Increased calcium and noradrenaline sensitivity in spontaneously hypertensive rat resistance vessels is an intrinsic vascular smooth muscle defect independent of blood pressure.
We have investigated media thickness and noradrenaline- and calcium-sensitivity of isolated mesenteric resistance vessels from spontaneously hypertensive (SHR) and control Wistar-Kyoto (WKY) rats, which had been treated in various ways. Vessels from untreated SHRs had an increased media thickness and increased noradrenaline- and calcium-sensitivity. Anti-hypertensive treatment of SHRs and WKYs with Felodipine reduced blood pressure, eliminated the difference in vessel media thickness, but did not reduce vessel noradrenaline- or calcium-sensitivity. Chemical sympathectomy of SHRs and WKYs at birth likewise resulted in reduced blood pressure, but did not eliminate the difference in vessel media thickness although again vessel noradrenaline- and calcium-sensitivity remained unchanged. Induction of renal hypertension in WKYs caused an increase in blood pressure and increase in vessel media thickness, but did not affect vessel noradrenaline-sensitivity. The results suggest that while vessel media thickness is influenced by blood pressure, the sensitivity differences of SHR resistance vessels are an intrinsic defect of their vascular smooth muscle, independent both of blood pressure and neurogenic influences.
Mulvany et al. (Thu,) conducted a other in Hypertension. Felodipine, chemical sympathectomy, or renal hypertension vs. Untreated controls was evaluated on Media thickness and noradrenaline- and calcium-sensitivity of isolated mesenteric resistance vessels. Increased calcium and noradrenaline sensitivity in spontaneously hypertensive rat resistance vessels is an intrinsic vascular smooth muscle defect independent of blood pressure.