports have demonstrated abnormalities of Ca2+ handling in vascular smooth muscle cells (SMC) of hypertensive animals which, regarding the important role played by Ca2+ in the regulation of vascular tone, could be responsible for marked changes in vessel reactivity (Kwan 1985; Sada et al. 1990). Different observations suggest that voltage-dependent Ca2+ Channels might be altered in vessels from hypertensive rats. The first argument for the implication of a change in Ca2+ Channels in hypertension is the blood pressure-lowering effect of dihydropyridine Ca2+ antagonists (MacGregor et al. 1982; Kazda and Knorr 1990). These antagonists have also been shown to suppress the myogenic active tone displayed by blood vessels from hypertensive rats (Aoki and Asano 1986; Sada et al. 1990).
KeywordsAngiotensin Acetylcholine Aldosterone Nifedipine Clonidine
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