Sympathetic cross-innervation of SHR and genetic controls suggests a trophic influence on vascular muscle membranes.

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Abstract
We have attempted to differentiate neural from humoral environmental factors as the cause of altered arterial muscle membrane properties in spontaneously hypertensive rats (SHR). This laboratory has previously reported that alterations in membrane electrical properties appear to be responsible for increased NE sensitivity in caudal arteries from SHR. In this study, caudal arteries were transplanted into innervated or denervated anterior eye chambers of the same (KNR in KNR, SHR in SHR) or the opposite (KNR in SHR, SHR in KNR) strain. Seven weeks later, we measured membrane potential (Em) and norepinephrine (NE) contractile sensitivity (EC50) in both transplanted and host caudal arteries. Caudal arteries from 2-week-old donor animals transplanted into hosts reinnervated and developed Em and NE EC50 values characteristic of the host strain, interconverting between SHR and KNR characteristics in cross-transplantations. In other experiments, the superior cervical ganglion ipsilateral to the transplanted eye chamber was removed 1 day before transplantation to eliminate the influence of sympathetic nerves. Em values were the same in transplants denied sympathetic innervation whether the arteries were transplanted into the same or opposite strains. Although denervation increased NE sensitivity of KNR caudal arteries, sensitivity of arteries from the SHR strain was unchanged. Therefore, without sympathetic reinnervation, there was no interconversion of Em or NE EC50 characteristics between SHR and KNR by cross-transplantation. These results suggest that neural factors control the development of membrane properties of vascular muscle. It appears that the sympathetic nervous system of the SHR has altered trophic influences that contribute importantly to altered membrane properties in hypertension.

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